An inorganic and water-soluble platinum complex. After undergoing hydrolysis, it reacts with DNA to produce both intra and interstrand crosslinks. These crosslinks appear to impair replication and transcription of DNA. The cytotoxicity of cisplatin correlates with cellular arrest in the G2 phase of the cell cycle.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
The use of two or more chemicals simultaneously or sequentially in the drug therapy of neoplasms. The drugs need not be in the same dosage form.
Platinum. A heavy, soft, whitish metal, resembling tin, atomic number 78, atomic weight 195.09, symbol Pt. (From Dorland, 28th ed) It is used in manufacturing equipment for laboratory and industrial use. It occurs as a black powder (platinum black) and as a spongy substance (spongy platinum) and may have been known in Pliny's time as "alutiae".
Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures.
Time schedule for administration of a drug in order to achieve optimum effectiveness and convenience.
A semisynthetic derivative of PODOPHYLLOTOXIN that exhibits antitumor activity. Etoposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent entry into the mitotic phase of cell division, and lead to cell death. Etoposide acts primarily in the G2 and S phases of the cell cycle.
Tumors or cancer of the LUNG.
Tumors or cancer of the OVARY. These neoplasms can be benign or malignant. They are classified according to the tissue of origin, such as the surface EPITHELIUM, the stromal endocrine cells, and the totipotent GERM CELLS.
The treatment of a disease or condition by several different means simultaneously or sequentially. Chemoimmunotherapy, RADIOIMMUNOTHERAPY, chemoradiotherapy, cryochemotherapy, and SALVAGE THERAPY are seen most frequently, but their combinations with each other and surgery are also used.
Antitumor alkaloid isolated from Vinca rosea. (Merck, 11th ed.)
The products of chemical reactions that result in the addition of extraneous chemical groups to DNA.
A pyrimidine analog that is an antineoplastic antimetabolite. It interferes with DNA synthesis by blocking the THYMIDYLATE SYNTHETASE conversion of deoxyuridylic acid to thymidylic acid.
A cyclodecane isolated from the bark of the Pacific yew tree, TAXUS BREVIFOLIA. It stabilizes MICROTUBULES in their polymerized form leading to cell death.
A cell line derived from cultured tumor cells.
Soft tissue tumors or cancer arising from the mucosal surfaces of the LIP; oral cavity; PHARYNX; LARYNX; and cervical esophagus. Other sites included are the NOSE and PARANASAL SINUSES; SALIVARY GLANDS; THYROID GLAND and PARATHYROID GLANDS; and MELANOMA and non-melanoma skin cancers of the head and neck. (from Holland et al., Cancer Medicine, 4th ed, p1651)
An organoplatinum compound that possesses antineoplastic activity.
Positional isomer of CYCLOPHOSPHAMIDE which is active as an alkylating agent and an immunosuppressive agent.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.
The forcible expulsion of the contents of the STOMACH through the MOUTH.
A carcinoma derived from stratified SQUAMOUS EPITHELIAL CELLS. It may also occur in sites where glandular or columnar epithelium is normally present. (From Stedman, 25th ed)
Methods of investigating the effectiveness of anticancer cytotoxic drugs and biologic inhibitors. These include in vitro cell-kill models and cytostatic dye exclusion tests as well as in vivo measurement of tumor growth parameters in laboratory animals.
A heterogeneous aggregate of at least three distinct histological types of lung cancer, including SQUAMOUS CELL CARCINOMA; ADENOCARCINOMA; and LARGE CELL CARCINOMA. They are dealt with collectively because of their shared treatment strategy.
A class of statistical procedures for estimating the survival function (function of time, starting with a population 100% well at a given time and providing the percentage of the population still well at later times). The survival analysis is then used for making inferences about the effects of treatments, prognostic factors, exposures, and other covariates on the function.
Antineoplastic antibiotic obtained from Streptomyces peucetius. It is a hydroxy derivative of DAUNORUBICIN.
The action of a drug in promoting or enhancing the effectiveness of another drug.
A group of diterpenoid CYCLODECANES named for the taxanes that were discovered in the TAXUS tree. The action on MICROTUBULES has made some of them useful as ANTINEOPLASTIC AGENTS.
The long-term (minutes to hours) administration of a fluid into the vein through venipuncture, either by letting the fluid flow by gravity or by pumping it.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
The relationship between the dose of an administered drug and the response of the organism to the drug.
Period after successful treatment in which there is no appearance of the symptoms or effects of the disease.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
Tumors or cancer of the TESTIS. Germ cell tumors (GERMINOMA) of the testis constitute 95% of all testicular neoplasms.
An unpleasant sensation in the stomach usually accompanied by the urge to vomit. Common causes are early pregnancy, sea and motion sickness, emotional stress, intense pain, food poisoning, and various enteroviruses.
An antineoplastic antibiotic produced by Streptomyces caespitosus. It is one of the bi- or tri-functional ALKYLATING AGENTS causing cross-linking of DNA and inhibition of DNA synthesis.
The proportion of survivors in a group, e.g., of patients, studied and followed over a period, or the proportion of persons in a specified group alive at the beginning of a time interval who survive to the end of the interval. It is often studied using life table methods.
An alkaloid isolated from the stem wood of the Chinese tree, Camptotheca acuminata. This compound selectively inhibits the nuclear enzyme DNA TOPOISOMERASES, TYPE I. Several semisynthetic analogs of camptothecin have demonstrated antitumor activity.
Methods which attempt to express in replicable terms the extent of the neoplasm in the patient.
Vinblastine derivative with antineoplastic activity against CANCER. Major side effects are myelosuppression and neurotoxicity. Vindesine is used extensively in chemotherapy protocols (ANTINEOPLASTIC COMBINED CHEMOTHERAPY PROTOCOLS).
A malignant epithelial tumor with a glandular organization.
The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.
Antagonist of urate oxidase.
Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION. These deviations may be caused by physical or chemical agents and occur by natural or unnatural, introduced circumstances. They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR). If the damage is extensive, it can induce APOPTOSIS.
An anaplastic, highly malignant, and usually bronchogenic carcinoma composed of small ovoid cells with scanty neoplasm. It is characterized by a dominant, deeply basophilic nucleus, and absent or indistinct nucleoli. (From Stedman, 25th ed; Holland et al., Cancer Medicine, 3d ed, p1286-7)
A decrease in the number of NEUTROPHILS found in the blood.
A complex of related glycopeptide antibiotics from Streptomyces verticillus consisting of bleomycin A2 and B2. It inhibits DNA metabolism and is used as an antineoplastic, especially for solid tumors.
Congener of FLUOROURACIL with comparable antineoplastic action. It has been suggested especially for the treatment of breast neoplasms.
Tumors or cancer of the STOMACH.
Neoplasms composed of primordial GERM CELLS of embryonic GONADS or of elements of the germ layers of the EMBRYO, MAMMALIAN. The concept does not refer to neoplasms located in the gonads or present in an embryo or FETUS.
Agents obtained from higher plants that have demonstrable cytostatic or antineoplastic activity.
The reconstruction of a continuous two-stranded DNA molecule without mismatch from a molecule which contained damaged regions. The major repair mechanisms are excision repair, in which defective regions in one strand are excised and resynthesized using the complementary base pairing information in the intact strand; photoreactivation repair, in which the lethal and mutagenic effects of ultraviolet light are eliminated; and post-replication repair, in which the primary lesions are not repaired, but the gaps in one daughter duplex are filled in by incorporation of portions of the other (undamaged) daughter duplex. Excision repair and post-replication repair are sometimes referred to as "dark repair" because they do not require light.
A malignant neoplasm of the germinal tissue of the GONADS; MEDIASTINUM; or pineal region. Germinomas are uniform in appearance, consisting of large, round cells with vesicular nuclei and clear or finely granular eosinophilic-staining cytoplasm. (Stedman, 265th ed; from DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, pp1642-3)
Any process by which toxicity, metabolism, absorption, elimination, preferred route of administration, safe dosage range, etc., for a drug or group of drugs is determined through clinical assessment in humans or veterinary animals.
The local recurrence of a neoplasm following treatment. It arises from microscopic cells of the original neoplasm that have escaped therapeutic intervention and later become clinically visible at the original site.
Diminished or failed response of an organism, disease or tissue to the intended effectiveness of a chemical or drug. It should be differentiated from DRUG TOLERANCE which is the progressive diminution of the susceptibility of a human or animal to the effects of a drug, as a result of continued administration.
Tumors or cancer of the ESOPHAGUS.
A tumor derived from mesothelial tissue (peritoneum, pleura, pericardium). It appears as broad sheets of cells, with some regions containing spindle-shaped, sarcoma-like cells and other regions showing adenomatous patterns. Pleural mesotheliomas have been linked to exposure to asbestos. (Dorland, 27th ed)
Drug therapy given to augment or stimulate some other form of treatment such as surgery or radiation therapy. Adjuvant chemotherapy is commonly used in the therapy of cancer and can be administered before or after the primary treatment.
Drugs used to prevent NAUSEA or VOMITING.
New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.
The highest dose of a biologically active agent given during a chronic study that will not reduce longevity from effects other than carcinogenicity. (from Lewis Dictionary of Toxicology, 1st ed)
An anthracycline which is the 4'-epi-isomer of doxorubicin. The compound exerts its antitumor effects by interference with the synthesis and function of DNA.
Neoplasms of the thin serous membrane that envelopes the lungs and lines the thoracic cavity. Pleural neoplasms are exceedingly rare and are usually not diagnosed until they are advanced because in the early stages they produce no symptoms.
Tumors or cancer of the URINARY TRACT in either the male or the female.
A subnormal level of BLOOD PLATELETS.
A competitive serotonin type 3 receptor antagonist. It is effective in the treatment of nausea and vomiting caused by cytotoxic chemotherapy drugs, including cisplatin, and has reported anxiolytic and neuroleptic properties.
Mutant mice homozygous for the recessive gene "nude" which fail to develop a thymus. They are useful in tumor studies and studies on immune responses.
A phosphorothioate proposed as a radiation-protective agent. It causes splenic vasodilation and may block autonomic ganglia.
A malignant neoplasm made up of epithelial cells tending to infiltrate the surrounding tissues and give rise to metastases. It is a histological type of neoplasm but is often wrongly used as a synonym for "cancer." (From Dorland, 27th ed)
Antimetabolites that are useful in cancer chemotherapy.
Nuclear phosphoprotein encoded by the p53 gene (GENES, P53) whose normal function is to control CELL PROLIFERATION and APOPTOSIS. A mutant or absent p53 protein has been found in LEUKEMIA; OSTEOSARCOMA; LUNG CANCER; and COLORECTAL CANCER.
Precursor of an alkylating nitrogen mustard antineoplastic and immunosuppressive agent that must be activated in the LIVER to form the active aldophosphamide. It has been used in the treatment of LYMPHOMA and LEUKEMIA. Its side effect, ALOPECIA, has been used for defleecing sheep. Cyclophosphamide may also cause sterility, birth defects, mutations, and cancer.
Inorganic compounds which contain platinum as the central atom.
Drugs used to potentiate the effectiveness of radiation therapy in destroying unwanted cells.
Initial drug treatment designed to bring about REMISSION INDUCTION. It is typically a short-term and high-dose drug treatment that is followed by CONSOLIDATION CHEMOTHERAPY and then MAINTENANCE CHEMOTHERAPY.
Preliminary cancer therapy (chemotherapy, radiation therapy, hormone/endocrine therapy, immunotherapy, hyperthermia, etc.) that precedes a necessary second modality of treatment.
Disorders of the blood and blood forming tissues.
Tumors or cancer of the UTERINE CERVIX.
A sarcoma originating in bone-forming cells, affecting the ends of long bones. It is the most common and most malignant of sarcomas of the bones, and occurs chiefly among 10- to 25-year-old youths. (From Stedman, 25th ed)
Therapeutic act or process that initiates a response to a complete or partial remission level.
Inorganic salts of thiosulfuric acid possessing the general formula R2S2O3.
Administration of the total dose of radiation (RADIATION DOSAGE) in parts, at timed intervals.

Tumour ablation and hepatic decompensation rates in multi-agent chemoembolization of hepatocellular carcinoma. (1/7975)

Thirty-seven cirrhotic patients with 62 hepatocellular carcinoma (HCC) foci--most Child-Pugh class B or C and/or with large, inoperable tumours--underwent 148 sessions of transcatheter arterial chemoembolization (TACE) using lipiodol, doxorubicin and cisplatin. Treatment efficacy was assessed by serial hepatic arteriography in 34/37 (91.9%) patients and abdominal CT scanning in 3/37 (8.1%) patients. Child-Pugh status was determined prior to each treatment session. Varying degrees of control of tumour neovascularity occurred for a median 390 days (range 90 to > 1680 days) in 33/34 (97.1%) patients in whom progress hepatic arteriography was performed. Ablation of tumour neovascularity occurred in 6/6 (100%), 4/12 (33.3%) and 6/16 (37.5%) patients with HCC diameters < 4 cm, 4-7 cm and > 8 cm, respectively (p < 0.02). Significantly more sessions were required for ablation of larger tumours (p < 0.05). Recurrent HCC was detected in 50% of patients after a median 240 days (range 60-1120 days). Deterioration in Child-Pugh status followed a session of TACE on 19/148 (12.8%) occasions but resulted in unscheduled hospitalization on only 4/148 (2.7%) occasions, the highest incidence (8.3%) in Child-Pugh C patients. Actuarial survival was 27/36 (75.0%) at 6 months, 17/34 (50.0%) at 12 months, 14/34 (41.2%) at 18 months, 9/31 (29.0%) at 24 months and 4/27 (14.8%) at 36 months. Multi-agent TACE with lipiodol, doxorubicin and cisplatin provides a useful anti-tumour effect, even in cirrhotic patients with large HCCs. The incidence of clinically significant deterioration in hepatic function due to ischaemia of non-tumorous liver is acceptably low, even in Child-Pugh C patients.  (+info)

Intensive weekly chemotherapy is not effective in advanced pancreatic cancer patients: a report from the Italian Group for the Study of Digestive Tract Cancer (GISCAD). (2/7975)

Twenty-two patients, with locally advanced unresectable and/or metastatic pancreatic carcinoma, received weekly administration of cisplatin 40 mg m(-2), 5-fluorouracil 500 mg m(-2), epidoxorubicin 35 mg m(-2), 6S stereoisomer of leucovorin 250 mg m(-2) and glutathione 1.5 mg m(-2), supported by a daily administration of lenograstim at a dose of 5 microg kg(-1). Nineteen patients were men and three were women. Median age was 63 years (range 47-70). At study entry, pain was present in 15 out of 22 patients (68%) with a mean value of Scott-Huskisson scale of 27.6+/-23.8, whereas a weight loss >10% was present in 15 patients. After eight weekly treatments, three partial responses were achieved for a response rate of 13% (95% CI 0-26%), five patients had stable disease and 14 progressed on therapy. Pain was present in 9 out of 22 patients (40%) with a mean value of Scott-Huskisson scale of 12.3+/-18.4. Eight patients (36%) (three partial response and five stable disease) had a positive weight change. Toxicity was mild: WHO grade III or IV toxicity was recorded in terms of anaemia in 7 out of 188 cycles (3.7%), of neutropenia in 9 out of 188 cycles (4.7%) and of thrombocytopenia in 3 out of 188 cycles (1.5%). Median survival of all patients was 6 months. The outcome of this intensive chemotherapy regimen does not support its use in pancreatic cancer.  (+info)

Role of dexamethasone dosage in combination with 5-HT3 antagonists for prophylaxis of acute chemotherapy-induced nausea and vomiting. (3/7975)

Dexamethasone (20 mg) or its equivalent in combination with 5-HT3 antagonists appears to be the gold-standard dose for antiemetic prophylaxis. Additional to concerns about the use of corticosteroids with respect to enhanced tumour growth or impaired killing of the tumour cells, there is evidence that high-dosage dexamethasone impairs the control of delayed nausea and emesis, whereas lower doses appear more beneficial. To come closer to the most adequate dose, we started a prospective, single-blind, randomized trial investigating additional dosage of 8 or 20 mg dexamethasone to tropisetron (Navoban), a 5-HT3 receptor antagonist, in cis-platinum-containing chemotherapy. After an interim analysis of 121 courses of chemotherapy in 69 patients, we have been unable to detect major differences between both treatment alternatives. High-dose dexamethasone (20 mg) had no advantage over medium-dose dexamethasone with respect to objective and subjective parameters of acute and delayed nausea and vomiting. In relation to concerns about the use of corticosteroids in non-haematological cancer chemotherapy, we suggest that 8 mg or its equivalent should be used in combination with 5-HT3 antagonists until further research proves otherwise.  (+info)

MycN sensitizes neuroblastoma cells for drug-induced apoptosis. (4/7975)

Amplification of the MYCN gene is found in a large proportion of neuroblastoma and considered as an adverse prognostic factor. To investigate the effect of ectopic MycN expression on the susceptibility of neuroblastoma cells to cytotoxic drugs we used a human neuroblastoma cell line harboring tetracycline-controlled expression of MycN. Neither conditional expression of MycN alone nor low drug concentrations triggered apoptosis. However, when acting in concert, MycN and cytotoxic drugs efficiently induced cell death. Apoptosis depended on mitochondrial permeability transition and activation of caspases, since the mitochondrion-specific inhibitor bongkrekic acid and the caspase inhibitor zVAD-fmk almost completely abrogated apoptosis. Loss of mitochondrial transmembrane potential and release of cytochrome c from mitochondria preceded activation of caspase-8 and caspase-3 and cleavage of PARP. CD95 expression was upregulated by treatment with cytotoxic drugs, while MycN cooperated with cytotoxic drugs to increase sensitivity to CD95-induced apoptosis and enhancing CD95-L expression. MycN overexpression and cytotoxic drugs also synergized to induce p53 and Bax protein expression, while Bcl-2 and Bcl-X(L) protein levels remained unchanged. Since amplification of MYCN is usually associated with a poor prognosis, these findings suggest that dysfunctions in apoptosis pathways may be a mechanism by which MycN-induced apoptosis of neuroblastoma cells is inhibited.  (+info)

A novel trinuclear platinum complex overcomes cisplatin resistance in an osteosarcoma cell system. (5/7975)

Multinuclear platinum compounds have been designed to circumvent the cellular resistance to conventional platinum-based drugs. In an attempt to examine the cellular basis of the preclinical antitumor efficacy of a novel multinuclear platinum compound (BBR 3464) in the treatment of cisplatin-resistant tumors, we have performed a comparative study of cisplatin and BBR 3464 in a human osteosarcoma cell line (U2-OS) and in an in vitro selected cisplatin-resistant subline (U2-OS/Pt). A marked increase of cytotoxic potency of BBR 3464 in comparison with cisplatin in U2-OS cells and a complete lack of cross-resistance in U2-OS/Pt cells were found. A detailed analysis of the cisplatin-resistant phenotype indicated that it was associated with reduced cisplatin accumulation, reduced interstrand cross-link (ICL) formation and DNA platination, microsatellite instability, and reduced expression of the DNA mismatch repair protein PMS2. Despite BBR 3464 charge and molecular size, in U2-OS and U2-OS/Pt cells, BBR 3464 accumulation and DNA-bound platinum were much higher than those observed for cisplatin. In contrast, the frequency of ICLs after exposure to BBR 3464 was very low. The time course of ICL formation after drug removal revealed a low persistence of these types of DNA lesions induced by BBR 3464, in contrast to an increase of DNA lesions induced by cisplatin, suggesting that components of the DNA repair pathway handle the two types of DNA lesions differently. The cellular response of HCT116 mismatch repair-deficient cells was consistent with a lack of influence of mismatch repair status on BBR 3464 cytotoxicity. Because BBR 3464 produces high levels of lesions different from ICLs, likely including intra-strand cross-links and monoadducts, the ability of the triplatinum complex to overcome cisplatin resistance appears to be related to a different mechanism of DNA interaction (formation of different types of drug-induced DNA lesions) as compared with conventional mononuclear complexes rather than the ability to overcome specific cellular alterations.  (+info)

Testicular cancer: an oncological success story. (6/7975)

Testicular cancer has become a model for a curable neoplasm. Our studies with cisplatin combination chemotherapy allow us to conclude that: (a) short-duration intensive induction therapy with the most active agents in optimal dosage is more important than maintenance therapy; (b) modest dose escalation increases toxicity without improving therapeutic efficacy; (c) it is possible to develop curative salvage therapy for refractory germ cell tumors; and (d) preclinical models predicting synergism, such as vinblastine + bleomycin or cisplatin + etoposide have clinical relevance. Finally, testicular cancer has also become a model for new drug development. Cisplatin was approved by the Food and Drug Administration for testis and ovarian cancer, and etoposide and ifosfamide were approved for refractory germ cell tumors. The success of these studies confirms the importance of the continued search for new investigational drugs in all solid tumors.  (+info)

Multimodality therapy for locally advanced and limited stage IV breast cancer: the impact of effective non-cross-resistance late-consolidation chemotherapy. (7/7975)

To determine the effectiveness of non-cross-resistant late-consolidation chemotherapy in locally advanced breast cancer (LABC) and stage IV breast cancer, we review our experience with two regimens. Between 1985 and 1991, we enrolled 56 patients with LABC, who were treated with a doxorubicin-based adjuvant regimen, followed by a late-consolidation non-cross-resistant regimen containing methotrexate, 5-fluorouracil, cisplatin, and cyclophosphamide. Between 1985 and 1996, a total of 45 patients with limited stage IV breast cancer underwent surgical excision of all evaluable disease, making them metastatic (stage IV) with no evaluable disease. Surgery was followed by a doxorubicin-containing regimen and then a late-consolidation non-cross-resistant regimen, which was either methotrexate, 5-fluorouracil, cisplatinum, and cyclophosphamide or 5-fluorouracil, mitomycin, etoposide, and cisplatin. Twenty-four patients with limited bone metastases that were unresectable were treated with a doxorubicin-containing regimen, radiation therapy to all sites of disease, and then one of the two late non-cross-resistant regimens. With a median follow-up of 84 months, 78% of patients with LABC are alive, and 68% are free of disease. After a median follow-up of 44 months, 53% of patients with stage IV with no evaluable disease are alive and free of disease. The use of non-cross-resistant late-consolidation chemotherapy is an effective strategy in the treatment of patients with LABC and selected patients with limited stage IV breast cancer.  (+info)

Modification of non-conservative double-strand break (DSB) rejoining activity after the induction of cisplatin resistance in human tumour cells. (8/7975)

The induction of collateral radioresistance after the development of cisplatin resistance is a well-documented phenomenon; however, the exact processes that are responsible for the cisplatin-induced radioresistance remain to be elucidated. There was no obvious difference in the level of radiation-induced DNA double strand breaks (DSBs), in DSB rejoining rates, or the level of the catalytic subunit of the DNA-dependent protein kinase (DNA-PKcs) in the cisplatin- and radiation-sensitive 2780/WT and cisplatin-resistant 2780/CP cell lines. However, there was a significantly (P < 0.01) lower level of DSB misrejoining activity within nuclear protein extracts derived from the cisplatin- and radiation-sensitive 2780/WT and OAW42/WT tumour cell lines than in similar extracts from their cisplatin- (and radiation-) resistant 2780/CP and OAW42/CP counterparts. All of the DSB misrejoining events involved deletions of between 134 and 444 bp that arose through illegitimate recombination at short repetitive sequences, such as those that arise through non-homologous repair (NHR). These data further support the notion that the radiosensitivity of DSB repair proficient human tumour cell lines may be partly determined by the predisposition of these cell lines to activate non-conservative DSB rejoining pathways. Furthermore, our data suggest that the induction of acquired cisplatin resistance is associated with a two- to threefold decrease in the activity of a non-conservative DSB rejoining mechanism that appears to be a manifestation of NHR.  (+info)

TY - JOUR. T1 - O6-methylguanine DNA methyltransferase repairs platinum-DNA adducts following cisplatin treatment and predicts prognoses of nasopharyngeal carcinoma. AU - Chen, Shang Hung. AU - Kuo, Ching Chuan. AU - Li, Chien Feng. AU - Cheung, Chun Hei Antonio. AU - Tsou, Tsui Chun. AU - Chiang, Huai Chih. AU - Yang, Yun Ning. AU - Chang, Shin Lun. AU - Lin, Li Ching. AU - Pan, Hsin Yi. AU - Chang, Kwang Yu. AU - Chang, Jang Yang. PY - 2015/9/1. Y1 - 2015/9/1. N2 - Cisplatin (CDDP) is an important anti-cancer drug commonly used in various human cancers, including nasopharyngeal carcinoma (NPC). How to overcome the drug resistance of CDDP provides opportunities to improve clinical outcomes of NPC. O6-methylguanine-DNA methyltransferase (MGMT) has been well-characterized to be a therapeutic determinant of O6-alkylguanine alkylating drugs. However, the underlying mechanism and clinical relevance between MGMT and CDDP remain poorly defined in NPC. In this study, we showed that MGMT-proficient ...
Ovarian cancer is the leading cause of death from gynecologic cancer in women worldwide. According to the National Cancer Institute, ovarian cancer has the highest mortality rate among all the reproductive cancers in women. Advanced stage diagnosis and chemo/radio-resistance is a major obstacle in treating advanced ovarian cancer. The most commonly employed chemotherapeutic drug for ovarian cancer treatment is cis-platin. As with most chemotherapeutic drugs, many patients eventually become resistant to cis-platin and therefore, diminishing its effect. The efficacy of current treatments may be improved by increasing the sensitivity of cancer cells to chemo/radiation therapies. The present study is focused on identifying the differential expression of regulatory microRNAs (miRNAs) between cis-platin sensitive (A2780), and cis-platin resistant (A2780/CP70) cell lines. Cell proliferation assays were conducted to test the sensitivity of the two cell lines to cis-platin. Differential expression patterns of
The aim of this work is to clarify the effect of curcumin and beta-carotene on cisplatin-induced tissue damage and to demonstrate the potential of Raman spectroscopy to detect tissue changes consistent with liver and kidney histopathology as a potential diagnostic adjunct. In the study, 56 Wistar albino female rats were used and randomly divided into 7 groups (n:8). Sham group received only sesame oil; Cisplatin group, received a single dose injection of cisplatin; Beta-carotene group, treated with beta-carotene orally; Cisplatin + Beta-carotene group, pretreated with beta-carotene 30 min prior to the cisplatin injection, then received cisplatin; Curcumin group, orally treated with curcumin; Cisplatin + Curcumin group, pretreated with curcumin 30min prior to the cisplatin injection, then received cisplatin. The second application was performed 1 week after the first application. One of the liver and kidney tissues was taken to 10% form for histopathological examinations and the others were taken ...
Salmon sperm DNA, treated with the antitumor agent cis-diamminedichloroplatinum(II) (cis-DDP), was enzymatically degraded to (oligo)nucleotides. Four Pt-containing products were identified by 1H NMR after preparative chromatography on a diethylaminoethyl-Sephacel column at pH 8.8. In all identified …
TY - JOUR. T1 - Ras-mediated activation of ERK by cisplatin induces cell death independently of p53 in osteosarcoma and neuroblastoma cell lines. AU - Woessmann, Willi. AU - Chen, Xinbin. AU - Borkhardt, Arndt. PY - 2002. Y1 - 2002. N2 - Activation of the mitogen-activated protein kinases ERK1/2 by the chemotherapeutic agent cisplatin has been shown to result in either survival or cell death. The downstream mediators of these opposing effects are unknown, as are the upstream signaling molecules. Activation of ERK is required for accumulation and phosphorylation of p53 following cisplatin treatment. We studied the role of ERK activation after cisplatin treatment under p53-negative and p53-positive conditions using a tetracycline-dependent expression vector in Saos-2 osteosarcoma cells. Dose-dependent activation of ERK first occurred 3-6 h after a 2-h cisplatin incubation and declined after 12-24 h in several tumor cell lines. Incubation of cell lines with the MEK1 inhibitors PD98059 or UO126 ...
Cisplatin-based chemotherapy is recommended as the primary treatment for advanced bladder cancer (BC) with unresectable or metastatic disease. However, the benefits are limited due to the acquisition of drug resistance. The mechanisms of resistance remain unclear. Although there are some reports that some molecules are associated with cisplatin resistance in advanced BC, those reports have not been fully investigated. Therefore, we undertook a new search for cisplatin resistance-related genes targeted by tumor suppressive microRNAs as well as genes that were downregulated in cisplatin-resistant BC cells and clinical BC tissues. First, we established cisplatin-resistant BOY and T24 BC cell lines (CDDP-R-BOY, CDDP-R-T24). Then, Next Generation Sequence analysis was performed with parental and cisplatin-resistant cell lines to search for the microRNAs responsible for cisplatin resistance. We conducted gain-of-function analysis of microRNAs and their effects on cisplatin resistance, and we searched target
TY - JOUR. T1 - The effects of the antioxidant α-tocopherol succinate on cisplatin-induced ototoxicity in HEI-OC1 auditory cells. AU - Kim, Sung Kyun. AU - Im, Gi Jung. AU - An, Yun Suk. AU - Lee, Se Hee. AU - Jung, Hak Hyun. AU - Park, Sang Yoo. PY - 2016/7/1. Y1 - 2016/7/1. N2 - Conclusion: D-α-tocopherol succinate significantly reduced a cisplatin-induced hair cell loss in HEI-OC1 cell lines. These effects were mediated by its scavenging activity against reactive oxygen species (ROS) and inhibition of apoptosis. Objectives: Alpha-tocopherol is a class of methylated phenols, known as fat-soluble antioxidants, and is a different form of vitamin E, which reduces free radicals and acts as an antioxidant. We hypothesized that the antioxidative effect of α-tocopherol could protect against cisplastin-induced cytotoxicity, and thus evaluated its effects on cisplatin-induced ototoxicity in HEI-OC1 auditory cells. Methods: HEI-OC1 cells were pretreated with D-α-tocopherol succinate at a ...
In the present work, we studied the molecular mechanisms by which sodium butyrate sensitizes cancer cells towards cisplatin. HeLa cells were treated with 5 mM butyrate, with 8 μM cis-diaminedichloroplatinum II (cisplatin), or with both. Cells treated with both agents showed approximately two-fold increase of the mortality rate in comparison with cells treated with cisplatin only. Accordingly, the life span of albino mice transfected with Ehrlich ascites tumor was prolonged almost two-fold by treatment with cisplatin and butyrate in comparison with cisplatin alone. This showed that the observed synergism of cisplatin and butyrate was not limited to specific cell lines or in vitro protocols, but was also expressed in vivo during the process of tumor development. DNA labeling and fluorescence activated cell sorting experiments showed that cisplatin treatment inhibited DNA synthesis and arrested HeLa cells at the G1/S transition and early S phase of the cell cycle. Western blotting and chromatin ...
Background: Cisplatin is a commonly used anti-cancer drug. However, its use is associated with severe side effects including ototoxicity that affects a large fraction of cisplatin-treated patients. Approved therapies that reduce cisplatin-induced ototoxicity are lacking. Among the candidate therapeutics, dexamethasone stands out. There is extensive experience of its use in combination with cisplatin for the prevention of chemotherapy-induced nausea and vomiting indicating that dexamethasone does not affect the anti-cancer effects of cisplatin. Objective: The objective of this study is to assess the potential of dexamethasone for the prevention of cisplatin-induced ototoxicity by a systematic analysis of the available evidence. Results: We identified 16 relevant original research articles. The analyzed studies reported conflicting results on the effects of dexamethasone on cisplatin-induced ototoxicity. However, studies in which dexamethasone was used prior to cisplatin treatment and directly ...
Our study analyzes the effect of magnesium supplementation on nephrotoxicity in patients receiving cisplatin for head and neck cancer. We retrospectively reviewed the medical records of patients with head and neck cancer who received two doses of cisplatin (80 mg/m2) and 5-fluorouracil (800 mg/m2) 3 weeks apart from August 2008 to October 2012. The regimen prior to 2011 (crystalloid-only) involved the administration of 1000 mL of lactated Ringers solution on the day prior to cisplatin infusion and 2000 mL of continuous infusion of saline on the day of cisplatin infusion. The regimen after 2011 (magnesium-supplemented) did not involve hydration on the day before cisplatin administration but used 1000 mL of 0.9% saline with magnesium sulfate (20 mEq) administered for 3 hours before cisplatin infusion. Sixty-five patients were treated with the crystalloid-only regimen and 56 patients with the magnesium-supplemented regimen. The mean creatinine clearance in the magnesium-supplemented group decreased by 4.9
Although modest improvements in the survival of patients with non-small cell lung cancer (NSCLC) can be achieved with cisplatin-based chemotherapy (CT), its value is disputed in the geriatric setting. In this study, we evaluate the feasibility of vinorelbine/cisplatin CT for elderly NSCLC patients. In this pilot phase I/II trial, all patients received CT with vinorelbine 25 mg/m2, on day 1 and 8, and cisplatin on day 1, in 28 days-cycles. After stratification for age (up to 75 years), younger patients were sequentially allocated to moderate cisplatin doses (80 mg/m2 or 90 mg/m2), and older patients were allocated to lower cisplatin doses (60 mg/m2 or 70 mg/m2). We recruited patients aged over 70 years with newly diagnosed NSCLC, clinical stage III or IV, Karnofsky performance status ≥ 70%, normal serum creatinine, peripheral neuropathy ≤ grade 1, and no prior cancer therapy. Analysis was by intention to treat. Main toxicities (grade 3-4) was as follows: neutropenia, 20%; anemia, 11%; and
The efficacy of the widely used chemotherapeutic drug cisplatin is limited by the occurrence of drug-resistant tumour cells. To fully exploit the potential of this drug in cancer therapy, it is imperative to understand the molecular basis of cisplatin resistance. Using an insertional mutagenesis technique in cells of Dictyostelium discoideum, we have identified six genes which are involved in cisplatin resistance. None of these genes has been previously linked to resistance to this drug. Several of these genes encode proteins that are involved in signal transduction pathways which regulate cell death, cell proliferation or gene regulation. The resistance of these mutant strains is specific for cisplatin, since deletion of these genes does not confer resistance to other DNA-damaging agents. Significantly, the disruption of three of these genes, encoding the sphingosine-1-phosphate lyase, the RegA cAMP phosphodiesterase and a phosphatidylinositol-4-phosphate 5-kinase, also results in abnormalities in the
TY - JOUR. T1 - The mTORC2 Component Rictor Contributes to Cisplatin Resistance in Human Ovarian Cancer Cells. AU - Im-aram, Akechai. AU - Farrand, Lee. AU - Bae, Seung Min. AU - Song, Gwonhwa. AU - Song, Yong Sang. AU - Han, Jae Yong. AU - Tsang, Benjamin K.. PY - 2013/9/23. Y1 - 2013/9/23. N2 - Resistance to cisplatin-based therapy is a major cause of treatment failure in human ovarian cancer. A better understanding of the mechanisms of cisplatin resistance will offer new insights for novel therapeutic strategies for this deadly disease. Akt and p53 are determinants of cisplatin sensitivity. Rictor is a component of mTOR protein kinase complex 2, which is required for Akt phosphorylation (Ser473) and full activation. However, the precise role of rictor and the relationship between rictor and p53 in cisplatin resistance remains poorly understood. Here, using sensitive wild-type p53 (OV2008 and A2780s), resistant wild-type p53 (C13* and OVCAR433), and p53 compromised (A2780cp, OCC1, and SKOV-3) ...
The DNA-binding inorganic compound cisplatin is one of the most successful anticancer drugs. The detailed mechanism by which cells recognize and process cisplatin−DNA damage is of great interest. Although the family of proteins that bind cisplatin 1,2- and 1,3-intrastrand cross-links has been identified, much less is known about cellular protein interactions with cisplatin interstrand cross-links (ICLs). In order to address this question, a photoreactive analogue of cisplatin, PtBP[subscript 6], was used to construct a DNA duplex containing a site-specific platinum ICL. This DNA probe was characterized and used in photo-cross-linking experiments to separate and identify nuclear proteins that bind to the ICL by peptide mass fingerprint analysis. Several such proteins were discovered, including PARP-1, hMutSβ, DNA ligase III, XRCC1, and PNK. The photo-cross-linking approach was independently validated by an electrophoretic mobility shift assay demonstrating hMutSβ binding to a cisplatin ICL. ...
TY - JOUR. T1 - erbB-2 Signaling Enhances Cisplatin-induced Cytotoxicity in Human Breast Carcinoma Cells. T2 - Association between an Oncogenic Receptor Tyrosine Kinase and Drug-induced DNA Repair. AU - Arteaga, Carlos L.. AU - Winnier, Angela R.. AU - Hurd, Stephen D.. AU - Stewart, Stanford J.. PY - 1994/7/15. Y1 - 1994/7/15. N2 - The c-erbB-2 (HER-2/neu) protooncogene encodes an Mr 185,000 transmembrane glycoprotein with intrinsic tyrosine kinase activity. Agonistic antibodies against pl85c-erbB-2 enhance the cytotoxic effect of the DNA alkylator, cisplatin, against c-erB-2-overexpressing human carcinoma cells (Hancock et al., Cancer Res., 51: 4575-4580,1991). We have studied the possible association between receptor signal transduction and cispla-tin-mediated cytotoxicity utilizing the SKBR-3 human breast cancer cell line and the anti-pl85 TAb 250 IgGl. TAb 250 induced tyrosine phosphorylation of pl85 and the receptor substrate phospholipase C-yl, as well as rapid association of these ...
The efficacy of treatment with a combination of radiotherapy and chemotherapy in the yeast Saccharomyces cerevisiae as suitable eukaryotic model is demonstrated by following the induction and repair of DNA double-strand breaks. These may be induced by ionizing radiation. Furthermore, the chemotherapeutic agent cisplatin may induce DNA double-strand breaks through cellular repair mechanisms. The aim of this study is to investigate the induction and repair of DNA double-strand breaks after a combination of treatment with cisplatin and radiation versus radiation alone under hypoxic conditions.The number of induced double-strand breaks caused by radiation under hypoxic conditions is dependent on dose. Following combined treatment with cisplatin and radiation, the radiation-induced double-strand breaks simply add to those induced by cisplatin. We identified no difference in the repair kinetics of double-strand breaks following radiation between cells treated with cisplatin and those not treated with ...
Malignant pleural mesothelioma (MPM) is an aggressive malignant tumor in which cisplatin therapy is commonly used, although its effectiveness is limited. It follows that research efforts dedicated to identify promising combinations that can synergistically kill cancer cells are needed. Because we recently demonstrated that ADP inhibits the proliferation of ZL55 cells, an MPM-derived cell line obtained from bioptic samples of asbestos-exposed patients. Our objective in this study was to investigate the hypothesis that ADP also potentiates the cytotoxic activity of cisplatin. Results show that in ZL55 cells ADP enhanced (a) the cytotoxicity of cisplatin by 12-fold, (b) the restraint of cell clonogenic potential cisplatin-mediated, and (c) the number of apoptotic cells. Cisplatin, but not ADP, caused caspases activation; nevertheless, poly(ADP-ribose) polymerase-1 was not only cleaved in cisplatin-treated cells but also in cells treated with ADP alone. Furthermore, ADP, but not cisplatin, decreased ...
This study assigned subjects to either cisplatin/vinorelbine or cisplatin/pemetrexed chemotherapy using a genomic based expression profile to determine chemotherapy sensitivity in completely resected early stage non-squamous non-small-cell lung cancer (NSCLC). The vinorelbine-sensitive tumors group received Vinorelbine followed by cisplatin, while the pemetrexed-sensitive tumors group received pemetrexed followed by cisplatin. The primary objective of this trial was to determine whether genomic-based adjuvant chemotherapy treatment increased the 2-year progression-free survival rate in completely resected patients with NSCLC compared to historic controls. Secondary objectives included: 1) estimation of the percentage of completely resected NSCLC tumors that can be adequately analyzed and used to direct specific adjuvant chemotherapy; 2) estimation of the proportion of patients who are assigned to treatment with vinorelbine and pemetrexed; 3) evaluation of drug sensitivity patterns of cisplatin ...
TY - JOUR. T1 - Epidermal Growth Factor Protects Squamous Cell Carcinoma against Cisplatin-Induced Cytotoxicity through Increased Interleukin-1β Expression. AU - Ko, Shian Chin. AU - Huang, Chi Ruei. AU - Shieh, Jiunn Min. AU - Yang, Jhen Hong. AU - Chang, Wen Chang. AU - Chen, Ben Kuen. PY - 2013/2/1. Y1 - 2013/2/1. N2 - The expression of cytokines, such as IL-1β, and the activation of the epidermal growth factor receptor (EGFR) are crucial regulators in the process of carcinogenesis. The correlation between growth factor and activated cytokine signals in the control of tumor development is a critical issue to be clarified. In our study, we found that the IL-1β gene and protein expression were induced by EGF in squamous cell carcinoma. To clarify the mechanism involved in EGF-regulated IL-1β expression, we examined the transcriptional activity and mRNA stability of IL-1β in EGF-treated cells. We found that EGF induced the expression of IL-1β and was mediated through transcriptional ...
This study determined the in vitro permeability of cisplatin through isolated human sclera as delivered by a collagen matrix vehicle. Short-term and long-term intraocular levels of cisplatin were also measured in the rabbit eye after a subconjunctival injection. Cisplatin in either a collagen matrix vehicle or a control balanced salt solution (BSS) vehicle was applied to human sclera mounted in a specially designed in vitro perfusion chamber. The amount of cisplatin that diffused across the sclera was measured in hourly samples for 24 h using atomic absorption spectrometry. In vivo studies were also performed in Dutch Belted rabbits given subconjunctival injections of cisplatin in collagen matrix or in BSS. Eyes were enucleated at 1.5 h and 2 weeks after injection, frozen, and dissected to determine the intraocular cisplatin concentrations. Cisplatin had a peak in vitro scleral permeability constant of 8.3+/-1.2 x 10(-6) and 20.1+/-1.8 x 10(-6) cm/s, delivered in collagen matrix and in BSS, respectively
The mechanisms underlying the proapoptotic effect of the chemotherapeutic agent, cisplatin, are undefined largely. MAPK-dependent system. Cisplatin treatment coupled with particular inhibitors to each MAPK pathway (c-Jun N-terminal kinase, extracellular signal-regulated kinase, and p38) led to reduced ATF3 induction on the proteins level. MAPK pathway inhibition resulted in reduced ATF3 messenger RNA appearance and decreased cytotoxic ramifications of cisplatin as assessed with the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide cell viability assay. In A549 lung carcinoma cells, concentrating on ATF3 with specific little hairpin RNA attenuated the cytotoxic ramifications of cisplatin also. Likewise, ATF3-/- murine embryonic fibroblasts (MEFs) had been been shown to be much less delicate to cisplatin-induced cytotoxicity weighed against ATF3+/+ MEFs. This research recognizes cisplatin being a MAPK pathway-dependent inducer of ATF3, whose expression influences cisplatins cytotoxic ...
Gemcitabine and cisplatin treatment were administered to patients with advanced-stage, non-small-cell lung cancer. During phase II studies, the treatment is performed using a 28-day cycle, with gemcitabine administered on days 1, 8, and 15. Although it is advised that cisplatin not be administered...
Cisplatin is the main chemotherapeutic drug for the treatment of cervical cancers, however resistance to cisplatin is increasingly common and therefore has limited the efficacy and use of this drug in the clinic. Dose-dependent toxicity poses an additional challenge since patients suffer long-term and often permanent side-effects after treatment. Bcl-2 up-regulation has been implicated in the resistance to cisplatin in a variety of cancer cell lines, however its role in cervical cancer is confounding. A low, non-cytotoxic concentration of cisplatin was used in the treatment of HeLa and CaSki cells. Bcl-2 expression was determined through Western blotting and immunocytochemistry before and after treatment with cisplatin. To assess the reliance of the cervical cancer cells on Bcl-2 in the presence of cisplatin, Bcl-2 knock-down was achieved through RNA interference, where after apoptosis was assessed through PARP cleavage (Western blotting), Caspase activity (Caspase-Glo©) and PI inclusion analysis (Flow
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Background: The cisplatin resistance of non-small cell lung cancer (NSCLC) patients results in low response rate and overall survival rate. Exosomes contribute to pathological processes of multiple cancers. Objective: In this study, we explored the function and mechanisms of exosomal miR-103a-3p derived from cancer-associated fibroblast (CAF) in cisplatin resistance in NSCLC. Results: MiR-103a-3p was highly expressed in CAFs and CAF exosomes, and exosomal miR-103a-3p derived from CAFs in NSCLC. CAFs exosomes co-cultured with NSCLC cells promoted miR-103a-3p expression both in NSCLC cells and its exosomes. Functional experiments showed that exo-miR-103a-3p derived from CAFs promoted cisplatin resistance and inhibited apoptosis in NSCLC cells. Pumilio2 (Pum2) bound with miR-103a-3p in cytoplasm and nucleus, and facilitated packaging into CAF-derived exosomes in NSCLC cells. Further analysis showed Bak1 was a direct target of miR-103a-3p, and miR-103a-3p accelerated cisplatin resistance in NSCLC cells via
As a dose-response relationship has been suggested for cisplatin, it appeared attractive to explore high-dose-intensity regimens in non-small-cell lung cancer. In a phase I study of weekly administration of cisplatin combined with oral etoposide we achieved a cisplatin dose intensity of 52.5-60 mg/m2 per week in most patients. We subsequently explored this regimen in advanced non-small-cell lung cancer. Patients were treated with cisplatin infused at 70 mg/m2 on days 1, 8, 15 and 29, 36, 43 in combination with oral etoposide given at 50 mg on days 1-15 and 29-43. Patients showing stable disease or a better response were continued on treatment with oral etoposide given at 50 mg/m2 per day on days 1-21 every 28 days for a maximum of four cycles. In all, 22 patients with stage III disease and 31 patients with stage IV disease entered the study. The median number of cisplatin administration was 6 per patient; 17 patients reached the planned cisplatin dose intensity of 60 mg/m2 per week, 11 patients ...
TY - JOUR. T1 - Peripheral neuroglial death induced by cisplatin administration in newborn rats. AU - Sugimoto, Tomosada. AU - Takeyama, Akihiro. AU - Fujita, Masako. AU - Ichikawa, Hiroyuki. AU - Takano-Yamamoto, Teruko. PY - 2001/1/22. Y1 - 2001/1/22. N2 - To determine the target of cytotoxicity of cisplatin (CDDP), we injected newborn rats with 2mg/kg CDDP and examined the trigeminal ganglion for possible cell death. A nick translation method for DNA fragmentation revealed CDDP-induced glial cell death. DNA fragmentation was detected in both Schwann cells and satellite cells. Satellite cell death was observed as early as 0.5 day after injection, most frequent at 1-3 days and subsided thereafter. The incidence of neuronal death was very low and comparable to that observed in vehicle control rats. CDDP has selective toxicity to peripheral glial cells, though the damage did not culminate in cell death in adults. The glial toxicity may contribute to clinical symptoms of CDDP neuropathy.. AB - To ...
Background: Methotrexate, vinblastine, doxorubicin, and cisplatin regimen, and gemcitabine and cisplatin regimen are widely used for advanced or metastatic urothelial carcinomas (UCs). However, a standard treatment for patients who fail these firstline chemotherapies is unavailable. We examined the efficacy and safety of secondline paclitaxel, gemcitabine, and cisplatin (PCG) chemotherapy in Japanese patients. Methods: Between 2004 and 2010, 25 patients with metastatic UCs who failed to respond to platinumbased regimens were treated with PCG. They received intravenous paclitaxel (60 mg/m2) and gemcitabine (1000 mg/m2) on days 1 and 8, and cisplatin (70 mg/m2) on day 2 of every 21 day course. We retrospectively collected patients clinical and pathological data and evaluated adverse effects and survivals. Results: Patients underwent 95 PCG cycles in all (average, 3.8 cycles per patient). One patient (4%) achieved complete response, 5 (20%) showed partial response, 8 (42%) had disease stabilization, and 5
TY - JOUR. T1 - Inhibition of PKCδ reduces cisplatin-induced nephrotoxicity without blocking chemotherapeutic efficacy in mouse models of cancer. AU - Pabla, Navjotsingh. AU - Dong, Guie. AU - Jiang, Man. AU - Huang, Shuang. AU - Kumar, M. Vijay. AU - Messing, Robert O.. AU - Dong, Zheng. PY - 2011/7. Y1 - 2011/7. N2 - Cisplatin is a widely used cancer therapy drug that unfortunately has major side effects in normal tissues, notably nephrotoxicity in kidneys. Despite intensive research, the mechanism of cisplatin-induced nephrotoxicity remains unclear, and renoprotective approaches during cisplatin-based chemotherapy are lacking. Here we have identified PKCδ as a critical regulator of cisplatin nephrotoxicity, which can be effectively targeted for reno-protection during chemotherapy. We showed that early during cisplatin nephrotoxicity, Src interacted with, phosphorylated, and activated PKCδ in mouse kidney lysates. After activation, PKCδ regulated MAPKs, but not p53, to induce renal cell ...
To the editor: We wish to call to your readers attention an unexpectedly severe and disabling neurotoxicity due to very-high-dose cisplatin therapy for cancer of the ovary. The attainment of complete remission, proven by second-look surgery, is the first step toward achieving prolonged survival and cure of stage III cancer of the ovary. Recently, Ozols and associates (1) have reported that administration of very high doses of cisplatin (200 mg/m2 body surface area over 5 consecutive days) has achieved frequent tumor regression in patients with advanced cancer of the ovary previously refractory to conventional doses of cisplatin. To improve complete ...
In an Indian phase III trial reported in the Journal of Clinical Oncology, Vanita Noronha, MD, of Tata Memorial Hospital, Mumbai, and colleagues found that curative-intent adjuvant chemoradiation with cisplatin at 100 mg/m2 every 3 weeks produced better locoregional control vs cisplatin at 30 mg/m2 every week in patients with locally advanced head and neck squamous cell cancer.1 Severe adverse events were more common in the every-3-week group.. Study Details. In the noninferiority trial, 300 patients with locally advanced head and neck cancer at Tata Memorial Center in Mumbai were randomized between 2013 and 2017 to receive cisplatin at 30 mg/ m2 given once a week (n = 150) vs cisplatin at 100 mg/m2 given once every 3 weeks (n = 150), both administered concurrently with curative-intent radiotherapy. Disease had to be locally advanced with no distant metastases with planned curative chemoradiation, either as adjuvant treatment for ≥ 1 high-risk feature (eg, extracapsular extension, close [≤ 5 ...
Drug resistance is still a major obstacle for efficient treatment of hepatocellular carcinoma (HCC) during the cisplatin-based chemotherapy. Recent studies have demonstrated that CD133 positive population of cancer cells are responsible for multiple drug resistance. We are supposed to take strategies to sensitize CD133+ HCC cells to cisplatin treatment. In the present study, CD133+ HCC cells showed significant cisplatin-resistance compared to the CD133- HCC cells. Downregulation of miR-124 was observed in CD133+ HCC cells. However, enforced expression of miR-124 can increase the sensitivity of CD133+ HCC cells to cisplatin treatment in vitro and in vivo. Mechanically, overexpression of miR-124 was found to inhibit the expression of SIRT1 and thus promoted the generation of ROS and phosphorylation of JNK. As the results, overexpression of miR-124 expanded the apoptosis in cisplatin-treated CD133+ HCC cells. We then demonstrated that
The combination of pemetrexed and cisplatin shows good clinical activity against mesothelioma and lung cancer. In order to study the potential cellular basis for this, and provide leads as to how to optimize the combination, we studied the schedule-dependent cytotoxic effects of pemetrexed and cisplatin against four human cancer cell lines in vitro. Tumor cells were incubated with pemetrexed and cisplatin for 24 h at various schedules. The combination effects after 5 days were analyzed by the isobologram method. Both simultaneous exposure to pemetrexed and cisplatin for 24 h and sequential exposure to cisplatin for 24 h followed by pemetrexed for 24 h produced antagonistic effects in human lung cancer A549, breast cancer MCF7, and ovarian cancer PA1 cells and additive effects in colon cancer WiDr cells. Pemetrexed for 24 h followed by cisplatin for 24 h produced synergistic effects in MCF7 cells, additive/synergistic effects in A549 and PA1 cells, and additive effects in WiDr cells. Cell cycle ...
Platinum complexes are clinically used as adjuvant therapy of cancers aiming to induce tumor cell death. Depending on cell type and concentration, cisplatin induces cytotoxicity, e.g., by interference with transcription and/or DNA replication mechanisms. Additionally, cisplatin damages tumors via induction of apoptosis, mediated by the activation of various signal transduction pathways, including calcium signaling, death receptor signaling, and the activation of mitochondrial pathways. Unfortunately, neither cytotoxicity nor apoptosis are exclusively induced in cancer cells, thus, cisplatin might also lead to diverse side-effects such as neuro- and/or renal-toxicity or bone marrow-suppression. Moreover, the binding of cisplatin to proteins and enzymes may modulate its biochemical mechanism of action. While a combination-chemotherapy with cisplatin is a cornerstone for the treatment of multiple cancers, the challenge is that cancer cells could become cisplatin-resistant. Numerous mechanisms of cisplatin
TY - JOUR. T1 - Use of organotypic cultures of Cortis organ to study the protective effects of antioxidant molecules on cisplatin-induced damage of auditory hair cells. AU - Kopke, Richard D.. AU - Liu, Wei. AU - Gabaizadeh, Ramin. AU - Jacono, Andrew. AU - Feghali, Joseph. AU - Spray, David. AU - Garcia, Phil. AU - Steinman, Howard. AU - Malgrange, Bridgitte. AU - Ruben, Robert J.. AU - Rybak, Leonard. AU - Van De Water, Thomas R.. PY - 1997/9/1. Y1 - 1997/9/1. N2 - Hypothesis: Cisplatin causes the generation of reactive oxygen species (ROS), which interferes with the antioxidant defense system of Cortis organ and results in damage to the hair cells. Background: Cisplatin is a widely used chemotherapeutic agent with the dose-limiting side effect of ototoxicity. Evidence is accumulating that cisplatin interferes with the antioxidant defense system of Cortis organ. Methods: Organotypic explants of P-3 rat organ of Corti were the in vitro model system. Presence of intact auditory hair cells and ...
TY - JOUR. T1 - Effect of miR-29 on cisplatin sensitivity of ovarian cancer cells. AU - Yu, Pei Ning. AU - Lin, Wen-Chi. AU - Kuo, Chih Chi. AU - Huang, Rui-Lan. AU - Yan, Ming De. AU - Shih, Yu Lueng. AU - Chou, Yu Ching. AU - Lai, Hung-Cheng. AU - Lin, Ya Wen. PY - 2014/11/21. Y1 - 2014/11/21. N2 - Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, ILIn clinical practice, the main dilemma to a successful ovarian cancer therapy is the development of drug resistance. The mounting evidence demonstrated that microRNAs (miRNAs) not only controlled cell proliferation, invasion and metastasis but also therapeutic resistance of ovarian cancer cell. Recently, we isolated CP70sps(CP70 side population spheres) from CP70 ovarian cancer cell line and proved that CP70sps exhibited more resistant to cisplatin than CP70. This phenomenon was correlated to other study which supported that side population of cancer cells was responsible for chemoresistance. In this study, we ...
Abstract Background Cisplatin is a platinum-based chemotherapeutic that damages genomic DNA leading to cell death. It also damages mitochondrial DNA and...
A statistically significant (p=0.0039) increase in IL6 was shown in the blood plasma of the cisplatin animals (131.9±31.91 pg/ml) compared to the vehicle animals (38.00±6.748 pg/ml). There were no significant differences between cisplatin and vehicle animals in dorsal horn neurones or astrocytes at either time point. Microglia cell counts in the dorsal horn were significantly decreased at the juvenile time point in the Cisplatin treatment group. Cisplatin induced significant increases in dorsal horn expression of Aβ-fibre and non-peptidergic C-fibre terminations at both time-points, in the Cisplatin treatment group. TrkA expression in dorsal horn peptidetgic C-fibre terminations was increased at both time-points, however, CGRP expression was only initially increased at the juvenile time-point but showed no difference to the veh at the adult time-point. Interneuron expression was increased at both time-points ...
TY - JOUR. T1 - Effect of N-acetylcysteine route of administration on chemoprotection against cisplatin-induced toxicity in rat models. AU - Dickey, D. Thomas. AU - Muldoon, Leslie L.. AU - Doolittle, Nancy D.. AU - Peterson, Darryl R.. AU - Kraemer, Dale F.. AU - Neuwelt, Edward A.. N1 - Funding Information: This work was supported by a Veterans Administration Merit Review Grant and by NIH grants NS33618, NS34608, and NS44687 from the National Institute of Neurological Disorders and Stroke to EAN. Copyright: Copyright 2008 Elsevier B.V., All rights reserved.. PY - 2008/7. Y1 - 2008/7. N2 - Dosing and route of administration of N-acetylcysteine (NAC) for protection against cisplatin (CDDP) nephrotoxicity was investigated in rats. Two models of toxicity were tested: a single high dose of CDDP (10 mg/kg intraperitoneally (IP)), and multiple low dose treatments (1 mg/kg IP twice a day for 4 days, 10 days rest, then repeated). NAC (50-1,200 mg/kg) was given to the rats by IP, oral (PO), intravenous ...
Patients. Twenty-eight cancer patients were included in this study and were treated with locoregional standard radiotherapy and simultaneous cisplatin-containing chemotherapy. They gave their written informed consent to be included in this study, which was approved by the local ethics committee. Patients were irradiated for intrathoracic, pelvic, or head and neck tumors in 21, 4, and 3 cases, respectively. All patients received cisplatin-containing chemotherapy concurrent with radiotherapy at weekly or longer intervals. The cisplatin doses per application ranged from 20 to 50 mg/m2 and were given at days 0 and 7 of each 21- to 28-d cycle. Cisplatin was given according to three schedules, either as cisplatin monochemotherapy or, for non-small cell lung cancer patients (n = 14), as cisplatin 50 mg/m2 and navelbine 15 mg/m2 doublet at days 0 and 7 after the start of radiotherapy (day −1). For small-cell lung cancer patients (n = 4), it was given as cisplatin 45 to 50 mg/m2 at days 0 and 7 ...
An unanswered question in first line treatment of non small cell lung cancer (NSCLC) is whether the administration of more than 2 active drugs provides greater efficacy than a two-drug combination. Docetaxel/gemcitabine combination is a well tolerated regimen, which has comparable efficacy to docetaxel/cisplatin or vinorelbine/cisplatin. In a recent phase II study in first line treatment of advanced or metastatic NSCLC, the sequential administration of vinorelbine/cisplatin followed by docetaxel/gemcitabine produced a response rate of 45.8% and a 1-year survival rate of 51%. The addition of bevacizumab to a platinum-based regimen provided a survival benefit in patients with advanced or metastatic NSCLC ...
Cisplatin-based chemotherapy is the standard therapy used for the treatment of several types of cancer. However, its efficacy is largely limited by the acquired drug resistance. To date, little is known about the RNA expression changes in cisplatin-resistant cancers. Identification of the RNAs related to cisplatin resistance may provide specific insight into cancer therapy. In the present study, expression profiling of 7 cancer cell lines was performed using oligonucleotide microarray analysis data obtained from the GEO database. Bioinformatic analyses such as the Gene Ontology (GO) and KEGG pathway were used to identify genes and pathways specifically associated with cisplatin resistance. A signal transduction network was established to identify the core genes in regulating cancer cell cisplatin resistance. A number of genes were differentially expressed in 7 groups of cancer cell lines. They mainly participated in 85 GO terms and 11 pathways in common. All differential gene interactions in the ...
Cisplatin is a widely used cancer therapy drug that unfortunately has major side effects in normal tissues, notably nephrotoxicity in kidneys. Despite intensive research, the mechanism of cisplatin-induced nephrotoxicity remains unclear, and renoprotective approaches during cisplatin-based chemotherapy are lacking. Here we have identified PKCδ as a critical regulator of cisplatin nephrotoxicity, which can be effectively targeted for renoprotection during chemotherapy. We showed that early during cisplatin nephrotoxicity, Src interacted with, phosphorylated, and activated PKCδ in mouse kidney lysates. After activation, PKCδ regulated MAPKs, but not p53, to induce renal cell apoptosis. Thus, inhibition of PKCδ pharmacologically or genetically attenuated kidney cell apoptosis and tissue damage, preserving renal function during cisplatin treatment. Conversely, inhibition of PKCδ enhanced cisplatin-induced cell death in multiple cancer cell lines and, remarkably, enhanced the chemotherapeutic ...
Cisplatin is a widely used cancer therapy drug that unfortunately has major side effects in normal tissues, notably nephrotoxicity in kidneys. Despite intensive research, the mechanism of cisplatin-induced nephrotoxicity remains unclear, and renoprotective approaches during cisplatin-based chemotherapy are lacking. Here we have identified PKCδ as a critical regulator of cisplatin nephrotoxicity, which can be effectively targeted for renoprotection during chemotherapy. We showed that early during cisplatin nephrotoxicity, Src interacted with, phosphorylated, and activated PKCδ in mouse kidney lysates. After activation, PKCδ regulated MAPKs, but not p53, to induce renal cell apoptosis. Thus, inhibition of PKCδ pharmacologically or genetically attenuated kidney cell apoptosis and tissue damage, preserving renal function during cisplatin treatment. Conversely, inhibition of PKCδ enhanced cisplatin-induced cell death in multiple cancer cell lines and, remarkably, enhanced the chemotherapeutic ...
TY - JOUR. T1 - IL-10 from dendritic cells but not from T regulatory cells protects against cisplatin-induced nephrotoxicity. AU - Wang, Wei Wei. AU - Wang, Yamei. AU - Li, Kang. AU - Tadagavadi, Raghu. AU - Friedrichs, William E.. AU - Budatha, Madhusudhan. AU - Reeves, W. Brian. N1 - Funding Information: This work was supported in part by grants from the National Institute of Diabetes and Digestive and Kidney Diseases (DK-081876 and DK-108185) to W.B.R. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. There was no additional external funding received for this study.. PY - 2020/9. Y1 - 2020/9. N2 - Interleukin-10 (IL-10), a cytokine with anti-inflammatory effects, is produced by renal parenchymal cells and bone marrow derived cells. Both endogenous and exogenous IL-10 are protective in cisplatin-induced acute kidney injury. However, the source of endogenous IL-10 in cisplatin-induced nephrotoxicity is not clear. Bone ...
Chemoresistance to platinums, such as cisplatin, is of critical concern in the treatment of ovarian cancer. Recent evidence has linked epithelial-mesenchymal transition (EMT) as a contributing mechanism. The current study explored the connection between cellular responses to cisplatin and EMT in ovarian cancer. Expression microarrays were utilized to estimate the EMT status as a binary phenotype, and the transcriptional responses of 46 ovarian cancer cell lines to cisplatin were measured at dosages equivalent to 50% growth inhibition. Phenotypic responses to cisplatin were quantified with respect to cell number, proliferation rate and apoptosis, and then compared with the epithelial or mesenchymal status. Ovarian cancer cell lines with an epithelial status exhibited higher resistance to cisplatin treatment in the MTS assay than those with a mesenchymal status. Pathway analyses revealed the induction of G1/S- and S-phase genes (P=0.001) and the activation of multiple NF-κB (nuclear factor kappa-light
Background. Erythropoietin (Epo) is a growth factor whose synthesis mainly takes place in the kidney. Epo has been shown to support the growth not only of erythroid progenitor cells but also of certain other cell types. We attempted to establish whether Epo enhances the recovery from acute renal failure induced by cisplatin.. Methods. Sprague‐Dawley rats were randomized into three groups. In the cisplatin group, animals received one intraperitoneal injection of cisplatin (6 mg/kg) and a daily injection of placebo for 9 days. In the cisplatin+Epo group, animals received intrapertoneal cisplatin and a daily injection of Epo (100 IU/kg) for 9 days. In the control group, animals received both placebo preparations alone. Para‐aminohippuric acid and inulin clearances were determined after 4 and 9 days to evaluate renal blood flow and glomerular filtration rate. In addition, light microscopy and immunohistochemistry examinations were performed, and in situ proliferating cell nuclear antigen (PCNA) ...
TY - JOUR. T1 - Combination chemotherapy with continuous 5-fluorouracil and low-dose cisplatin infusion for advanced hepatocellular carcinoma. AU - Tanioka, Hiroaki. AU - Tsuji, Akihito. AU - Morita, Sojiro. AU - Horimi, Tadashi. AU - Takamatsu, Masahiro. AU - Shirasaka, Tetsuhiko. AU - Mizushima, Takaaki. AU - Ochi, Koji. AU - Kiura, Katsuyuki. AU - Tanimoto, Mitsune. PY - 2003/3/1. Y1 - 2003/3/1. N2 - Background: In this study we evaluated the efficacy and toxicities of combination chemotherapy consisting of continuous 5-fluorouracil (5-FU) infusion and low-dose cisplatin infusion (low-dose FP therapy) in the treatment of advanced hepatocellular carcinoma (HCC). Materials and Methods: Thirty-eight patients with advanced HCC in whom local treatment was not indicated were enrolled. The low-dose FP therapy consisted of 5-FU (170mg/m2/day on days 1 to 7/week, continuous infusion) and cisplatin (3mg/m2/day in 100ml normal saline, infusion more than 30 minutes, on days 1 to 5/week). The patients ...
TY - JOUR. T1 - High temperature requirement A3 (HtrA3) promotes etoposide- and cisplatin-induced cytotoxicity in lung cancer cell lines. AU - Beleford, Daniah. AU - Rattan, Ramandeep. AU - Chien, Jeremy. AU - Shridhar, Viji. PY - 2010/4/16. Y1 - 2010/4/16. N2 - Lung cancer is the leading cause of cancer-related deaths worldwide. Here we show for the first time that HtrA3 is a mitochondrial stress-response factor that promotes cytotoxicity to etoposide and cisplatin in lung cancer cell lines. Exogenous expression of wild type HtrA3 domain variants significantly attenuated cell survival with etoposide and cisplatin treatment in lung cancer cell lines H157 and A549 compared with expression of protease inactive mutants (S305A) or vector control. Conversely, HtrA3 suppression promoted cell survival with etoposide and cisplatin treatment in lung cancer cell lines Hop62 and HCC827. Survival was attenuated by re-expression of wild type HtrA3 variants during treatment but not by protease inactive ...
TY - JOUR. T1 - Expression of p53 in cisplatin-resistant ovarian cancer cell lines. T2 - Modulation with the novel platinum analogue (1R, 2R- diaminocyclohexane)(trans-diacetato)(dichloro)platinum(IV). AU - Hagopian, George S.. AU - Mills, Gordon B.. AU - Khokhar, Abdul R.. AU - Bast, Robert C.. AU - Siddik, Zahid H.. N1 - Copyright: Copyright 2007 Elsevier B.V., All rights reserved.. PY - 1999/3. Y1 - 1999/3. N2 - The compound (IR,2R- diaminocyclohexane)(transdiacetato)(dichloro)platinum(IV) (DACH-acetato-Pt) is a novel platinum-based antitumor agent with clinical potential against cisplatin-resistant disease that is under development in our laboratory. In view of the central role of the wild-type p53 tumor suppressor gene in drug- induced apoptosis, we evaluated the cytotoxicity of cisplatin and DACH- acetato-Pt in a panel of cisplatin-resistant ovarian tumor models with differing p53 status. Cisplatin was relatively more effective against mutant or null p53 cell lines (continuous drug ...
TY - JOUR. T1 - Phase II study of irinotecan plus cisplatin in patients with advanced non-small-cell lung cancer. AU - DeVore, Russell F.. AU - Johnson, David H.. AU - Crawford, Jeffrey. AU - Garst, Jennifer. AU - Dimery, Isaiah W.. AU - Eckardt, John. AU - Eckhardt, S. Gail. AU - Elfring, Gary L.. AU - Schaaf, Larry J.. AU - Hanover, Cristy K.. AU - Miller, Langdon L.. PY - 1999/9. Y1 - 1999/9. N2 - Purpose: To evaluate the antitumor efficacy and safety of a combination of irinotecan (CPT-11) and cisplatin in patients with inoperable non-small- cell lung cancer (NSCLC). A secondary objective was to characterize the pharmacokinetics and pharmacodynamics of CPT-11 and its active metabolite, SN-38. Patients and Methods: Patients with stage IIIB or IV NSCLC were treated with repeated 4-week courses comprising CPT-11 (60 mg/m2) administered on days 1, 8, and 15, and a single dose of cisplatin (80 mg/m2) after CPT-11 administration on day 1. Results: Fifty-two patients were enrolled, including 33 men ...
TY - JOUR. T1 - Cisplatin resistant spheroids model clinically relevant survival mechanisms in ovarian tumors. AU - Chowanadisai, Winyoo. AU - Messerli, Shanta M.. AU - Miller, Daniel H.. AU - Medina, Jamie E.. AU - Hamilton, Joshua W.. AU - Messerli, Mark A.. AU - Brodsky, Alexander S.. N1 - Funding Information: This work was funded by the National Institutes of Health (NIH) NCRR supplement grant P41 RR001395-27S1 (JWH), National Science Foundation (NSF) DBI-1005378 ?REU Site: Biological Discovery in Woods Hole?, faculty startup funds from the Office of Research at Oklahoma State University (WC), and the Mary Kay Foundation (ASB). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. We thank Joel Commisso at the Interdisciplinary Center for Plasma Mass Spectrometry at the University of California, Davis, for his technical expertise. We thank Milton C. Gum for his advice regarding dataset analyses. This work was funded by ...
Background: Osteosarcoma (OS) is the most predominant bone tumor in individuals between 10-25 yrs of age. Cisplatin is the most widely used chemotherapeutic agent for OS management, it significantly enhances the survival rate. Resistance to the drug, toxicities of high doses and metastasis are the major concerns in the treatment. Objective: Our primary objective is to investigate effects of calcitriol in combination with cisplatin on the osteosarcoma cell apoptosis, invasion and migration. Our hypothesis is pretreatment of OS cells with calcitriol would sensitize them for cisplatin therapy leading to decrease in concentration for IC50. Secondary objective was to evaluate the effect of calcitriol on migration and invasion of OS cell lines, and the role of matrix metalloproteins (MMPs) in migration/invasion. Design: Previous findings in our lab suggests, calcitriol act as differentiation agent in human osteosarcoma cell lines 143B and SaOS-2. The dose response of cisplatin with and without ...
TY - JOUR. T1 - NSC109268 potentiates cisplatin-induced cell death in a p53-independent manner. AU - Shankar, Eswar. AU - Basu, Chandreyi. AU - Adkins, Brett. AU - Siede, Wolfram. AU - Basu, Alakananda. N1 - Copyright: Copyright 2017 Elsevier B.V., All rights reserved.. PY - 2010/5/10. Y1 - 2010/5/10. N2 - Background: Ovarian cancer is the leading cause of death among gynecological cancers. Cisplatin is one of the most effective anticancer drugs used in the treatment of ovarian cancer. Development of resistance to cisplatin limits its therapeutic use. Most of the anticancer drugs, including cisplatin, are believed to kill cancer cells by inducing apoptosis and a defect in apoptotic signaling can contribute to drug resistance. The tumor suppressor protein p53 plays a critical role in DNA damage-induced apoptosis. During a yeast-based drug screening, NSC109268 was identified to enhance cellular sensitivity to cisplatin. The objective of the present study is to determine if p53 is responsible for ...
In a Chinese phase III trial reported in The New England Journal of Medicine, Yuan Zhang, MD, PhD, and colleagues found that the addition of gemcitabine/cisplatin induction chemotherapy to standard platinum-based chemoradiotherapy improved recurrence-free survival vs chemoradiotherapy alone in locoregionally advanced nasopharyngeal carcinoma.. Study Details. The open-label trial included 480 patients with newly diagnosed disease from 12 centers. Patients were randomly assigned between December 2013 and September 2016 to receive gemcitabine at 1 g/m2 on days 1 and 8 and cisplatin at 80 mg/m2 on day 1 every 3 weeks for three cycles plus standard chemoradiotherapy (n = 242) or standard chemoradiotherapy alone (n = 238). Chemoradiotherapy consisted of 100 mg/m2 of cisplatin every 3 weeks on days 1, 22, and 43, plus intensity-modulated radiotherapy. Randomization was stratified by treatment center and disease stage III or IV. It was recommended that patients in the induction chemotherapy group begin ...
TY - JOUR. T1 - Preventive effect of prostaglandin E1 on cisplatin-induced nephrotoxicity. AU - Takayama, K.. AU - Nakanishi, Y.. AU - Takano, K.. AU - Harada, T.. AU - Inoue, K.. AU - Osaki, S.. AU - Minami, T.. AU - Hara, N.. N1 - Copyright: This record is sourced from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine. PY - 1999/3. Y1 - 1999/3. N2 - In order to prevent the nephrotoxicity induced by cisplatin (CDDP), prostaglandin E1 (PGE1) was administered intravenously after anticancer chemotherapy to six patients with lung cancer. All patients underwent two courses of multi-drug chemotherapy with the same regimen including a single administration of 80 mg/m2 CDDP. From the 7th day of the 2nd course of chemotherapy, 120 micrograms PGE1 had been administered for five days. During the two courses of chemotherapy, serum creatinine, blood urea nitrogen, creatinine clearance (Ccr), 24-h excretions of beta 2-microglobulin (beta 2-MG) and N-acetylglucosaminidase (NAG) in urine ...
Introduction: Cisplatin is used as a chemotherapeutic agent for the treatment of human ovarian and testicular cancers. This study was designed to investigate the protective role of taurine against cisplatin-induced kidney injury. Methods: Male Wistar rats were divided into 4 groups (n=8) (1) saline-treated group (2) cisplatin-treated group (10 mg/kg, i.p.), (3) ...
TY - JOUR. T1 - Salicylate protects hearing and kidney function from cisplatin toxicity without compromising its oncolytic action. AU - Li, Geming. AU - Sha, Su Hua. AU - Zotova, Elena. AU - Arezzo, Joseph. AU - Van De Water, Thomas R.. AU - Schacht, Jochen. PY - 2002/1/1. Y1 - 2002/1/1. N2 - Salicylate has recently been demonstrated to protect against the auditory and vestibular side effects of aminoglycoside antibiotics. Similarities in the toxic mechanisms suggest salicylate as a treatment strategy to prevent the ototoxic side effects of cisplatin (CDDP). We first tested protection of the inner ear in Wistar rats receiving a single infusion of 16 mg CDDP/kg body weight with or without treatment with 100 mg/kg salicylate (bid) for 5 days beginning one day before the CDDP infusion. Cisplatin induced a threshold shift of more than 30 dB (at 14 kHz; measured by auditory evoked brain stem response) that was significantly reduced by salicylate. We then examined the protective potential of ...
TY - JOUR. T1 - Protective effects of apocynin on cisplatin-induced ototoxicity in an auditory cell line and in zebrafish. AU - Choi, June. AU - Im, Gi Jung. AU - Chang, Jiwon. AU - Chae, Sung Won. AU - Lee, Seung Hoon. AU - Kwon, Soon Young. AU - Chung, Ah Young. AU - Park, Hae Chul. AU - Jung, Hak Hyun. PY - 2013/2. Y1 - 2013/2. N2 - Cisplatin is a very effective anticancer drug and generates reactive oxygen species (ROS) such as superoxide anions that can deplete antioxidant protective molecules in the cochlea. These processes result in the death of cochlear hair cells by induction of apoptosis. Apocynin, which is used as a specific nicotinamide adenine dinucleotide phosphate oxidase inhibitor, has a preventive effect for intracellular ROS generation. In this study, the effect of apocynin was investigated in a cochlear organ of Corti-derived cell line, HEI-OC1 cells, and in transgenic zebrafish (Brn3C: EGFP). To investigate the protective effects of apocynin, HEI-OC1 cells were treated with ...
TY - JOUR. T1 - Prophylactic effect of diacerein against cisplatin-induced nephrotoxicity in rats. AU - Abdel-Aziz, Asmaa Mohamed. AU - Ibrahim, Mohamed Abdellah. AU - El-Shiekh, Azza Ali. AU - Osman, Nisreen Abdel Tawab. AU - Geddawy, Ayman. AU - Abdelrahman, Aly. PY - 2018. Y1 - 2018. N2 - Background and Objective: Cisplatin is an effective chemotherapeutic agent for solid tumors, however its use is limited by nephrotoxicity. The current study investigated the effect of diacerein in cisplatin-induced nephrotoxicity in rats. Materials and Methods: Rats were randomly divided into 5 groups; control (untreated), diacerein control (100 mg kgG1), cisplatin (5 mg kgG1 i.p.), cisplatin+diacerein (50 mg kgG1) and cisplatin+diacerein (100 mg kgG1). Data were analyzed by one way ANOVA using GraphPad Prism. Results: Administration of cisplatin caused significant deterioration in renal function, designated by the increase in serum levels of both urea and creatinine, reduction in creatinine clearance, ...
Several lines of evidence correlate the overexpression of glutathione S-transferase omega 1-1 (GSTO1-1) with the onset of drug resistance of cancer cells; however, no direct evidence is yet available. In order to investigate the mechanisms involved, stable transfection with GSTO1-1 complementary DNA was performed in HeLa cells, which spontaneously express very low levels of GSTO1-1. When transfected cells were seeded at low density, a sharp increase in GSTO1-1 expression was observed as compared with controls, along with an increased resistance against cisplatin cytotoxicity. When seeded at increasing densities, control untransfected cells also presented with an increase in GSTO1-1 expression, again accompanied by cisplatin resistance; the latter was significantly reduced after transfection with GSTO1-1 small interfering RNA. Cisplatin resistance of transfected cells was not accounted for by changes in the intracellular drug concentration nor in the amount of DNA cross-links or content of ...
TY - JOUR. T1 - Cisplatin-induced apoptosis in p53-deficient renal cells via the intrinsic mitochondrial pathway. AU - Jiang, Man. AU - Wang, Cong Yi. AU - Huang, Shuang. AU - Yang, Tianxin. AU - Dong, Zheng. N1 - Copyright: Copyright 2009 Elsevier B.V., All rights reserved.. PY - 2009/5. Y1 - 2009/5. N2 - Nephrotoxicity is the major limiting factor for the use of cisplatin in cancer therapy. Recent studies have demonstrated an important role for p53 in cisplatin-induced renal injury. Nevertheless, pharmacological and genetic blockade of p53 only provides partial renoprotective effects, suggesting the presence of p53-independent injury mechanisms. To understand the p53-independent mechanisms, we have now examined cisplatin-induced apoptosis in p53-deficient kidney cells. We show that cisplatin could induce Bax activation, cytochrome c release, and apoptosis in primary cultures of p53-deficient renal tubular cells, albeit at a level that was lower than in the wild-type cells. Cisplatin could also ...
cisplatin on cell viability of NSCLC cell lines. A three-dimensional spherification assay was used to simulate in vivo tumor formation. Flow cytometry was performed to examine cell cycle distribution and the percentages of apoptotic cells. The associated proteins and mRNA of cell cycle, apoptosis, and autophagy were measured by western blotting and real-time fluorescence quantitative PCR. Immunofluorescence assay was used to test apoptotic nuclei and autolysosome. Small interfering RNA experiments were used to silence the expression of p21. Combination treatment of AKBA and cisplatin inhibited cell viability, clone formation, and three-dimensional spherification, enhanced G0/G1 phase arrest, increased the percentages of apoptotic cells, and decreased the ratio of positive autolysosomes, compared with cisplatin alone. AKBA in combination with cisplatin suppressed the protein expressions of cyclin A2, cyclin E1, p-cdc2, CDK4, Bcl-xl, Atg5, and LC3A/B, and upregulated p27 and p21 mRNA levels in ...
Ovarian cancer is currently the second leading cause of gynecological malignancy and cisplatin or cisplatin-based regimens have been the standard of care for the treatment of advance epithelial ovarian cancers. However, the efficacy of cisplatin treatment is often limited by the development of drug resistance either through the inhibition of apoptotic genes or activation of antiapoptotic genes. We have previously reported the overexpression of human UO-44 (HuUO-44) in ovarian cancers and the HuUO-44 antisera markedly inhibited NIH-OVCAR3 ovarian cancer cell attachment and proliferation (Oncogene 23: 5707-5718, 2004). In the present study, we observed through the cancer cell line profiling array that the expression of HuUO-44 was suppressed in the ovarian cancer cell line (SKOV-3) after treatment with several chemotherapeutic drugs. Similarly, this suppression in HuUO-44 expression was also correlated to the cisplatin sensitivity in two other ovarian cancer cell lines NIH-OVCAR3 and OV-90 in a ...
This small phase II study provides a direct comparison between cisplatin and paclitaxel used as weekly concurrent chemotherapy with definitive radiation for advanced carcinoma of the cervix. Our data indicate that the overall response and progression free survival rates with the use of paclitaxel, which is the experimental arm, are not superior to those with cisplatin. In fact, there were non-significant trends for a higher relapse rate, higher gastrointestinal toxicity, and more allergic reactions in the concurrent paclitaxel group. Taken together, these results indicate that paclitaxel does not provide any clinical advantage over the current standard of concurrent cisplatin in CTRT for patients with advanced cervical carcinoma.. Although many prospective studies had shown that CTRT with cisplatin-based chemotherapy clearly improve the outcome of patients with carcinoma of the cervix, many patients treated on these protocols continue to fail in the pelvis and at distant sites [6, 16, 22, 23]. ...
334 patients were randomised to cisplatin (n = 166) or cetuximab (n = 168). Two-year overall survival (97·5% vs 90·0%, HR: 3.268 [95% CI 1·451 to 7·359], p = 0·0251) and recurrence rates (6·4% vs 16·0%, HR: 2·67 [1·38 to 5·15]; p = 0·0024) favoured cisplatin. No significant differences in EQ-5D-5L utility scores were detected at any time point. At 24 months PT, mean difference was 0·107 QALYs in favour of cisplatin (95% CI: 0·186 to 0·029, p = 0·007) driven by the mortality difference. Health care costs were similar across all categories except the procurement cost and delivery of the systemic agent, with cetuximab significantly more expensive than cisplatin (£7779 [P , 0.001]). Consequently, total costs at 24 months PT averaged £13517 (SE: £345) per patient for cisplatin and £21064 (SE: £400) for cetuximab (mean difference £7547 [95% CI: £6512 to £8582]).. ...
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Looking for online definition of Cis-diamminedichloroplatinum in the Medical Dictionary? Cis-diamminedichloroplatinum explanation free. What is Cis-diamminedichloroplatinum? Meaning of Cis-diamminedichloroplatinum medical term. What does Cis-diamminedichloroplatinum mean?
TY - JOUR. T1 - Foxo3a expression and acetylation regulate cancer cell growth and sensitivity to cisplatin. AU - Shiota, Masaki. AU - Yokomizo, Akira. AU - Kashiwagi, Eiji. AU - Tada, Yasuhiro. AU - Inokuchi, Junichi. AU - Tatsugami, Katsunori. AU - Kuroiwa, Kentaro. AU - Uchiumi, Takeshi. AU - Seki, Narihito. AU - Naito, Seiji. N1 - Copyright: Copyright 2010 Elsevier B.V., All rights reserved.. PY - 2010/5. Y1 - 2010/5. N2 - Many advanced cancers receive cisplatin-based chemotherapy. However, cisplatin resistance is a major obstacle for cancer chemotherapy. Foxo3a is a member of the Foxo transcription factor family, which modulates the expression of genes involved in DNA damage repair, apoptosis, and other cellular processes. In this study, we found that cisplatin-resistant cells were more sensitive to the anticancer agent mithramycin than their parental cells, and had a decreased level of Foxo3a expression. Foxo3a knockdown increased cell proliferation and resistance to cisplatin. On the other ...
Cisplatin induces protective autophagy through activation of BECN1 in human bladder cancer cells Ji-Fan Lin,1 Yi-Chia Lin,2 Te-Fu Tsai,2,3 Hung-En Chen,2 Kuang-Yu Chou,2,3 Thomas I-Sheng Hwang2–4 1Central Laboratory, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, 2Division of Urology, School of Medicine, Fu-Jen Catholic University, New Taipei, 3Division of Urology, Department of Surgery, Shin Kong Wu Ho-Su Memorial Hospital, 4Department of Urology, Taipei Medical University, Taipei, Taiwan Purpose: Cisplatin-based chemotherapy is the first line treatment for several cancers including bladder cancer (BC). Autophagy induction has been implied to contribute to cisplatin resistance in ovarian cancer; and a high basal level of autophagy has been demonstrated in human bladder tumors. Therefore, it is reasonable to speculate that autophagy may account for the failure of cisplatin single treatment in BC. This study investigated whether cisplatin induces autophagy and the mechanism involved using human BC
Plant-derived BEC with its main component solamargine possesses anticancer activities via its effect on a variety of biological pathways in a wide range of human cancer cells. High cure rates with BEC therapy have been obtained in animals with deadly cancers, and, in humans with terminal cancers promising results have been reported. At a clinical level, optimal concentrations of BEC have been established in a topical cream formulation Curaderm, for effective removal of skin cancers, but optimal concentrations of BEC have not been reported for other cancers. The objective of this study was to determine whether combination therapy of Cisplatin with BEC would result in synergism using cure rates as end points. BEC on its own cures Sarcoma 180 in mice, whereas, Cisplatin on its own has no effect on Sarcoma 180 activity. A combination of BEC and Cisplatin shows synergism, resulting in higher cure rates than BEC and Cisplatin at comparable individual concentrations.
The chemotherapeutic drug cisplatin is an important treatment for many types of solid tumours, in particular non-small cell lung cancer (NSCLC). Platinum(IV) complexes offer several advantages to cisplatin due to their requirement for reduction to the active platinum(II) form to elicit cytotoxicity. This should minimise non-specific effects and facilitate higher amounts of the active complexes reaching the target DNA. Hypoxia and a quiescent cell population are features of the tumour microenvironment known to lead to resistance to many chemotherapeutic agents. It is unclear how these microenvironmental factors will impact on the efficacy of novel platinum(IV) complexes. Consequently, the cytotoxicities of several platinum drugs were determined in monolayer and tumour spheroid cultures derived from NSCLC lines. Platinum(IV) reduction potential correlated well with cytotoxicity. The complex containing a chloro axial ligand demonstrated the greatest potency and the drug with the hydroxy ligand was the
Bleomycin, vincristine, cisplatin/bleomycin, etoposide, cisplatin chemotherapy: an alternating, dose intense regimen producing promising results in untreated patients with intermediate or poor prognosis malignant germ-cell ...
TY - JOUR. T1 - Cisplatin and vindesine combination chemotherapy for advanced carcinoma of the lung. T2 - A randomized trial investigating two dosage schedules. AU - Gralla, R. J.. AU - Casper, E. S.. AU - Kelsen, D. P.. AU - Braun, D. W.. AU - Dukeman, M. E.. AU - Martini, N.. AU - Young, C. W.. AU - Golbey, R. B.. PY - 1981/1/1. Y1 - 1981/1/1. N2 - Eighty-five patients with advanced squamous carcinoma or adenocarcinoma of the lung were randomly assigned to receive vindesine with either high dose (120 mg/m2 of body surface area) or low dose (60 mg/m2) cisplatin. All patients had measurable disease and had not previously received chemotherapy. The response rate was similar with both treatments (43% complete and partial remission rate), but the high dose cisplatin regimen was superior to the low dose in median duration of response (12 versus 5.5 months; p = 0.05) and in median survival for responding patients (21.7 versus 10 months; p = 0.02). Myelosuppression was generally not a treatment ...
Background Urothelial bladder cancer (UBC) accounts for 10,000 new diagnoses and 5000 deaths annually in the UK (Cancer Research UK,, Cancer Research UK, Accessed 26 Mar 2018). Cisplatin-based chemotherapy is standard of care therapy for UBC for both palliative first-line treatment of advanced/metastatic disease and radical neoadjuvant treatment of localised muscle invasive bladder cancer. However, cisplatin resistance remains a critical cause of treatment failure and a barrier to therapeutic advance in UBC. Based on supportive pre-clinical data, we hypothesised that DNA methyltransferase inhibition would circumvent cisplatin resistance in UBC and potentially other cancers. Methods The addition of SGI-110 (guadecitabine, a DNA methyltransferase inhibitor) to conventional doublet therapy of gemcitabine and cisplatin (GC) is being tested within the phase Ib/IIa SPIRE clinical trial. SPIRE ...
Background: Much research has confirmed the favorable effect of irinotecan/cisplatin (IP) and etoposide/cisplatin (EP) on extensive-stage small cell lung c
Background: Considering the uprising number of Head and neck cancer in the state with limited options of medical and surgical treatment, the focus of this study involved on chemotherapy in advanced Head and neck cancers. The aim of this study was to evaluate the efficacy and toxicity of combination of Cisplatin and 5-Fluorouracil (PF) as induction chemotherapy in patients in locally advanced squamous cell cancer of head and neck. Materials and Methods: Forty four patients with previously untreated stage III -IV advanced and inoperable cases were included in this prospective study. Induction chemotherapy consisted of 3 cycles of Cisplatin 100mg/mt2 as infusion on day 1, 5-Fluorouracil of 750mg/mt2 on day 2, 5-Fluorouracil of 1000mg/mt2 as infusion on day 3 in an inpatient basis. Cycles were repeated with an interval of 21 days. Patients were evaluated within a period of 3 weeks at the end of completion of third cycle of chemotherapy. Post chemotherapy local therapy was individualized based on the ...
TY - JOUR. T1 - The roles of copper transporters in cisplatin resistance. AU - Kuo, Macus Tien. AU - Chen, Helen H.W.. AU - Song, Im Sook. AU - Savaraj, Niramol. AU - Ishikawa, Toshihisa. PY - 2007/3/1. Y1 - 2007/3/1. N2 - Platinum-based antitumor agents have been effective in the treatments of many human malignancies but the ultimate success of these agents is often compromised by development of drug resistance. One mechanism associated with resistance to platinum drugs is reduced intracellular accumulation owing to impaired drug intake, enhanced outward transport, or both. Mechanisms for transporting platinum drugs were not known until recent demonstrations that import and export transporters involved in maintenance copper homeostasis are also involved in the transport of these drugs. Ctr1, the major copper influx transporter, has been convincingly demonstrated to transport cisplatin and its analogues, carboplatin, and oxaliplatin. Evidence also suggests that the two copper efflux transporters ...
We have developed a simple, rapid, selective and sensitive method for detecting the antitumour agent cis-diamminedichloroplatinum (II) (cisplatin) (CDDP) and its toxic impurities trans-diamminedichloroplatinum (II) (transplatin) (TDDP) amminetri-chloroplatinat (ATCP) anion using HPLC in one run. By using 4-methyl-2-thiouracil (MTU) as a derivatizing agent, new compounds have been formed from the Pt compounds and separated on a mu-Bondapak C-18 column with isocratic elution and detection at 315 nm. ...
According to the statistics for 2018, cervical cancer is the fourth most common cancer in women worldwide, with 569,847 patients yearly [1]. Patients with cervical cancer who have progressed to an inoperable stage or have experienced recurrence receive widely used anti-cancer chemotherapy and platinum-based chemotherapy [2]. Cisplatin is a platinum-based chemotherapeutic agent that is widely used for the treatment of malignant tumors, such as cervical cancer, lung cancer, and ovarian cancer [3]. Cisplatin mainly induces cross-linking at the N7-position of guanosine, which modifies DNA to induce apoptosis and kill cancer cells [4]. However, the use of cisplatin as a cancer treatment has been limited owing to its serious side effects involving the kidney or hearing impairment and the emergence of resistant cancer cells [5]. In order to overcome anti-cancer drug resistance, high-dose chemotherapy with increasing dose combination therapy that combines several chemotherapy agents, and concurrent ...
In this study, we have assessed the mechanism of cytotoxicity in a series of cisplatin-sensitive and -resistant ovarian carcinoma cells following treatment with equitoxic concentrations of cisplatin. The specific proteolytic degradation and the enzymatic activities of the DNA-dependent protein kinase (DNA-PK) were assessed in the cisplatin-sensitive A2780 cell line and two resistant derivative cell lines, CP70 and C30. Forty-eight h following cisplatin treatment, unattached, apoptotic A2780 cells demonstrated a 20-30% decrease in DNA-PK phosphorylation activity. The resistant CP70 and C30 cell lines showed greater decreases in activity approaching 80 and 90%, respectively. The decreases in kinase activity were attributed to proteolytic degradation of the catalytic subunit of DNA-PK (DNA-PKcs). The extent of degradation mimicked the loss of DNA-PK activity, with the resistant cell lines showing the greatest portion of degraded DNA-PKcs. At the same time point, the ability of the DNA-PK Ku ...

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Reduce cisplatin by 25%. 30 to less than 50. Reduce fluorouracil by 25% and cisplatin by 50% or consider substituting ... Cisplatin. Commence prehydration for cisplatin:. *administer 10 mmol magnesium sulphate (MgSO4) in 1000 mL sodium chloride 0.9 ... Arm 1 (TPF): docetaxel 75mg/m2 and cisplatin 100 mg/m2 on day 1 followed by fluorouracil 1000 mg/m2/day from day 1 to day 4 Arm ... ciSplatin. 100 mg/m2 (IV infusion) in 1000 mL sodium chloride 0.9% over 60 minutes. ...
Gill KRS, Gross SA, Al-Haddad M, Patel T, Scolapio JS.Cisplatin induced ischemic colitis: a case report. American Journal of ... Cisplatin. React. Wkly. 1175, 11 (2007). ...
Yang Q, et al. Concurrent chemoradiotherapy versus intensitymodulated radiotherapy alone for elderly nasopharyngeal carcinoma patients with pre-treatment Epstein-Barr virus DNA: A cohort study in an endemic area with long-term follow-up. Journal of Cancer 9: 3023-3031, No. 17, 30 Jul 2018. Available from: URL: - ChinaCrossRefPubMedPubMedCentralGoogle Scholar ...
A list of US medications equivalent to Cisplatin Accord is available on the website. ... Cisplatin Accord is a medicine available in a number of countries worldwide. ... Cisplatin Accord may be available in the countries listed below.. Ingredient matches for Cisplatin Accord. Cisplatin. Cisplatin ...
This page contains brief information about cisplatin and a collection of links to more information about the use of this drug, ... Cisplatin is approved to be used alone or with other drugs to treat:. *Bladder cancer that cannot be treated with surgery or ... More About Cisplatin. Definition from the NCI Drug Dictionary - Detailed scientific definition and other names for this drug. ... MedlinePlus Information on Cisplatin - A lay language summary of important information about this drug that may include the ...
Get an overview of CISPLATIN (injection, solution), including warnings and precautions, directions, and the names of other ...
"Cisplatin". Drug Information Portal. U.S. National Library of Medicine. IARC Monograph: "Cisplatin" Medicine portal. ... It is suggested that an antibody reacting with a cisplatin-red-cell membrane is responsible for hemolysis. Cisplatin interferes ... cisplatin is used in Auger therapy.[medical citation needed] Cisplatin has a number of side effects that can limit its use: ... adducts formed by cisplatin in abundance. Cisplatin is the square planar coordination complex cis-[Pt(NH3)2Cl2]. The prefix cis ...
Cisplatin is a platinum-based chemotherapy medicine used to treat cancer. Heres how it works, who should avoid it and the ... How cisplatin treatment given?. Cisplatin infusion is given via a drip into a vein (intravenous infusion). The infusion can ... Cisplatin is often used in combination with other chemotherapy medicines.. Heres everything you need to know about cisplatin, ... Cisplatin: uses and side effects. Cisplatin is a platinum-based chemotherapy medicine used to treat cancer. ...
If cisplatin accidentally seeps out of the vein into which it is injected, it may damage some tissues and cause scarring. Tell ... Cisplatin may lower your bodys resistance and there is a chance you might get the infection the immunization is meant to ... Cisplatin can temporarily lower the number of white blood cells in your blood, increasing the chance of getting an infection. ... While you are being treated with cisplatin, and after you stop treatment with it, do not have any immunizations (vaccinations) ...
Cisplatin (Platinol, CDDP) chemotherapy side effects, how its given, how it works, precautions and self care tips for treatent ... If cisplatin escapes from the vein it can cause tissue damage. The nurse or doctor who gives cisplatin must be carefully ... Cisplatin side effects will improve after therapy is complete.. *Cisplatin side effects may be quite manageable. There are many ... How Cisplatin Is Given:. *Cisplatin is administered through a vein (intravenously or IV) as an infusion. ...
cisplatin (UNII: Q20Q21Q62J) (cisplatin - UNII:Q20Q21Q62J) cisplatin. 1 mg in 1 mL. ... The active ingredient, cisplatin USP, is a yellow to orange crystalline powder. Cisplatin is a heavy metal complex containing a ... Cisplatin is mutagenic in bacteria and produces chromosome aberrations in animal cells in tissue culture. In mice cisplatin is ... Cisplatin Injection is a clear, colorless, sterile aqueous solution. Each 100 mL amber vial of Cisplatin Injection contains: 1 ...
Cisplatin: The Invention of an Anticancer Drug by Andri Smith. *Anti-cancer Agents: A treatment of Cisplatin and their ... Cisplatin resistanceEdit. Cisplatin combination chemotherapy is the cornerstone of treatment of many cancers. Initial platinum ... "Cisplatin". International Drug Price Indicator Guide. Retrieved 8 December 2016.. *^ British national formulary: BNF 69 (69 ed ... Cisplatin". Annals of Internal Medicine. 100 (5): 704-13. doi:10.7326/0003-4819-100-5-704. PMID 6370067.. ...
Cisplatin is used together with other medications to treat bladder cancer, testicular cancer, or ovarian cancer. Cisplatin may ... Cisplatin is a cancer medication that interferes with the growth of cancer cells and slows their growth and spread in the body ... How is cisplatin given?. Cisplatin is injected into a vein through an IV. You will receive this injection in a clinic or ... What other drugs will affect cisplatin?. Cisplatin can harm your kidneys. This effect is increased when you also use certain ...
Interaction of Cisplatin with Glutathione. When cancer cells are exposed to cisplatin, the platinum atom in cisplatin is ... How cells respond to cisplatin-induced DNA damage plays a critical role in deciding cisplatin sensitivity. Cisplatin-induced ... Efflux of cisplatin from the cells by the ATP-dependent transporters, ATP7A and ATP7B. [. 3. ]. Cisplatin binds to cellular ... Cisplatin increased p53 and decreased XIAP in cisplatin-sensitive ovarian cancer 2008 cells but not in cisplatin-resistant ...
Cisplatin and fluorouracil (5FU) chemotherapy treats cancers of the gullet (oesophagus), head and neck, and anus. It may also ... How cisplatin and 5FU is given. You will have cisplatin and 5FU in the chemotherapy day unit or during a short stay in hospital ... What is cisplatin and 5FU?. Cisplatin and fluorouracil (5FU) is a combination chemotherapy treatment used to treat cancers of ... Your course of cisplatin and 5FU. You usually have a course of several cycles of treatment over a few months. Cisplatin and 5FU ...
What is cisplatin?. Cisplatin is a chemotherapy drug used to treat testicular, ovarian, bladder, head and neck, and non-small ... How cisplatin is given. You usually have cisplatin in the chemotherapy day unit or during a stay in hospital. A chemotherapy ... Each cycle of cisplatin usually takes 21 days (three weeks). You usually have the cisplatin on the first day of the cycle. But ... Possible side effects of cisplatin. We explain the most common side effects of cisplatin here. But we dont include all the ...
... with fecal pellets before chemotherapy reduces intestinal damage and systemic inflammation in response to cisplatin. ... Bacteriotherapy Heals Cisplatin Damage * NHLBI selects Moffitt Cancer Center as one of the Cell Therapies Processing Facilities ... Bacteriotherapy Heals Cisplatin Damage * S100A9-Induced Overexpression of Pd-1/Pd-L1 Contributes to Ineffective Hematopoiesis ... The new study indicates that cisplatin induces significant changes in the repertoire of intestinal commensal bacteria, which ...
Sodium thiosulfate can be used to prevent cisplatin-induced ototoxicity in children and adolescents with cancer, according to a ... Cisplatin-induced ototoxicity is permanent and progressive. A clinical-practice guideline is available for ototoxicity ... NEW YORK (Reuters Health) - Sodium thiosulfate can be used to prevent cisplatin-induced ototoxicity in children and adolescents ... Cite this: New Guideline Recommends Sodium Thiosulfate to Prevent Cisplatin-Induced Ototoxicity - Medscape - Jan 16, 2020. ...
Abstract Background Cisplatin is a platinum-based chemotherapeutic that damages genomic DNA leading to cell death. It also ... Cisplatin is known to damage the DNA of oocytes, but the possibility that cisplatin also compromises oocyte survival and ... To begin to address this question, neonatal mice were treated with saline or cisplatin (2 mg/kg or 4 mg/kg) and the short and ... Abstract Background Cisplatin is a platinum-based chemotherapeutic that damages genomic DNA leading to cell death. It also ...
Phenotypic responses to cisplatin were quantified with respect to cell number, proliferation rate and apoptosis, and then ... Overall, our results suggest that, in epithelial-like ovarian cancer cells, NF-κB activation by cisplatin may lead to defective ... Ovarian cancer cell lines with an epithelial status exhibited higher resistance to cisplatin treatment in the MTS assay than ... The current study explored the connection between cellular responses to cisplatin and EMT in ovarian cancer. Expression ...
Several mechanisms have been implicated in cisplatin resistance, including reduced drug uptake, increased cellular … ... Cisplatin is among the most widely used broadly active cytotoxic anticancer drugs; however, its clinical efficacy is often ... Cisplatin resistance and oncogenes--a review Anticancer Drugs. 2000 Apr;11(4):225-36. doi: 10.1097/00001813-200004000-00001. ... Cisplatin is among the most widely used broadly active cytotoxic anticancer drugs; however, its clinical efficacy is often ...
Capecitabine and streptozocin ± cisplatin in advanced gastroenteropancreatic neuroendocrine tumours.. Meyer T1, Qian W2, Caplin ... with or without cisplatin (Cis) 70 mg/m(2) intravenously on day 1. The primary outcome measure was objective response. ... to investigate whether capecitabine combined with streptozocin was an acceptable regimen with or without adding cisplatin. ...
Concurrent Daily Cisplatin and High-Dose Radiation Therapy in Patients With Stage III Non-Small Cell Lung Cancer. *Dieleman E ... Concurrent Daily Cisplatin and High-Dose Radiation Therapy in Patients With Stage III Non-Small Cell Lung Cancer. International ... CCRT consisted of daily low-dose cisplatin (6 mg/m 2 ) combined with 24 fractions of 2.75 Gy to a total dose of 66 Gy. Results ... CCRT with daily low-dose cisplatin for locally advanced stage III NSCLC resulted in promising overall survival (3-year survival ...
The claims of eight cisplatin analogues as viable alternatives to the parent drug are discussed in terms of their toxicities, ... Preclinical studies identifying carboplatin as a viable cisplatin alternative Cancer Treat Rev. 1985 Sep;12 Suppl A:21-33. doi ... The claims of eight cisplatin analogues as viable alternatives to the parent drug are discussed in terms of their toxicities, ...
Infection-Cisplatin decreases your bodys ability to fight infection * Kidney disease-Effects of cisplatin may be increased ... Information about this cisplatin-intravenous-route. Pregnancy Category. Explanation. All Trimesters. D. Studies in pregnant ... If cisplatin accidentally seeps out of the vein into which it is injected, it may damage some tissues and cause scarring. Tell ... Cisplatin belongs to the group of medicines known as alkylating agents. It is used to treat cancer of the bladder, ovaries, and ...
Cisplatin Injection) may treat, side effects, dosage, drug interactions, warnings, patient labeling, reviews, and related ... Cisplatin Injection (cisplatin injection (cisplatin (cisplatin injection) injection) ) is supplied as follows:. NDC 55390-099- ... Cisplatin (cisplatin injection) can cause fetal harm when administered to a pregnant woman. Cisplatin (cisplatin injection) is ... Cisplatin injection (cisplatin injection (cisplatin (cisplatin injection) injection) ) is indicated as therapy to be employed ...
頭痛,発熱,痙攣,意識障害で発症し,経過中に一過性の皮質盲を呈したシスプラチン脳症の1剖検例 [in Japanese] Clinicopathological report of cisplatin encephalopathy [in ... Encephalopathy following cisplatin, bleomycin and vinblastine therapy for non-seminomatous germ cell tumor of testis HITCHINS ... Ototoxicity in patients receiving cisplatin : Importance of dose and method of drug administration REDDEL RR. ... Seizures and cortical dysfunction
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The combined use of 1,25(OH)2D3 and cisplatin may be used as a strategy to overcome resistance to cisplatin and dose ... Magnesium improves cisplatin-mediated tumor killing while protecting against cisplatin-induced nephrotoxicity.Jul 31, 2017. ... Curcumin potentiates Cisplatin-induced proliferation inhibitory effect and apoptosis in A549 and Cisplatin resistant lung ... Additional Keywords : Chemotherapeutic Synergy: Cisplatin, Chemotherapy-Induced Toxicity: Cisplatin, Inflammation, Lipid ...
Find user ratings and reviews for cisplatin intravenous on WebMD including side effects and drug interactions, medication ... 6 Cisplatin treatments @ 1/wk. 7 wks radiation to head and neck. Now cancer free ... BUT ... severe fatigue and chemo brain 6 ... 6 Cisplatin treatments @ 1/wk. 7 wks radiation to head and neck. Now cancer free ... BUT ... severe fatigue and chemo brain 6 ... Read user comments about the side effects, benefits, and effectiveness of cisplatin intravenous. ...
  • Cisplatin injection must be given in a hospital or medical facility under the supervision of a doctor who is experienced in giving chemotherapy medications for cancer. (
  • You will be given docetaxel and cisplatin in the chemotherapy day unit or during a stay in hospital. (
  • Cisplatin is a platinum-based chemotherapy medicine used to treat cancer. (
  • Cisplatin is a platinum-based chemotherapy medicine used to treat a variety of cancers, including bladder cancer, cervical cancer , head and neck cancer, lung cancer, testicular cancer and cancer of the ovaries. (
  • Cisplatin is often used in combination with other chemotherapy medicines. (
  • Etoposide and cisplatin, known as EP (or sometimes PE), is a combination chemotherapy treatment used to treat different cancers. (
  • Cisplatin is an anti-cancer ("antineoplastic" or "cytotoxic") chemotherapy drug. (
  • Cisplatin is a chemotherapy medication used to treat a number of cancers . (
  • cisplatin is one of the most emetogenic chemotherapy agents, but this symptom is managed with prophylactic antiemetics ( ondansetron , granisetron , etc.) in combination with corticosteroids . (
  • Bacteriotherapy with fecal pellets before chemotherapy reduces intestinal damage and systemic inflammation in response to cisplatin, according to new research from Moffitt Cancer Center that was published online by The Journal of Leukocyte Biology . (
  • Cisplatin and Teysuno (pronounced tay-soon-oh) is a combination of chemotherapy drugs. (
  • Cisplatin is a chemotherapy drug that works by damaging the DNA in cancer cells and stopping them from multiplying. (
  • Cisplatin (cisplatin injection) , as a single agent, is indicated as secondary therapy in patients with metastatic ovarian tumors refractory to standard chemotherapy who have not previously received cisplatin (cisplatin injection) therapy. (
  • As compared with the standard regimen of cisplatin and fluorouracil, induction chemotherapy with the addition of docetaxel significantly improved progression-free and overall survival in patients with unresectable squamous-cell carcinoma of the head and neck. (
  • He said that patients who are candidates for chemotherapy should now receive topotecan/cisplatin, rather than single-agent cisplatin. (
  • nearly 80% received radiation therapy, and almost 60% had received prior cisplatin-based chemotherapy. (
  • This research study is evaluating how well triple negative breast cancer responds to preoperative treatment with Cisplatin or Paclitaxel chemotherapy, and if use of a research test Homologous Recombination Deficiency (HRD) assay can predict response to preoperative treatment. (
  • Paclitaxel plus ifosfamide and cisplatin is considered as a standard salvage chemotherapy in relapsed good prognosis GCTs, however, up to 40% of favourable prognosis patients failed to achieve durable response to this combination, and therefore new treatment strategies are warranted. (
  • The resurgence of platinum-based chemotherapy in the last few years has renewed interest in the field, including clinical studies of cisplatin in combination with resistance modulators. (
  • or induction chemotherapy with cisplatin and 5FU followed by radiation. (
  • Otonomy also intends to initiate clinical development for OTO-104 in a second indication, the prevention of hearing loss associated with cisplatin chemotherapy. (
  • Many testicular cancer survivors experience hearing loss after cisplatin-based chemotherapy, according to researchers at Indiana University. (
  • The researchers, led by Lois B. Travis, M.D., Sc.D., the Lawrence D. Einhorn Professor of Cancer Research at the IU School of Medicine and a researcher at the Indiana University Melvin and Bren Simon Cancer Center, studied for the first time the cumulative effects of cisplatin-based chemotherapy on hearing levels in testicular cancer survivors through comprehensive audiometry measurements. (
  • They indicate that it will be important to follow patients given cisplatin-based chemotherapy long term to better understand the extent to which the natural aging process may further add to hearing deficits, as it does in the general population. (
  • Our findings suggest that health care providers should, at a minimum, annually query patients who have received cisplatin-based chemotherapy about their hearing status, consulting with audiologists as indicated. (
  • The researchers found that the sugar was abundant in the cells of invasive bladder cancers that were previously treated but did not respond to the standard chemotherapy drug, cisplatin . (
  • The chemotherapy drug cisplatin is often administered before surgical treatment to reduce the size of cancer. (
  • One of the most effective chemotherapy drugs against cancer is cisplatin because it attaches to cancer DNA and disrupts repair. (
  • Delayed administration of sodium thiosulfate after cisplatin chemotherapy may prevent treatment-related hearing loss in children with standard-risk hepatoblastoma without affecting survival outcomes, according to a study published online June 21 in the New England Journal of Medicine . (
  • WEDNESDAY, June 27, 2018 (HealthDay News) -- Delayed administration of sodium thiosulfate after cisplatin chemotherapy may prevent treatment-related hearing loss in children with standard-risk hepatoblastoma without affecting survival outcomes, according to a study published online June 21 in the New England Journal of Medicine . (
  • Cisplatin (CDDP)-based combination chemotherapy remains the mainstream treatment for advanced bladder cancer. (
  • Adjuvant cisplatin-based chemotherapy for resected NSCLC: one size fits all? (
  • The standard of care for resected stage II - IIIA non-small-cell lung cancer includes adjuvant chemotherapy based on the results of randomized trials using cisplatin regimens. (
  • However, long-term results of the International Adjuvant Lung Cancer Trial evaluating adjuvant cisplatin-based chemotherapy in resected non-small-cell lung cancer indicated a possible late adjuvant chemotherapy-related over-mortality. (
  • In the knowledge of late adjuvant chemotherapy-related over-mortality it is therefore critical to identify subsets of patients who would or would never benefit from adjuvant cisplatin. (
  • Despite highly effective cisplatin-based chemotherapy, around 20% of patients with metastatic disease will still die from the disease. (
  • Evaluation of exposures to healthcare personnel from cisplatin during a mock demonstration of intra-operative intraperitoneal chemotherapy administration. (
  • In preparation for a clinical trial in which chemotherapy would be administered intraoperatively, the question of exposure to healthcare personnel arose, therefore, the purpose of this study was to perform an evaluation of healthcare personnel exposure to cisplatin during a mock demonstration of intraperitoneal chemotherapy administration. (
  • Chemotherapy is considered as the standard treatment for patients with advanced or recurrent cervical cancer, and cisplatin appears to treat the disease effectively. (
  • Nausea and vomiting: cisplatin is one of the most emetogenic chemotherapy agents, but this symptom is managed with prophylactic antiemetics (ondansetron, granisetron, etc.) in combination with corticosteroids. (
  • Concomitant treatment with cilastatin reduced cisplatin-induced changes. (
  • green coffee reduced cisplatin-induced renal apoptosis. (
  • The clinically acquired resistance can be caused by decreased drug accumulation which includes reduced uptake or increased efflux of cisplatin, increased drug detoxification by cellular thiols, increased DNA repair or tolerance of cisplatin-damaged DNA and the ability of the cancer cells to evade cisplatin-induced cell death. (
  • There are many options to help minimize or prevent the side effects of cisplatin. (
  • Common neurological side effects of cisplatin include visual perception and hearing disorder, which can occur soon after treatment begins. (
  • What are the possible side effects of cisplatin? (
  • Hearing problems and loss of balance are more likely to occur in children, who are usually more sensitive to the effects of cisplatin. (
  • These are not all the possible side effects of Cisplatin. (
  • No data were available to evaluate the teratogenic potential or the mutagenicity or chromosomal effects of cisplatin in humans. (
  • Camel milk has protective effects against the clastogenic and cytotoxic effects of cisplatin. (
  • For patients treated with cisplatin-based regimens for other types of cancer, it might also influence a physician to offer an alternative to those patients found to be genetically susceptible to the ototoxic effects of cisplatin after carefully weighing the risks and benefits of alternative treatments. (
  • OBJECTIVE: The purpose of this study was to investigate whether resveratrol adds to the growth inhibitory effects of cisplatin and doxorubicin on ovarian and uterine cancer cells and to evaluate whether resveratrol diminishes the cardiac toxicity of doxorubicin in rodent heart. (
  • The common side-effects of cisplatin usage are generally induced by oxidative stress due to strong electrophilic nature of activated cisplatin ( 3 ). (
  • An ultimate goal is to use the genetic results to develop effective agents that will protect the ear during the administration of cisplatin. (
  • Extra intravenous fluid is given prior to and following administration of cisplatin to reduce side effects to the kidneys. (
  • Kidney function tests and some electrolyte levels may be taken prior to each administration of cisplatin. (
  • The extracellular levels of HMGB1, TNF-α and IFN-γ were also significantly decreased by the administration of cisplatin. (
  • The administration of cisplatin reduced the cytoplasmic levels of HMGB1 and increased nuclear HMGB1 levels in vitro and in vivo . (
  • This was the first study evaluating the exposure of healthcare personnel to the administration of cisplatin intra-operatively. (
  • After the intravenous administration of cisplatin, abnormal motor activity was produced in the involved vagus nerve and in the involved serotonergic neurons via another pathway. (
  • The success of cisplatin therapy is compromised due to dose-limiting toxicity, especially nephrotoxicity as well as resistance by tumor cells to cisplatin. (
  • It has many similarities to human cisplatin nephrotoxicity, which are mentioned in the paper. (
  • Thymoquinone and curcumin combination protects cisplatin-induced kidney injury, nephrotoxicity. (
  • Thymoquinone and curcumin combination protects cisplatin-induced kidney injury, nephrotoxicity by attenuating NFκB, KIM-1 and ameliorating Nrf2/HO-1 signalling. (
  • In summary, Tq + Cur had protective effects on cisplatin-induced nephrotoxicity and renal injury, which could be mediated by up-regulation of survival signals like Akt, Nrf2/HO-1 and attenuation of KIM-1, NFκB. (
  • Effect of short hydration on cisplatin-induced nephrotoxicity in cancer patients: A retrospective study. (
  • A major area in cancer therapy is the search for protective strategies against cisplatin-induced nephrotoxicity. (
  • Effect of TNF-α inhibitors on cisplatin nephrotoxicity. (
  • G1: control negative group was received isotonic saline (0.5 ml, i.p.) for 30 consecutive days, G2: sham operated group mice were received green coffee extract in water (40 mg/kg/day) for 30 consecutive days, animals of G3 and G4 were administered cisplatin (8 mg/kg/day, i.p.) at 10th day, which is well known to produce significant nephrotoxicity in rats. (
  • Cisplatin alone, 90 mg/m 2 body surface area intraperitoneally, produced nephrotoxicity. (
  • medical citation needed] Cisplatin has a number of side effects that can limit its use: Nephrotoxicity (kidney damage) is a major concern. (
  • 2 SUMMARY The principal target organ for cisplatin toxicity is the kidney. (
  • Cisplatin is usually administered in hospital and the administering clinician must monitor the patient for any signs and symptoms of toxicity. (
  • Cumulative renal toxicity associated with cisplatin is severe. (
  • Another active area of research has been to develop analogs of cisplatin to minimize toxicity and circumvent cisplatin resistance. (
  • Conclusions: CCRT with daily low-dose cisplatin for locally advanced stage III NSCLC resulted in promising overall survival (3-year survival rate of 52% and 5-year survival rate of 40%) with low toxicity. (
  • An additional 63 patients were randomized to MVAC (methotrexate/vinblastine/doxorubicin/cisplatin) every 4 weeks, but this arm was closed prematurely due to excessive toxicity and did not yield data for presentation. (
  • This study evaluates the protective effects of Thymoquinone (Tq) and Curcumin (Cur) in models of cisplatin-induced renal toxicity. (
  • This is a phase I dose escalation study of cisplatin and radiation to determine the toxicity of this combined treatment and establish an MTD. (
  • Resveratrol adds to the growth inhibitory/anticancer activity of cisplatin and doxorubicin in vitro and protects against doxorubicin-induced cardiac toxicity both in vitro and in mice. (
  • However, in addition to the efforts against to its toxicity, the amelioration of cisplatin sensitivity is an important point in treatment of cervical cancer. (
  • Multiple mechanisms contribute to renal toxicity following exposure to cisplatin. (
  • [9] While triggering apoptosis through interfering with DNA replication remains the primary mechanism of cisplatin, this has not been found to contribute to neurological side effects. (
  • We have discussed various steps, including the entry of cisplatin inside cells, DNA repair, drug detoxification, DNA damage response, and regulation of cisplatin-induced apoptosis by protein kinases. (
  • Cisplatin, like many other chemotherapeutic drugs, can induce apoptosis. (
  • Thus, the signaling pathways that regulate apoptosis have significant impact on deciding cellular responsiveness to cisplatin. (
  • However, TMRM staining intensity, a marker of mitochondrial membrane potential, was decreased in immature oocytes from cisplatin treated mice compared to saline treated controls, consistent with the induction of apoptosis. (
  • Phenotypic responses to cisplatin were quantified with respect to cell number, proliferation rate and apoptosis, and then compared with the epithelial or mesenchymal status. (
  • Overall, our results suggest that, in epithelial-like ovarian cancer cells, NF-κB activation by cisplatin may lead to defective apoptosis, preferential proliferation arrest and a consequential decreased sensitivity to cisplatin. (
  • Cisplatin (cis-diamminedichloroplatinum [II]) is a platinum compound that forms DNA adducts, which are subsequently involved in the activation of various signal transduction pathways involved in DNA damage recognition, DNA repair, cell cycle arrest and apoptosis. (
  • Furthermore, considerable evidence indicates that mutated p53 plays a significant role in the development of cisplatin resistance since several genes implicated in drug resistance and apoptosis (e.g. mismatch repair, bcl-2, high mobility group proteins, DNA polymerases alpha and beta, PCNA, and insulin-like growth factor) are known to be regulated by the p53 oncoprotein. (
  • Tq + Cur combination synergistically reduced the proliferation inhibition of HEK-293 cells resulted from cisplatin treatment and brought down cisplatin-induced apoptosis in these cells.studies revealed serum levels of BUN, creatinine, CK and pro-inflammatory cytokines like TNF-α, IL-6 and MRP-1 to be elevated in the cisplatin-treated group while reducing glomerular filtration rate. (
  • NP mediated controlled release of Platin-M and subsequent reduction of this prodrug to cisplatin allowed cross-links to be formed with the mitochondrial DNA, which have no nucleotide excision repair system, forcing the overactive cancer cells to undergo apoptosis. (
  • Our observations revealed that EGCG increases the sensitization of cisplatin to cervical cancer cells by inhibiting cell survival and inducing apoptosis. (
  • Two mTORC1/2 inhibitors, AZD8055 and MLN0128, strongly enhanced cisplatin-induced apoptosis in all tested TC cell lines. (
  • Inhibition of caspase activity by caspase-9 inhibitor (z-LEHD-fmk) or by overexpression of Bcl-2 potently inhibited apoptosis induced by cisplatin. (
  • Since Bcl-2 is overexpressed in many cancer cell types and resistance to cisplatin-induced apoptosis is a major limitation for effective therapy, the knowledge from this study could be beneficial to the design of more effective therapy for cancer treatment. (
  • Green coffee administration in cisplatin-induced renal apoptosis groups produced significant lower levels of BUN, creatinine, uric acid and H 2 O 2 (24.4 ± 4.14, 1.730 ± 0.2830, 5.50 ± 0.850 and 0.51 ± 0.12 respectively) as compared with cisplatin-induced renal apoptosis group not administrated green coffee (27.4 ± 6, 2.04 ± .31, 7.00 ± 1.25 and 1.1 ± 0.16 respectively). (
  • Green coffee improved the general condition of cisplatin-induced renal apoptosis rats due to its antioxidant and anti-apoptotic effects. (
  • Cisplatin may cause severe allergic reactions, especially if you have received more than one dose of cisplatin injection. (
  • Cisplatin injection comes as a solution (liquid) to be injected over 6 to 8 hours intravenously (into a vein) by a doctor or nurse in a medical facility. (
  • tell your doctor and pharmacist if you are allergic to cisplatin, carboplatin (Paraplatin), any other medications, or any of the ingredients in cisplatin injection. (
  • 1.7 Presentation/formulation Cisplatin powder for injection: Yellowish-white freeze-dried cake in clear glass vials containing 10mg or 50mg cisplatin. (
  • Cisplatin solution for injection: Clear, practically colourless solution in amber glass vials containing cisplatin 1mg/ml, sodium chloride 9mg/ml and mannitol 1mg/ml with a pH of 3.5-4.0. (
  • Cisplatin Injection is a clear, colorless, sterile aqueous solution. (
  • Each 100 mL amber vial of Cisplatin Injection contains: 1 mg per mL cisplatin USP, 9 mg per mL sodium chloride, hydrochloric acid and/or sodium hydroxide to adjust pH, and water for injection USP to a final volume of 50 mL and 100 mL, respectively. (
  • The pH range of Cisplatin Injection is 3.8 to 5.9. (
  • Call your doctor if you miss an appointment for your cisplatin injection. (
  • Anaphylactic-like reactions to cisplatin (cisplatin injection) have been reported. (
  • Cisplatin Injection (cisplatin injection (cisplatin (cisplatin injection) injection) ) is a sterile aqueous solution, available in 50, 100 and 200 mL multiple dose vials, each mL containing 1 mg of cisplatin (cisplatin injection) and 9 mg sodium chloride in water for injection. (
  • Cisplatin (cisplatin injection) (cis-diamminedichloroplatinum) is a heavy metal complex containing a central atom of platinum surrounded by two chloride atoms and two ammonia molecules in the cis position. (
  • An established combination consists of cisplatin (cisplatin injection) and cyclophosphamide. (
  • PLATINOL® (cisplatin injection) infusion concentrate is a clear, colorless, sterile aqueous solution available in amber vials. (
  • A formulation for preparing Cisplatin 1-mg/mL Injection. (
  • Care must be taken to avoid inadvertent cisplatin overdose due to confusion with carboplatin or prescribing practices that fail to differentiate daily doses from total dose per cycle. (
  • You should not receive this medication if you are allergic to cisplatin or similar medications such as carboplatin (Paraplatin) or oxaliplatin (Eloxatin). (
  • In addition to cisplatin, its analogs, such as carboplatin and oxaliplatin, are also currently being used in the clinic. (
  • Platinum-based anticancer agents such as cisplatin and carboplatin display a broad range of activities against solid tumors ( 11 , 12 ). (
  • It was found that tetracycline-resistant bacteria expressing the TnlO gene of tetracycline resistance, upon induction with tetracycline, became extremely susceptible to destruction by the DNA-damaging anti-cancer drug cisplatin. (
  • By targeting mitochondria with the anticancer drug cisplatin, chemists have developed a new way to kill cancer cells that have shown resistance to cisplatin. (
  • The Saccharomyces cerevisiae PP4R3 ortholog Psy2 was identified previously in a screen for sensitivity to the DNA-damaging agent and anticancer drug cisplatin. (
  • Interestingly deletion of the yeast PP4R3 ortholog PSY2 was demonstrated previously to elicit hypersensitivity to the DNA damage-inducing drug cisplatin ( 10 ). (
  • GOG 179, a multicenter phase II trial, showed the combination of topotecan (Hycamtin) plus cisplatin to be superior in multiple outcome parameters over single-agent cisplatin in the treatment of recurrent or persistent cancer of the cervix, reported Harry J. Long, III, MD, associate professor of oncology, Mayo Clinic College of Medicine, Rochester, Minnesota. (
  • Treatment with topotecan plus cisplatin improved not only response rates and progression-free survival but also overall survival, and is the first controlled trial to show this. (
  • Combination therapy with pemetrexed plus cisplatin is the standard first line therapy for malignant mesothelioma, but results in a median overall survival of only 12.1 months. (
  • Combination of SS1(dsFv)PE38 with pemetrexed plus cisplatin could result in improved outcomes for patients with mesothelioma. (
  • To determine the MTD of SS1(dsFv)PE38 that can be safely administered in combination with pemetrexed plus cisplatin in patients with mesothelioma. (
  • To observe anti-tumor activity, if any of SS1(dsFv)PE38 in combination with pemetrexed plus cisplatin. (
  • Docetaxel plus cisplatin might be an effective therapeutic option for thymoma-associated MG patients complicated with hypertension /diabetes post thymectomy without worsening thymoma and hypertension / diabetes. (
  • Fluorouracil plus cisplatin and radiation twice a day (FCT) is an established chemoradiation (CRT) regimen for selective bladder-sparing treatment of muscle-invasive bladder cancer. (
  • You should not receive cisplatin if you have kidney disease, bone marrow suppression, or hearing loss. (
  • Before you receive cisplatin, tell your doctor about all other medications you use. (
  • You may be given IV fluids for 8 to 12 hours before you receive cisplatin. (
  • After 1 week of imatinib mesylate and folic acid, you will receive cisplatin and pemetrexed by IV infusion. (
  • Cats are vulnerable to severe pulmonary (lung) side effects and cannot receive cisplatin. (
  • In some cases, health care professionals may use the trade name Platinol® and Platinol®-AQ, or other names such as CDDP, when referring to the generic drug name cisplatin. (
  • Chemoresistance is one key factor for the failure of cisplatin (CDDP)-based therapy in colorectal cancer (CRC). (
  • Cisplatin (cis-diamminedichloroplatinum II, CDDP), an inorganic platinum compound, is one of the effective chemotherapeutic agents in the treatment of several types of cancer, including cervical carcinomas ( 1 ). (
  • Cisplatin (cis-diamminedichloroplatinum (II), CDDP) is widely used as a chemotherapeutic drug used in the treatment of numerous human cancers, including bladder, head and neck, ovarian and testicular cancers, lung, and breast. (
  • Cisplatin is used together with other medications to treat bladder cancer, testicular cancer, or ovarian cancer. (
  • Cisplatin has been used as a first-line therapy for several cancers, including testicular, ovarian, cervical, head, and neck and small-cell lung cancers either alone or in combination with other anticancer agents. (
  • Conclusions These findings suggest that mitochondrial dysfunction may contribute to the depletion of the ovarian reserve caused by cisplatin, but long-term impacts on mitochondria may be minimal as those immature oocytes that survive cisplatin treatment develop into mature oocytes with normal mitochondrial parameters. (
  • Chemoresistance to platinums, such as cisplatin, is of critical concern in the treatment of ovarian cancer. (
  • The current study explored the connection between cellular responses to cisplatin and EMT in ovarian cancer. (
  • Expression microarrays were utilized to estimate the EMT status as a binary phenotype, and the transcriptional responses of 46 ovarian cancer cell lines to cisplatin were measured at dosages equivalent to 50% growth inhibition. (
  • Ovarian cancer cell lines with an epithelial status exhibited higher resistance to cisplatin treatment in the MTS assay than those with a mesenchymal status. (
  • Cisplatin is a prescription medicine used to treat the symptoms of cancer in the testicles (Metastatic Testicular Tumors), bladder (Advanced Bladder Cancer ) and ovaries (Metastatic Ovarian Carcinoma). (
  • Cisplatin has been used since the 1970s primarily in the treatment of testicular and ovarian cancer, often in combination with other antineoplastic drugs. (
  • Bitter melon extract functions as a natural AMPK activator in the inhibition of ovarian cancer cell growth and might be useful as a supplement to improve the efficacy of cisplatin. (
  • RUDN biochemists studied the mechanism of drug resistance development in ovarian cancer cells under treatment with cisplatin. (
  • Although this study was conducted in patients with testicular cancer, the authors point out that the general conclusions are likely applicable to patients with other types of adult-onset cancers that are commonly treated with cisplatin. (
  • The researchers pointed out that because alterations in the highly successful testicular cancer regimens are unlikely for patients with advanced disease, their results underscore the importance of ongoing research aimed at the identification of genetic variants associated with cisplatin-related ototoxicity. (
  • The aim of this study was to explore the use of kinase inhibitors to sensitize testicular cancer cells to cisplatin treatment. (
  • How cells respond to cisplatin-induced DNA damage plays a critical role in deciding cisplatin sensitivity. (
  • Furthermore, the identification of oncogenes involved in cisplatin resistance has already led to in vitro approaches which successfully inactivated these genes using ribozymes or antisense oligodeoxynucleotides, thus restoring cisplatin sensitivity. (
  • Previously, it was showed that cisplatin resistant TGCTs overexpress ALDH isoforms and inhibition of ALDH activity by disulfiram is associated with reconstitution of cisplatin sensitivity. (
  • Cisplatin-resistant TGCTs exhibited increased sensitivity to ALDH inhibitor disulfiram in vitro. (
  • Investigators hypothesize that inactivation of ALDH by disulfiram recover cisplatin sensitivity in patients with progressing or relapsing germ cell cancer. (
  • A ) Effect of CHIP overexpression and MAST1 knockdown on cisplatin sensitivity and MAST1 protein level. (
  • B ) Effect of MAST1 WT rescue expression on cisplatin sensitivity and MAST1 protein level in cells with CHIP overexpression and MAST1 knockdown. (
  • miR-1271 enhances the sensitivity of colorectal cancer cells to cisplatin. (
  • Cisplatin is administered through a vein (intravenously or IV) as an infusion. (
  • Cisplatin is administered intravenously as short-term infusion in normal saline for treatment of solid malignancies. (
  • You have cisplatin as a drip into your bloodstream (intravenously). (
  • Patients with advanced, unresectable NETs of pancreatic, gastrointestinal foregut or unknown primary site were randomised to receive three-weekly capecitabine (Cap) 625 mg/m(2) twice daily orally, streptozocin (Strep) 1.0 g/m(2) intravenously on day 1, with or without cisplatin (Cis) 70 mg/m(2) intravenously on day 1. (
  • Cisplatin can be given intravenously (into a vein), or intraperitoneally (into the peritoneum of the abdominal cavity). (
  • Cisplatin is usually used intravenously and is given in conjunction with a process called "diuresis. (
  • Cisplatin given intravenously produced abnormal motor activity that lasted up to 5 h. (
  • In normal intact dogs with resection of the vagus nerve that were administered kytril, cisplatin given intravenously did not produce abnormal motor activity. (
  • Cisplatin is administered intravenously as short-term infusion in normal saline for treatment of solid and haematological malignancies. (
  • NEW YORK (Reuters Health) - Sodium thiosulfate can be used to prevent cisplatin-induced ototoxicity in children and adolescents with cancer, according to a new clinical-practice guideline. (
  • Cisplatin-induced ototoxicity is permanent and progressive. (
  • Dr. Sung and colleagues on a multidisciplinary, multinational panel used a systematic review of 27 randomized trials to develop a guideline for the prevention of cisplatin-induced ototoxicity in children and adolescents with cancer. (
  • The authors strongly recommend against using amifostine or sodium diethyldithiocarbamate for the prevention of cisplatin-induced ototoxicity in these patients, based on high-quality and low-quality evidence, respectively. (
  • Based on low-quality evidence, the guideline strongly discourages both using intratympanic middle-ear therapy and altering cisplatin-infusion duration, as a means in itself, to prevent ototoxicity in these patients. (
  • Cite this: New Guideline Recommends Sodium Thiosulfate to Prevent Cisplatin-Induced Ototoxicity - Medscape - Jan 16, 2020. (
  • This study demonstrated that intratympanic administration of 6% OTO-104 protected against ototoxicity observed following both acute and repeat administration of the chemotherapeutic agent cisplatin. (
  • Currently, no drugs or therapeutic strategies have been approved for the treatment of cisplatin-induced ototoxicity by the FDA.Purpose: The purpose of this study was to investigate the otoprotective effects of dexamethasone (DEX)-loaded silk-polyethylene hydrogel (DEX-SILK) following round window membrane administration in the cisplatin-induced ototoxicity mouse model.Methods: The morphology, gelation kinetics, viscosity and secondary structure of the DEX-SILK hydrogel were analyzed. (
  • DEX-SILK (5-60 ng/ml) exhibited significant protective effects against cisplatin-induced cellular ototoxicity and notably reduced the production of reactive oxygen species (ROS). (
  • Other drugs (such as the aminoglycoside antibiotic class) may also cause ototoxicity, and the administration of this class of antibiotics in patients receiving cisplatin is generally avoided. (
  • The ototoxicity of both the aminoglycosides and cisplatin may be related to their ability to bind to melanin in the stria vascularis of the inner ear or the generation of reactive oxygen species. (
  • However, patients who initially respond to cisplatin therapy often develop resistance to the drug during the course of the treatment. (
  • Tumor cells, in contrast to normal cells, respond to cisplatin exposure with transient gene expression to protect or repair their chromosomes. (
  • However, many patients do not respond to cisplatin and need more treatment options. (
  • The antitumor activity of cisplatin is believed to be due to its interaction with chromosomal DNA [ 4 ]. (
  • HeLa cells were used to control the effect of cilastatin on the tumoricidal activity of cisplatin. (
  • Cilastatin attenuates cisplatin-induced cell death in proximal tubular cells without reducing the cytotoxic activity of cisplatin in tumor cells. (
  • There is no relationship between the presence or severity of Cisplatin side effects and effectiveness of cisplatin. (
  • Read user comments about the side effects, benefits, and effectiveness of cisplatin intravenous. (
  • Use of resveratrol to improve the effectiveness of cisplatin and doxorubicin: study in human gynecologic cancer cell lines and in rodent heart. (
  • Cisplatin infusion is given via a drip into a vein (intravenous infusion). (
  • Day 1 - Intravenous (through a vein) infusions of pemetrexed and cisplatin. (
  • Dose Escalation: Begin with Level 1 dose of enzalutamide (orally), with standard doses of cisplatin and gemcitabine via intravenous (IV). (
  • Diuresis employs intravenous fluids to perfuse the kidneys and assist them in their toxin filtration duties which means your pet will have to be hospitalized on the day of treatment and receive intravenous fluids for several hours along with the intravenous cisplatin. (
  • Seventeen patients with intraperitoneal tumors were treated by 4-hour intraperitoneal dialysis with cisplatin alone, or in combination with an intravenous neutralizing agent, sodium thiosulfate. (
  • When intraperitoneal cisplatin therapy was combined with intravenous thiosulfate treatment, the dose of cisplatin could be escalated to 270 mg/m 2 body surface area without causing an increase in serum creatinine levels or undue myelosuppression. (
  • Abstract Background Cisplatin is a platinum-based chemotherapeutic that damages genomic DNA leading to cell death. (
  • SAN DIEGO-For the first time, a combination regimen has shown improved survival over single-agent cisplatin (Platinol) for the treatment of advanced cervical cancer, according to the Gynecologic Oncology Group (GOG) protocol 179, which was presented at the 35th Annual Meeting of the Society of Gynecologic Oncologists (abstract 9). (
  • An understanding of how various signaling pathways regulate cisplatin-induced cell death should aid in the development of more effective therapeutic strategies for the treatment of cancer. (
  • An Oncofetal Glycosaminoglycan Modification Provides Therapeutic Access to Cisplatin-resistant Bladder Cancer. (
  • Furthermore, pharmaceutical inhibition of ITPKB displayed synergistic attenuation of tumor growth with cisplatin, suggesting ITPKB as a promising synthetic lethal target for cancer therapeutic intervention to overcome cisplatin resistance. (
  • Because HMGB1 is a powerful inflammatory mediator in many diseases, the aim of this study is to evaluate the therapeutic effect of cisplatin acute liver failure. (
  • Doses of cisplatin which produce changes in renal function may cause no histopathological changes. (
  • Plasma concentrations of the parent compound, cisplatin, decay monoexponentially with a half-life of about 20 to 30 minutes following bolus administrations of 50 or 100 mg/m 2 doses. (
  • In mice, high doses of cisplatin can induce embryolethality. (
  • Consequently, the protocols among studies differ significantly (i.e., from low nephrotoxic to extremely high lethal doses of cisplatin). (
  • They found that increasing doses of cisplatin were associated with increased hearing loss at most of the tested frequencies, involving 4, 6, 8, 10, and 12 kHz. (
  • 400 mg/m2 cisplatin) doses. (
  • At cumulative doses of cisplatin higher than 300 mg/m2 the patients lost distal tendon and H-reflexes and displayed reduced vibration sense in the feet and the fingers. (
  • Motor conduction studies, autonomic function and warm and cold temperature sensation remained unchanged at all doses of cisplatin treatment. (
  • The results of these studies are consistent with degeneration of large sensory neurons whereas there was no evidence of distal axonal degeneration even at the lowest toxic doses of cisplatin. (
  • The dosing regimen of cisplatin and gemcitabine will be at standard doses of Gemcitabine at 1000 mg/m^2 IV on days 1, 8 and cisplatin at 70 mg/m2 IV on day 1, repeated every 21 days for total of 6 cycles. (
  • Dose Expansion: Enzalutamide at recommended dose level with standard doses of cisplatin and gemcitabine. (
  • Cisplatin, fluorouracil, and docetaxel in unresectable head and neck cancer. (
  • Phase 2 studies suggest that the standard regimen of cisplatin and fluorouracil (PF) plus docetaxel (TPF) improves outcomes in squamous-cell carcinoma of the head and neck. (
  • Cisplatin should not replace mitomycin when given with fluorouracil and radiotherapy in the primary treatment of localized anal canal carcinoma," they concluded. (
  • Combination cisplatin and 5-fluorouracil-induced takotsubo cardiomyopathy in oropharyngeal cancer: A case report. (
  • Bladder Preservation With Twice-a-Day Radiation Plus Fluorouracil/Cisplatin or Once Daily Radiation Plus Gemcitabine for Muscle-Invasive Bladder Cancer: NRG/RTOG 0712-A Randomized Phase II Trial. (
  • Further complicating these mechanisms of platinum resistance, growing evidence has suggested an association between epithelial-mesenchymal transition (EMT) and cellular resistance to many cytotoxic reagents, including cisplatin. (
  • Spreckelmeyer S, Orvig C, Casini A. Cellular Transport Mechanisms of Cytotoxic Metallodrugs: An Overview beyond Cisplatin. (
  • Cisplatin is also used alone or in combination with other medications to treat bladder cancer that can not be treated with surgery or radiation therapy alone. (
  • The main purpose of this study is to find out the dose of enzalutamide that can be safely given with gemcitabine and cisplatin in patients with advanced bladder cancer. (
  • The cohort expansion will then be done by enrolling 12 patients with stage IV bladder cancer, who express androgen receptor (AR) staining of 1+ and above by immunohistochemistry (IHC), to determine the safety and tolerability of cisplatin and gemcitabine with the recommended dose level of enzalutamide (80 mg or 160 mg, depending upon the safety results from dose escalation part) in this expanded cohort of patients with AR + bladder cancer. (
  • Autonomic neuropathy after treatment with cisplatin, vinblastine, and bleomycin for germ cell cancer. (
  • Therefore, cilastatin administration might represent a novel strategy in the prevention of cisplatin-induced acute renal injury. (
  • Our recent financing enables us to expand the scope of our development efforts, and the clinical evaluation of OTO-104 for the prevention of cisplatin-induced hearing loss is a priority based on the high unmet medical need, attractive market potential, and preclinical proof-of-concept presented in this publication," said David A. Weber, Ph.D., president and CEO of Otonomy. (
  • We found that cell viability and liver injury were greatly improved by cisplatin treatment. (
  • Patients may experience an allergic-type reaction within minutes of cisplatin administration consisting of wheezing, difficulty breathing and low blood pressure. (
  • Dexamethasone and high dose metoclopramide: efficacy in controlling cisplatin induced nausea and vomiting. (
  • This page contains brief information about cisplatin and a collection of links to more information about the use of this drug, research results, and ongoing clinical trials. (
  • Find Clinical Trials for Cisplatin - Check for trials from NCI's list of cancer clinical trials now accepting patients. (
  • Cisplatin was indeed demonstrated to possess antitumor activity in a mouse model [ 3 ] and was first used in the clinical trial almost 30 years ago. (
  • Improved understanding of molecular factors for the development of cisplatin resistance may allow the prediction of clinical response to cisplatin-based treatment. (
  • It is conceivable that these strategies, once transferred to a clinical setting, may have the potential to enhance the efficacy of cisplatin against a great variety of malignancies and thus more fully exploit the antineoplastic and curative potential of this drug. (
  • Cisplatin rodent model has been recognized as a simple and reproducible model with high clinical relevance [ 9 ]. (
  • To evaluate clinical and pathologic responses in TNBC treated with preoperative cisplatin and paclitaxel. (
  • Originally my gyno oncologist treatment plan was 1x weekly for each of the 5 weeks of radiation.At Center closer to my home where I receive treatment says there was a new clinical trial that the showed no different results for most that received Cisplatin Week 1 and Week 4 of radiation. (
  • TY - JOUR T1 - Neuronal involvement in cisplatin neuropathy: prospective clinical and neurophysiological studies. (
  • We have published hundreds of Cisplatin Gemcitabine Hydrochloride Radiation Therapy Pancreatic Cancer news stories on BioPortfolio along with dozens of Cisplatin Gemcitabine Hydrochloride Radiation Therapy Pancreatic Cancer Clinical Trials and PubMed Articles about Cisplatin Gemcitabine Hydrochloride Radiation Therapy Pancreatic Cancer for you to read. (
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  • Nausea beginning six hours after treatment and persisting for another six hours is expected with use of cisplatin. (
  • We propose here a new mechanism of cisplatin resistance mediated by glutathione transferase (GST) P1-1, as a cisplatin-binding protein. (
  • At this time, the mechanism of increased DNA damage formation and the mechanism underlying sensitization to cisplatin are still matters of speculation. (
  • However, the molecular mechanism regulating MAST1 levels in cisplatin-resistant tumors is unknown. (
  • Our study not only uncovers the regulatory mechanism of MAST1 in tumors but also suggests a promising combinatorial therapy to overcome cisplatin resistance in human cancers. (
  • As other anti-cancer drugs, the mechanism of cisplatin action occurs by induction of cell death through DNA damage. (
  • The detailed mechanism by which cells recognize and process cisplatin−DNA damage is of great interest. (
  • Mechanism of gastrointestinal abnormal motor activity induced by cisplatin in conscious dogs. (
  • Non-randomized, open-label, single center trial to assess efficacy (as measured by overall response rate (ORR) by RECIST 1.1 of disulfiram and cisplatin in patients with multiple relapsed/refractory germ cell tumors (GCTs). (
  • EGCG improved efficacy of cisplatin treatment in HeLa cells by regulating NFκB p65, COX-2, p-Akt, and p-mTOR pathways, whereas it increased the expression levels of Nrf2/HO-1 in combined therapy. (
  • Use of antioxidant supplements may mitigate this side effect but also can reduce the efficacy of cisplatin against the cancer it is combatting. (
  • However, resistance to cisplatin may develop, thus substantially compromising the efficacy of cisplatin to treat advanced or recurrent cervical cancer. (
  • Cisplatin does not undergo the instantaneous and reversible binding to plasma proteins that is characteristic of normal drug-protein binding. (
  • In addition, AP-2 transcription factors, modulated by protein kinase A, are also implicated in cisplatin resistance by regulating genes encoding for DNA polymerase beta and metallothionines. (
  • Our results show that cisplatin can be inactivated by this protein with the aid of 2 solvent-accessible and reactive cysteines. (
  • The research team studied the effect of the malaria protein - drug combo in mice, whose bladders were implanted with highly aggressive cancers that were resistant to treatment with cisplatin. (
  • Because cisplatin binds covalently to protein, labeling remains strong through subsequent steps used in downstream mass cytometry staining protocols. (
  • Recent studies have focused on the ability of cisplatin to retain the high mobility group box 1 (HMGB1) protein in cisplatin-DNA adducts, thereby preventing its release from the nucleus. (
  • Although the family of proteins that bind cisplatin 1,2- and 1,3-intrastrand cross-links has been identified, much less is known about cellular protein interactions with cisplatin interstrand cross-links (ICLs). (
  • Cisplatin administration increased expression of the apoptotic protein caspase-3. (
  • Using a combination of tandem affinity purification tagging and mass spectrometry, we characterized a novel, evolutionarily conserved protein phosphatase 4 (PP4)-containing complex (PP4cs, protein phosphatase 4, cisplatin-sensitive complex) that plays a critical role in the eukaryotic DNA damage response. (
  • Day one - you have etoposide as a drip (infusion) over an hour and cisplatin as a drip (infusion). (
  • Before and/or after the cisplatin infusion, extra IV fluids are given and care is taken to ensure adequate hydration before both during and after cisplatin, to protect your kidney function. (
  • Cisplatin also has been used as an infusion into the abdominal cavity (contains the abdominal organs). (
  • Targeting hsp90B sensitized cancer cells to cisplatin predominantly through MAST1 destabilization. (
  • Targeting ITPKB with shRNA or its small-molecule inhibitor resulted in attenuation of NOX4 activity, imbalanced redox status, and sensitized cancer cells to cisplatin treatment in patient-derived xenografts. (
  • Cisplatin may cause serious kidney problems. (
  • To help understand mechanisms involved in the development of kidney injury, cisplatin rodent model has been developed. (
  • Given the complex pathogenesis of kidney injury, which involves both local events in the kidney and interconnected and interdependent systemic effects in the body, cisplatin rodent model is indispensable in the investigation of underlying mechanisms and potential treatment strategies of both acute and chronic kidney injury. (
  • Nowadays, 20-30% of patients develop acute kidney injury (AKI) after cisplatin treatment despite improvements in therapy [ 1 ]. (
  • The investigation of the development of CKI was not gaining any attention, although it was known that cisplatin can have long term effects on the structure and function of the rat kidney after single [ 10 - 12 ] or multiple [ 13 - 15 ] administration. (
  • Cisplatin can cause kidney damage. (
  • Cisplatin is used combination with other medications to treat cancer of the testicles that has not improved or that has worsened after treatment with other medications or radiation therapy. (
  • Cisplatin is used alone or in combination with other medications to treat cancer of the ovaries (cancer that begins in the female reproductive organs where eggs are formed) that has not improved or that has worsened after treatment with other medications or radiation therapy. (
  • Slight changes in liver function and histopathology are also observed following cisplatin therapy. (
  • Cisplatin side effects will improve after therapy is complete. (
  • In addition, cisplatin is used in Auger therapy . (
  • Microbiota Reconstitution Restores Intestinal Integrity After Cisplatin Therapy. (
  • The study randomized 145 patients to single-agent cisplatin, 50 mg/m 2 every 3 weeks, and 148 patients to combination therapy with cisplatin 50 mg/m 2 on day 1 plus topotecan 0.75 mg/m 2 on days 1 to 3 every 3 weeks. (
  • The results were the most favorable in the 40% of patients who had not received prior cisplatin as a radiosensitizer, although prior cisplatin therapy did not hold up as an independent predictor in a multivariate analysis. (
  • To evaluate the performance of the HRD-LOH assay, the HRD-TAI assay, and the HRDLST assay, to predict pathologic response to cisplatin or taxane therapy in TNBC. (
  • Although Disulfiram (Antabuse) is an approved drug to support the treatment of chronic alcoholism, it may serve as an antitumor agent suitable for the drug repurposing in combination therapy in order to inhibit ALDH activity thus overcoming a cisplatin resistance in refractory TGCTs. (
  • Standard therapy for mesothelioma is a combination of the drugs pemetrexed and cisplatin. (
  • HOUSTON -- In patients with anal canal carcinoma, a rare malignancy, cisplatin-based induction therapy did not pan out, a randomized trial revealed. (
  • The authors reported colostomy rates of 10% with the mitomycin regimen and 19% with the cisplatin therapy ( P =0.02). (
  • This effect is used in cancer therapy, and cisplatin may operate on a similar principle. (
  • To determine the maximum tolerated dose of cisplatin when given concurrently with radiation therapy for participants with Stage II or III breast cancer who have undergone breast conserving surgery. (
  • We aimed to investigate the possible molecular pathways to potentiate cervical cancer cell (HeLa) growth inhibition by combination therapy of cisplatin and EGCG. (
  • Here you can see the latest Cisplatin Gemcitabine Hydrochloride Radiation Therapy Pancreatic Cancer articles that have been published worldwide. (
  • You can also find out about relevant Cisplatin Gemcitabine Hydrochloride Radiation Therapy Pancreatic Cancer Drugs and Medications on this site too. (
  • Herein, we have demonstrated that EGCG works synergistic with cisplatin in inhibiting growth of cervical cancer cells. (
  • In this article, we systematically review the recent literature and summarize the recent advances in our understanding of the molecular mechanisms underlying cisplatin resistance in cervical cancer. (
  • Treatment of the cells with cisplatin induced rapid generation of reactive oxygen species (ROS) and a concomitant increase in apoptotic cell death. (
  • Recent studies have shown that cisplatin noncompetitively inhibits an archetypal, membrane-bound mechanosensitive sodium-hydrogen ion transporter known as NHE-1 . (
  • In 33 percent of children in the cisplatin-sodium thiosulfate group and 63 percent in the cisplatin-alone group, hearing loss of grade 1 or higher occurred, which indicated a 48 percent lower incidence of hearing loss in the cisplatin-sodium thiosulfate group. (
  • At a median of 52 months of follow-up, the three-year rates of event-free survival were 82 percent in the cisplatin-sodium thiosulfate group and 79 percent in the cisplatin-alone group, while the three-year rates of overall survival were 98 percent and 92 percent, respectively. (
  • We found that the delayed administration of sodium thiosulfate resulted in a significantly lower incidence of cisplatin-induced hearing loss, with no evidence of tumor protection," conclude the authors. (
  • Inhibition of ROS by the antioxidant enzyme catalase or glutathione peroxidase (H2O2 scavenger), but not by superoxide dismutase (O2*- scavenger) or sodium formate (OH* scavenger), inhibited cisplatin-induced Bcl-2 downregulation. (
  • Cisplatin is one of the most effective anticancer agents widely used in the treatment of solid tumors. (
  • Since its approval by the Food and Drug administration in 1978, cisplatin continues to be one of the most effective anticancer drugs used in the treatment of solid tumors. (
  • Indeed, cisplatin is one of the most successful anticancer agents, effective against a wide range of solid tumors. (
  • To see if SS1(dsFV)PE38 given with pemetrexed and cisplatin has any effect on patients tumors. (
  • 5Department of Otology and Laryngology, Eaton-Peabody Laboratory, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Decibel Therapeutics, Boston, MA, 02215, USABackground: Cisplatin is an extensively used anti-neoplastic agent for the treatment of various solid tumors. (
  • Cisplatin is the generic name for the trade name drug Platinol® and Platinol®-AQ. (
  • This treatment takes 1 to 3 hours depending on the dose of Cisplatin. (
  • The researchers found that every 100 mg/m2 increase in cumulative dose of cisplatin resulted in a 3.2 dB impairment in hearing. (
  • After 6 cycles of cisplatin and Teysuno, you may be able to continue to take Teysuno for as long as it works. (
  • After you complete 6 treatment cycles of cisplatin and pemetrexed, you will continue to take imatinib mesylate tablets every day up to 1 month after the 6 treatment cycles. (
  • Although it is well known that cisplatin causes a sensory neuropathy, the primary site of involvement is not established. (
  • Your doctor will order certain tests before, during, and after your treatment to check your body's response to cisplatin. (
  • In this paper, we primarily focused on recent studies on cellular responses to cisplatin-induced DNA damage although we briefly discussed steps leading to cisplatin-induced DNA damage. (
  • Docetaxel and cisplatin is used to treat non-small cell lung cancer. (
  • Each cycle of docetaxel and cisplatin takes 21 days (3 weeks). (
  • On the first day, you will have docetaxel and cisplatin. (
  • This study will also help in finding out the effect on tumor of the combination of enzalutamide, gemcitabine and cisplatin. (
  • Cisplatin and other platinum-based chemotherapeutic agents are routinely used in treating numerous tumor types with approximately 500,000 patients including 2,000 children treated each year in the United States. (
  • Cisplatin should be administered under the supervision of a qualified physician experienced in the use of cancer chemotherapeutic agents. (
  • Cisplatin (CP) is one of important tumour chemotherapeutic agents in humans. (
  • Furthermore, combined treatment with a hsp90 inhibitor and the MAST1 inhibitor lestaurtinib further abrogated MAST1 activity and consequently enhanced cisplatin-induced tumor growth arrest in a patient-derived xenograft model. (
  • Through a metabolism-related kinome RNAi screen, we identified inositol-trisphosphate 3-kinase B (ITPKB) as a critical enzyme that contributes to cisplatin-resistant tumor growth. (
  • We demonstrated that inositol 1,3,4,5-tetrakisphosphate (IP4), the product of ITPKB, plays a critical role in redox homeostasis upon cisplatin exposure by reducing cisplatin-induced ROS through inhibition of a ROS-generating enzyme, NADPH oxidase 4 (NOX4), which promotes cisplatin-resistant tumor growth. (
  • Combined AZD8055 and cisplatin treatment resulted in effective mTORC1/2 inhibition, increased caspase-3 activity, and enhanced tumor growth inhibition. (

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