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
DBL CISPLATIN INJECTION medication page for healthcare professionals to search for scientific information on Pfizer medications. Also find the prescibing information, announcements, resources, and channels to connect with Pfizer Medical Information.
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]).. ...
Fingerprint Dive into the research topics of Randomized, multinational, phase III study of docetaxel plus platinum combinations versus vinorelbine plus cisplatin for advanced non-small-cell lung cancer: The TAX 326 Study Group. Together they form a unique fingerprint. ...
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 ...
... was the first to be developed. In 1983 pediatric oncologist Roger Packer began incorporating cisplatin into adjuvant ... "Cisplatin". Drug Information Portal. U.S. National Library of Medicine. IARC Monograph: "Cisplatin" Portal: Medicine (Articles ... It is suggested that an antibody reacting with a cisplatin-red-cell membrane is responsible for hemolysis. Cisplatin can ... adducts formed by cisplatin in abundance. Cisplatin is the square planar coordination complex cis-[Pt(NH3)2Cl2].: 286-8 : 689 ...
Examples: iron pentacarbonyl, titanium tetrachloride, cisplatin Usually, organometallic compounds are considered to contain the ... Cisplatin). The field, which incorporates many aspects of biochemistry, includes many kinds of compounds, e.g., the phosphates ...
When cisplatin forms interstrand crosslinks (5'-GC), there is a severe distortion to the DNA helix due to a shortened distance ... "Cisplatin". National Cancer Institute. 2007-03-02. Retrieved 2017-10-09. Cimino, G. D.; Gamper, H. B.; Isaacs, S. T.; Hearst, J ... When cisplatin generates DNA crosslinks, it more frequently forms 1,2-intrastrand crosslinks (5'-GG), but also forms 1,3- ... Cisplatin (cis-diamminedichloroplatinum(II)) and its derivatives mostly act on adjacent guanines at their N7 positions. The ...
"Cisplatin". Science & Research (Drugs). United States Food and Drug Administration. Reuther LO, Vainer B, Sonne J, Larsen NE ( ... Genetic variants of TPMT have also been associated with cisplatin-induced ototoxicity in children. TPMT is now listed as a ... "Genetic variants in TPMT and COMT are associated with hearing loss in children receiving cisplatin chemotherapy". Nat. Genet. ... pharmacogenomic biomarker for adverse drug reactions to cisplatin by the FDA. Cancer pharmacogenomics GRCh38: Ensembl release ...
Several chemotherapeutic agents, for example Cisplatin, are associated with acute and chronic kidney injuries. Newer agents ... Cisplatin nephrotoxicity. In: UpToDate, Palevsky PM (Ed), UpToDate, Waltham, MA, 2013. ... cisplatin-nephrotoxicity Robinson, Emily S.; Khankin, Eliyahu V.; Karumanchi, S. Ananth; Humphreys, Benjamin D. (1 November ...
Unlike cisplatin, carboplatin may be susceptible to alternative mechanisms. Some results show that cisplatin and carboplatin ... or the like-cisplatin hypothesis. Activation, or the unlike-cisplatin hypothesis. The former is more accepted owing to the ... It may be used for some types of testicular cancer but cisplatin is generally more effective. It has also been used to treat ... Relative to cisplatin, the greatest benefit of carboplatin is its reduced side effects, particularly the elimination of ...
... and cisplatin. These treatment regimens have been reported to lower local recurrence rates, prolong disease-free survival rates ... plus dacarbazine or cisplatin; cyclophosphamide, doxorubicin, plus dacarbazine; high dose methotrexate; or etoposide, ...
TMEM205 has been shown to be involved in Cisplatin resistance. Cisplatin is a chemotherapeutic drug that is commonly used to ... In addition to being involved in Cisplatin resistance there is growing evidence that the protein is also involved in the ... Shen DW, Gottesman MM (March 2012). "RAB8 enhances TMEM205-mediated cisplatin resistance". Pharmaceutical Research. 29 (3): 643 ... is associated with cisplatin resistance". Journal of Cellular Physiology. 225 (3): 822-8. doi:10.1002/jcp.22287. PMC 2971691. ...
The test is still used to assay samples of the drug cisplatin, but it is mainly of pedagogical interest, as it illustrates the ... The Kurnakov test is sometimes used to detect transplatin in samples of the drug cisplatin. In hot aqueous solution, the cis- ... "The Discovery and Development of Cisplatin". Journal of Chemical Education. 83 (5): 728-773. Bibcode:2006JChEd..83..728A. doi: ...
Alderden, Rebecca A.; Hall, Matthew D.; Hambley, Trevor W. (1 May 2006). "The Discovery and Development of Cisplatin". J. Chem ... An illustrative example is the preparation of the anti-cancer drug cisplatin from potassium tetrachloroplatinate. Beilstein ...
Cisplatin, or cis-diamminedichloroplatinum(II) is the first of a series of square planar platinum(II)-containing chemotherapy ... Side effects of cisplatin include nausea and vomiting, hair loss, tinnitus, hearing loss, and nephrotoxicity.) Organoplatinum ... The hexachloroplatinate ion The anion of Zeise's salt Dichloro(cycloocta-1,5-diene)platinum(II) Cisplatin Archaeologists have ... Riddell, Imogen A.; Lippard, Stephen J. (2018). "Cisplatin and Oxaliplatin:Our Current Understanding of Their Actions". In ...
Cisplatin and etoposide, Carboplatin and etoposide. The drug paclitaxel may be useful in the treatment of cisplatin-resistant ... About 68.1% of cisplatin-resistant cells appear to be sensitive to paclitaxel and 66.7% of paclitaxel-resistant cells to ... In Japan, first-line treatment is shifting to irinotecan and cisplatin. When the primary site is in the skin, it is referred to ... In cases of LS-SCLC, combination chemotherapy (usually cisplatin or carboplatin plus etoposide) is administered together with ...
Such agents include cisplatin and bleomycin. Cisplatin is known as a platinum coordination complex. Carboplatin and oxaliplatin ... Cisplatin and other platinum coordination complexes work by reacting with various sites on DNA in mainly cancer cells in order ... The mechanism of cisplatin in inducing ototoxicity is believed to involve the accumulation of reactive oxygen species, which ... The use of D-methionine to protect against hearing loss induced by drugs like cisplatin and aminoglycosides is preliminarily ...
Cleft lip and palate transmembrane protein 1-like protein (CLPTM1-like protein), also known as cisplatin resistance-related ... CRR9p is associated with cisplatin-induced apoptosis. CLPTM1L, which lies within a cancer susceptibility locus on chromosome 5 ...
Barnett Rosenberg, 82, American chemist, discovered cisplatin. Raul Solnado, 79, Portuguese actor and comedian, cardiovascular ...
Zamble, Deborah B.; Mu, David; Reardon, Joyce T.; Sancar, Aziz; Lippard, Stephen J. (1996-01-01). "Repair of Cisplatin−DNA ... Lippard on cisplatin, an anti-cancer drug. Her research considered the role of p53 in the cellular response to the drug. Zamble ... "Cisplatin and DNA repair in cancer chemotherapy". Trends in Biochemical Sciences. 20 (10): 435-439. doi:10.1016/S0968-0004(00) ... "HMG-domain proteins specifically inhibit the repair of the major DNA adduct of the anticancer drug cisplatin by human excision ...
... and cisplatin, which is used in chemotherapy. Amikacin should not be used with neuromuscular blocking agents, as they can ...
"Partial reversibility of cisplatin nephrotoxicity in children". The Journal of Pediatrics. 118 (4): 531-534. doi:10.1016/S0022- ...
Cisplatin was the first to be developed. Cisplatin is particularly effective against testicular cancer; the cure rate was ... In this form of chemotherapy, commonly used drugs include cisplatin, oxaliplatin, and carboplatin, but several have been ... As studied mainly on cisplatin, but presumably for other members as well, platinum-based antineoplastic agents cause ... Rudd GN, Hartley JA, Souhami RL (1995). "Persistence of cisplatin-induced DNA interstrand crosslinking in peripheral blood ...
Basu A, Krishnamurthy S (August 2010). "Cellular responses to Cisplatin-induced DNA damage". Journal of Nucleic Acids. 2010: 1- ...
2003). "Effect of cisplatin treatment on speckled distribution of a serine/arginine-rich nuclear protein CROP/Luc7A". Biochem. ... "Entrez Gene: CROP cisplatin resistance-associated overexpressed protein". Human LUC7L3 genome location and LUC7L3 gene details ... LUC7 like 3 pre-mRNA splicing factor (LUC7L3), also known as Cisplatin resistance-associated overexpressed protein, or CROP, is ... This gene encodes a cisplatin resistance-associated overexpressed protein (CROP). The N-terminal half of the CROP contains ...
Aziridines include thiotepa, mytomycin and diaziquone (AZQ). Cisplatin and derivatives include cisplatin, carboplatin and ... Drugs with medium risk include doxorubicin and platinum analogs such as cisplatin and carboplatin. On the other hand, therapies ... October 2014). "Strategic targeting of the PI3K-NFκB axis in cisplatin-resistant NSCLC". Cancer Biology & Therapy. 15 (10): ... Rybak LP, Mukherjea D, Jajoo S, Ramkumar V (November 2009). "Cisplatin ototoxicity and protection: clinical and experimental ...
Rybak LP, Mukherjea D, Jajoo S, Ramkumar V (November 2009). "Cisplatin ototoxicity and protection: clinical and experimental ... and platinum based chemotherapeutics such as cisplatin and carboplatin. In addition to medications, hearing loss can also ...
Cisplatin resistance occurs when cancer cells develop an enhanced ability to reverse such damage by removing the cisplatin from ... The cisplatin-resistant cells upregulate expression of the excision repair cross-complementing (ERCC1) gene and protein. Some ... In ovarian cancer, the ATP7B gene encodes for a copper efflux transporter, found to be upregulated in cisplatin-resistant cell ... Platinum-based chemotherapies, such as cisplatin, target tumour cells by cross-linking their DNA strands, causing mutation and ...
The major elements are cisplatin, carboplatin, and oxaliplatin. It has been reported with full recovery among early-stage ... It is known as the hyperthermic intraperitoneal chemotherapy (HIPEC), containing docetaxel, and cisplatin. Given the drug is ... and cisplatin, also known as the BEP treatment. Patients should be issued with 3-4 cycles of BEP to ensure full salvage. ... which consists of cisplatin, ifosfamide and paclitaxel. Yet, it is likely that OGCT survivors after BEP therapy will have ...
Commonly used drugs include cisplatin, vincristine, and methotrexate.[clarification needed] Side effects include anemia ( ...
July 2003). "Phase III study of pemetrexed in combination with cisplatin versus cisplatin alone in patients with malignant ... Cisplatin and pemetrexed together give patients a median survival of 12.1 months. Cisplatin in combination with raltitrexed has ... albeit with similar survival figures to patients receiving cisplatin. Cisplatin in combination with premetrexed disodium, folic ... For patients in whom cisplatin cannot be used, carboplatin can be substituted but non-randomised data have shown lower response ...
Rybak LP, Mukherjea D, Jajoo S, Ramkumar V (November 2009). "Cisplatin ototoxicity and protection: clinical and experimental ... and platinum based chemotherapeutics such as cisplatin and carboplatin. In 2007, the U.S. Food and Drug Administration (FDA) ...
"Investigation into ubiquitin signalling in response to cisplatin". Discovery Research Portal. University of Dundee. Retrieved 2 ... predicted to be a part of the ubiquitin ligase family and involved with DNA repair mechanisms after treatment with cisplatin, a ...
Cisplatin ("Platinol") was given instead of carboplatin ("Paraplatin"). He resided in Rome, New York with his second wife, ...
Cisplatin is a type of chemotherapy. It is a treatment for a number of different types of cancer. Find out about how you have ... Cisplatin. Cisplatin is a chemotherapy drug. You might have it as a treatment for a number of different types of cancer. ... How does cisplatin work?. Cisplatin is a type of chemotherapy. It destroys quickly dividing cells, such as cancer cells. ... How often do you have cisplatin?. You usually have cisplatin as cycles of treatment. Each cycle varies depending on what type ...
Cisplatin Injection: learn about side effects, dosage, special precautions, and more on MedlinePlus ... Cisplatin may cause severe allergic reactions, especially if you have received more than one dose of cisplatin injection. If ... Before taking cisplatin,. *tell your doctor and pharmacist if you are allergic to cisplatin, carboplatin (Paraplatin), any ... If you become pregnant while receiving cisplatin, call your doctor. Cisplatin may harm the fetus. ...
... weekly cisplatin plus radiotherapy has been shown to be not only less toxic than dosing once every three weeks but also ... For Saba, the take-home message of the trial is that weekly cisplatin "is now, finally, an accepted standard of care in the ... For the first time, weekly cisplatin plus radiotherapy (CDDP+RT) has been shown to be not only less toxic than dosing once ... Cite this: Weekly Cisplatin New Standard in Postop Head and Neck Cancer - Medscape - Jun 10, 2020. ...
JavaScript is disabled for your browser. Some features of this site may not work without it ...
Drug Information on cisplatin includes side effects, uses, drug interactions, dosage, drug pictures, overdose symptoms, and ... What is cisplatin (Platinol, Platinol (Restricted Access), Platinol-AQ)?. *What are the possible side effects of cisplatin ( ... You should not breastfeed while using cisplatin.. How is cisplatin given (Platinol, Platinol (Restricted Access), Platinol-AQ)? ... Nervous system problems may occur up to several weeks after you receive cisplatin, and these effects may not be reversible. ...
Phase II Gemcitabine + Cisplatin +/- Iressa Bladder CCT. The safety and scientific validity of this study is the responsibility ... Drug Information available for: Cisplatin Gemcitabine Gemcitabine hydrochloride Gefitinib Genetic and Rare Diseases Information ... Cisplatin. Gefitinib. Antineoplastic Agents. Antimetabolites, Antineoplastic. Antimetabolites. Molecular Mechanisms of ... An Open Randomised Phase II Study Of Gemcitabine Plus Cisplatin +/- Concomitant or Sequential ZD1839 in Patients With Advanced ...
... no drug or FDA approved treatment is currently available to prevent cisplatin … ... Cisplatin is a potent drug used in about 40% of cancer treatment but also leads to severe deafness in 60-80% of the cases. ... Cisplatin is a potent drug used in about 40% of cancer treatment but also leads to severe deafness in 60-80% of the cases. ... Systemic application of honokiol prevents cisplatin ototoxicity without compromising its antitumor effect Am J Cancer Res. 2020 ...
Thirty-six rats were administered intraperitoneally (i.p.) single dose cisplatin 10 mg/kg and divided in to 3 groups. ... This study was conducted to investigate the preventive effect of oxytocin (OT) on cisplatin-induced neurotoxicity in rats. ... We suggest that oxytocin may have beneficial effects against cisplatin-induced neurotoxicity. ... nontreated cisplatin-injected rats showed significantly higher TNF-,i,α,/i, and MDA levels and lower GSH level than ...
Peripheral sensory neuropathy and cisplatin chemotherapy. Robert I. Roelofs, William Hrushesky, Joanne Rogin, Leon Rosenberg ... Patients with advanced cancer, previously untreated, were given 60 mg/m2 cisplatin plus 60 mg/m2 adriamycin by monthly ...
Istradefylline protects from cisplatin-induced nephrotoxicity and peripheral neuropathy while preserving cisplatin antitumor ... Istradefylline protects from cisplatin-induced nephrotoxicity and peripheral neuropathy while preserving cisplatin antitumor ... 0.001 versus cisplatin; 2-way ANOVA (. n. = 5/group). (. B. and C. ) mRNA levels of Il1b. (. B. ) and Ccl2. (. C. ) in DRGs 8 ... 0.01 versus cisplatin; 2-way ANOVA (. n. = 5/group). (. D. -. G. ) Time-course evaluation of mechanical sensitivity in mice ...
... cisplatin) is a platinum-based chemotherapy drug often used in combination to treat a variety of cancers, including ... Platinol (cisplatin) Rheumatrex (methotrexate) Sutent (sunitinib) Taxol (paclitaxel) Medical Marijuana Care Providers Clinical ... Recent Studies Using Cisplatin. Cisplatin has been in use for decades, but researchers continue to use it in studies as a ... What Is Cisplatin?. Cisplatin is a platinum-containing chemotherapy drug that specifically attacks fast-growing cells in the ...
Seventeen biopsies of osteosarcoma patients receiving primary metotrexate, cisplatin and adryamicin chemotherapy followed by ... L. Richter, M. Buzzi and C. Dantas-Barbosa, "TP53 Mutations and Chemotherapy Response to Neoadjuvant Metotrexate, Cisplatin and ... 2010) TP53 mutations and pathologic complete response to neoadjuvant cisplatin and fluorouracil chemotherapy in resected oral ... TP53 Mutations and Chemotherapy Response to Neoadjuvant Metotrexate, Cisplatin and Adryamicin Chemotherapy in Resected ...
6 Studies found for: mesothelioma AND tumor AND Cisplatin AND Cisplatin , Recruiting, Not yet recruiting, Available Studies , ...
How then should cisplatin-resistant cancers be treated? Cisplatin-resistant cell lines are often more sensitive to another ... but not directly to cisplatin resistance. There are multiple resistance mechanisms induced by cisplatin treatment, even in the ... Many mechanisms of cisplatin resistance have been proposed from studies of cellular models of resistance including changes in ... Two models were developed from H69 SCLC cells, H69-CP and H69CIS200 using 100 ng/ml or 200 ng/ml cisplatin respectively. Both ...
... cisplatin and capecitabine for stage IV gastric cancer in Japanese patients: A feasibility study ... Figure 3 Case 8. Computed tomography images before (A, C) and after (B, D) four courses of modified docetaxel, cisplatin and ... cisplatin and capecitabine for stage IV gastric cancer in Japanese patients: A feasibility study. World J Gastroenterol 2017; ... cisplatin and capecitabine (DCX) (mDCX). The primary lesion (A, B), swollen lymph nodes along the common hepatic artery (#8) (C ...
Understanding Cisplatin Resistance Mediated by a Copper Efflux Protein. *Boal, Amie Kathleen (PI) ... Preliminary data indicate that cisplatin can directly bind these proteins, all of which share a common fold and bind Cu(I) via ... DESCRIPTION (provided by applicant): Cisplatin is a widely used anticancer drug but its efficacy is limited due to intrinsic ... The proposed study will examine the interaction between cisplatin and regulatory copper binding domains (MBDs) from the ...
Using a sensitive technique to measure and map cisplatin in mouse and human ear tissues researchers found that forms of ... By looking at inner ear tissue of mice after the first, second, and third cisplatin treatment, researchers saw that cisplatin ... NIH Researchers Find Link Between Cisplatin Build-up and Hearing Loss. Dec 19, 2017 , Research , 0 , ... The NIH team pursued a new angle on the problem: What if the inner ear is not able to get rid of cisplatin, and cells in the ...
This document is a guide only and cannot cover every possible situation. The health professionals caring for you should always consider your individual situation when making decisions about your care. Contact your cancer clinic staff or doctor if you have any questions or concerns about your treatment, or you are having problems coping with side effects. While eviQ endeavours to link to reliable sources that provide accurate information, eviQ and the Cancer Institute NSW do not endorse or accept responsibility for the accuracy, currency, reliability or correctness of the content of linked external information sources. Use of this document is subject to eviQs disclaimer available at ...
3. Patients who will receive TAI using cisplatin or oxaliplatin. 4. Must give informed consent. 5. If patient is female and of ... Effects of Acupoint Electro-stimulation on Preventing Nausea and Vomiting Induced by Cisplatin or Oxaliplatin. Trial Phase:. N/ ...
Aminoglycoside (AG) antibiotics are widely used to prevent life-threatening infections, and cisplatin is used in the treatment ... the AGs and cisplatin. ORC-13661 also prevents both hearing loss in a dose-dependent manner in rats treated with amikacin and ... ORC-13661 protects sensory hair cells from aminoglycoside and cisplatin ototoxicity. JCI Insight, 4 (15). pp. 1-19. ISSN 2379- ... that it may reduce the toxicity of AGs by directly competing for entry at the level of the MET channel and of cisplatin by a ...
The pharmacogenomics of cisplatin-induced hearing loss Pussegoda, Kusala Abstract. Cisplatin is a widely used chemotherapeutic ... Cisplatin is a widely used chemotherapeutic agent for the treatment of solid tumours. A serious complication of cisplatin ... A serious complication of cisplatin treatment is permanent hearing loss. The study hypothesis is that genetic variants in genes ... These findings have the potential to influence treatment modifications for cisplatin therapy and may improve safety in children ...
Phase III study of pemetrexed in combination with cisplatin versus cisplatin alone in patients with malignant pleural ... Siddik ZH: Cisplatin: Mode of cytotoxic action and molecular basis of resistance. Oncogene. 22:7265-7279. 2003. View Article : ... Chen H, Landen CN, Li Y, Alvarez RD and Tollefsbol TO: Enhancement of cisplatin-mediated apoptosis in ovarian cancer cells ... Bax, Bcl-2 associated X protein; Bcl-2, B-cell lymphoma 2; CDDP, cis-dichlorodiammineplatinum (cisplatin); PARP, poly(ADP- ...
... compared to methotrexate/vinblastine/doxorubicin/cisplatin (MVAC) for locally advanced or metastatic transitional cell ... of the urothelium treated with gemcitabine/cisplatin (GC) or methotrexate/vinblastine/doxorubicin/cisplatin (MVAC).. PATIENTS ... Long-Term Survival Results of a Randomized Trial Comparing Gemcitabine Plus Cisplatin, With Methotrexate, Vinblastine, ... Doxorubicin, Plus Cisplatin in Patients with Bladder Cancer December 12, 2018 PURPOSE: To compare long-term survival in ...
2012) Randomized phase Ⅲ study comparing paclitaxel/cisplatin/gemcitabine and gemcitabine/cisplatin in patients with locally ... Background: Methotrexate, vinblastine, doxorubicin, and cisplatin regimen, and gemcitabine and cisplatin regimen are widely ... received another cisplatin-based regimen (e.g., a combination regimen with ifosfamide, 5-fluorouracil, etoposide, and cisplatin ... 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 ...
DENVER-September 12, 2021, 9 a.m. GMT/10 a.m. CDT/11 a.m. EDT)-Neoadjuvant cisplatin and pemetrexed plus atezolizumab followed ... "Neoadjuvant cisplatin and pemetrexed plus atezolizumab followed by surgical resection and maintenance atezolizumab met safety ... Patients received four cycles of neoadjuvant cisplatin and pemetrexed plus atezolizumab (CPA), resection, then radiation (EPP ... Neoadjuvant Atezolizumab in Combination with Cisplatin/Pemetrexed and as Maintenance for Resectable Pleural Mesothelioma Meets ...
A Phase III Randomized Trial of Gemcitabine, Cisplatin, and Nab-Paclitaxel Versus Gemcitabine and Cisplatin in Newly Diagnosed ... and cisplatin (GC) versus those treated with gemcitabine, cisplatin, and nab-Paclitaxel (GCN). SECONDARY OBJECTIVES: I. To ... It is not known if giving gemcitabine hydrochloride and cisplatin with or without nab-paclitaxel may work better at treating ... ARM II: Patients receive cisplatin IV over 60 minutes and gemcitabine hydrochloride IV over 30 minutes on days 1 and 8. Courses ...
We established an in vitro approach wherein ovarian cancer cells with various sensitivities to cisplatin or paclitaxel were ... Four days after treatment the lethality of cisplatin-paclitaxel was evidenced by reduced number of cells, increased hypodiploid ... Seven days after receiving cisplatin-paclitaxel, cultures showed signs of relapse with escaping colonies that repopulated the ... Conversely, cultures exposed to cisplatin-paclitaxel followed by mifepristone not only did not display signs of repopulation ...
In addition, we show that the acquired cisplatin resistance in vitro alters the expression of specific genes and the highly ... We hypothesize that these epigenetic alterations affecting MGMT play a major role in the exquisite sensitivity to cisplatin, ... We studied epigenetic changes in relation to cisplatin response by examining promoter hypermethylation in a cohort of resistant ... These results also implicate defects in epigenetic pathways that regulate gene transcription in cisplatin resistant GCT. ...
All enrolled patients received cisplatin with hydration, magnesium supplementation and mannitol. Cisplatin-induced AKI was ... Nephrotoxicity of cisplatin combination chemotherapy in thoracic malignancy patients with CKD risk factors. BMC cancer ... BACKGROUND: Nephrotoxicity is the major side effect that limits the dose of cisplatin that can be safely administered, and it ... CONCLUSIONS: We should consider avoiding administration of cisplatin to patients with CKD risk factors, particularly cardiac ...
  • Our findings suggest that if we can prevent cisplatin from entering the stria vascularis in the inner ear during treatment, we may be able to protect cancer patients from developing cisplatin-induced hearing loss," said Cunningham. (
  • Patients with more risk factors for CKD tended to have a greater risk of developing cisplatin-induced AKI. (
  • Autotoxicity, neurotoxicity, and nephrotoxicity are the dose-limiting side effects of cisplatin [ 2 ]. (
  • In the present study, we show that the FDA-approved adenosine A2A receptor antagonist istradefylline (KW6002) protected from cisplatin-induced nephrotoxicity and neuropathic pain in mice with or without tumors. (
  • Nephrotoxicity of cisplatin combination chemotherapy in thoracic malignancy patients with CKD risk factors. (
  • BACKGROUND: Nephrotoxicity is the major side effect that limits the dose of cisplatin that can be safely administered, and it is a clinical problem in cancer patients who received cisplatin combination chemotherapy. (
  • Univariate analysis revealed that cardiac disease and use of non-steroidal anti-inflammatory drugs (NSAIDs) were associated with cisplatin-induced nephrotoxicity (odds ratios [OR] 6 and 3.56, 95% confidence intervals [CI] 1.21-29.87 and 1.11-11.39, p = 0.04 and p = 0.04, respectively). (
  • Multivariate analysis revealed that cisplatin nephrotoxicity occurred significantly more often in patients with both risk factors (OR 13.64, 95% CI 1.11-326.83, p = 0.04). (
  • A Canadian Study of Cisplatin Metabolomics and Nephrotoxicity (ACCENT)" by Anshika Jain, Ryan Huang et al. (
  • The A Canadian study of Cisplatin mEtabolomics and NephroToxicity (ACCENT) team was established to harness the power of metabolomics to identify novel biomarkers that predict risk and discriminate for presence of cisplatin nephrotoxicity, so that early intervention strategies to mitigate onset and severity of AKI can be implemented. (
  • Objective: Describe the design and methods of the ACCENT study which aims to identify and validate metabolomic profiles in urine and serum associated with risk for cisplatin-mediated nephrotoxicity in children and adults. (
  • Cisplatin is a widely used chemotherapeutic medication the clinical usage of which is bound by the advancement of dose-dependent nephrotoxicity. (
  • These outcomes may have essential medical implications for preventing the cisplatin-induced nephrotoxicity with PARP inhibitors, IKBA which currently show powerful anticancer actions in medical tests and synergistic anticancer impact with cisplatin in multiple experimental paradigms. (
  • The purpose of this study was to evaluate the role of LA in a model of cisplatin-induced nephrotoxicity. (
  • We demonstrated that use of MAZ51, a selective VEGFR3 inhibitor, caused significantly worse structural and functional kidney damage in cisplatin nephrotoxicity. (
  • Cisplatin nephrotoxicity is associated with vascular congestion due to endothelial dysfunction. (
  • Our findings identify a protective role for de novo LA in cisplatin nephrotoxicity and provide a rationale for the development of therapeutic approaches targeting LA. Our study also suggests off-target effects of MAZ51 on the vasculature in the setting of cisplatin nephrotoxicity. (
  • Objective: The current study was designed to evaluate the protective effect of standardized hydroalcoholic extract of Plumeria rubra (HAEPR) against cisplatin-induced nephrotoxicity in Wistar rats. (
  • tell your doctor and pharmacist if you are allergic to cisplatin, carboplatin (Paraplatin), any other medications, or any of the ingredients in cisplatin injection. (
  • Thus, cisplatin and paclitaxel, and later carboplatin plus paclitaxel, have been broadly accepted as first-line chemotherapy for advanced epithelial ovarian cancer. (
  • Previous results suggested that a combination of HSP90 inhibitors and the cisplatin analogue carboplatin resulted in a strong antitumour synergy in ovarian cancer cells. (
  • Patients were treated on sequential dose escalation cohorts of tarextumab (5-15mg/kg) administered every three weeks with etoposide and either cisplatin or carboplatin (platinum-based therapy). (
  • Recently, our group identified several predictive genetic variants that were highly associated with cisplatin-induced hearing loss in children. (
  • We identified novel variants in ABCB5 (rs10950831, P=1.06×10⁻⁶, OR 2.0) and DPYD (rs6667550, P=0.0047, OR 1.9) that were significantly associated with cisplatin-induced hearing loss. (
  • issue 16, pages 1725-1739) discuss the involvement of TLR2 and TLR4 in autophagy associated with cisplatin-induced acute kidney injury. (
  • To combat this resistance, cisplatin is typically combined with doxorubicin, pemetrexed , and gemcitabine. (
  • Combined with doxorubicin, cisplatin is often used for patients in advanced stages of mesothelioma. (
  • A combination of radical surgery, radiation, and chemotherapy with cisplatin, doxorubicin, and cyclophosphamide significantly improved survival times for patients. (
  • PURPOSE: To compare long-term survival in patients with locally advanced or metastatic transitional cell carcinoma (TCC) of the urothelium treated with gemcitabine/cisplatin (GC) or methotrexate/vinblastine/doxorubicin/cisplatin (MVAC). (
  • Background: Methotrexate, vinblastine, doxorubicin, and cisplatin regimen, and gemcitabine and cisplatin regimen are widely used for advanced or metastatic urothelial carcinomas (UCs). (
  • In patients with advanced or metastatic urothelial cancers (UCs), combination chemotherapy with methotrexate, vinblastine, doxorubicin, and cisplatin (M-VAC) was frequently used as standard treatment [1,2]. (
  • The combination of methotrexate, vinblastine, doxorubicin (Adriamycin), and cisplatin (MVAC) is the standard treatment for metastatic bladder cancer. (
  • A series of resistant models were developed from CCRF-CEM leukaemia cells with increasing doses of cisplatin from 100 ng/ml. (
  • We established an in vitro approach wherein ovarian cancer cells with various sensitivities to cisplatin or paclitaxel were exposed to a round of lethal doses of cisplatin for 1 h plus paclitaxel for 3 h. (
  • Cytostatic concentrations of mifepristone after exposure to lethal doses of cisplatin and paclitaxel in combination blocks repopulation of remnant cells surviving and escaping the cytotoxic drugs. (
  • The first two studies used the Src inhibitor as a cotreatment with single doses of cisplatin in Fischer 344/NHsd rats and nude rats, respectively. (
  • Although the mechanism is known to be related to the accumulation of reactive oxygen species (ROS), no drug or FDA approved treatment is currently available to prevent cisplatin ototoxicity. (
  • Targeting CXCL1 chemokine signaling for treating cisplatin ototoxicity. (
  • However, cisplatin -induced ototoxicity limits the utility of this agent in cancer patients , especially when dose escalations are needed. (
  • Previous studies have demonstrated a role of CXC chemokines in cisplatin ototoxicity . (
  • These results implicate the CXCL1 chemokine as an early player in cisplatin ototoxicity , possibly by initiating the immune cascade, and indicate that CXCR2 is a relevant target for treating cisplatin ototoxicity . (
  • An Src-protein tyrosine kinase inhibitor to reduce cisplatin ototoxicity while preserving its antitumor effect. (
  • Ototoxicity remains a major dose-limiting side effect of cisplatin. (
  • The current studies were carried out to evaluate the effectiveness of a novel Src-protein tyrosine kinase inhibitor in protecting the ear from cisplatin ototoxicity without compromising cisplatin's antitumor effects. (
  • Group-Wide, Prospective Study of Ototoxicity Assessment in Children Receiving Cisplatin Chemotherapy (ACCL05C1): A Report From the Children's Oncology Group. (
  • The objectives of our study were to compare different ototoxicity classification systems, to evaluate the feasibility of including otoacoustic emissions and extended high frequency audiometry, and to evaluate a central review mechanism for audiologic results for cisplatin-treated children in the cooperative group setting. (
  • The SIOP scale may be superior to ASHA, Brock, and CTCAE scales for classifying ototoxicity in pediatric patients who were treated with cisplatin. (
  • DESCRIPTION (provided by applicant): Cisplatin is a widely used anticancer drug but its efficacy is limited due to intrinsic and acquired cellular resistance. (
  • We examined the efficacy and safety of secondline paclitaxel, gemcitabine, and cisplatin (PCG) chemotherapy in Japanese patients. (
  • We, therefore, investigated the efficacy and safety of PCG as second-line chemotherapy regimen after failure of cisplatin-based treatment. (
  • We conducted this prospective, non-randomized phase II study to evaluate the feasibility and efficacy of cisplatin and gemcitabine as adjuvant treatment in patients with resected BTC. (
  • Results: The efficacy of HAEPR was compared with Cisplatin (CP) treated group. (
  • For the first time, weekly cisplatin plus radiotherapy (CDDP+RT) has been shown to be not only less toxic than dosing once every three weeks but also achieves better outcomes in patients with postoperative squamous cell carcinoma of the head and neck (SCCHN), say Japanese researchers. (
  • For Saba, the take-home message of the trial is that weekly cisplatin "is now, finally, an accepted standard of care in the postoperative high-risk setting, which is a major change at this ASCO meeting. (
  • Furthermore, this study demonstrates that predictive models can classify patients based on predicted risk of cisplatin-induced hearing loss. (
  • As oxidative stress and inflammation play the major role in the pathogenesis of cisplatin-induced neurotoxicity and the antioxidant/anti-inflammatory effects of OT are well known, we hypothesized that OT may be beneficial in preventing the cisplatin-induced neurotoxicity. (
  • You usually have cisplatin as cycles of treatment. (
  • Your doctor will order certain tests before, during, and after your treatment to check your body's response to cisplatin. (
  • 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. (
  • Cisplatin is a potent drug used in about 40% of cancer treatment but also leads to severe deafness in 60-80% of the cases. (
  • Cisplatin ( cis -diamminedichloroplatinum) is the first antineoplastic agent which has been used in cancer treatment. (
  • Cisplatin is a potent chemotherapeutic drug that is widely used in the treatment of various solid cancers. (
  • Altogether, our results support the use of istradefylline as a valuable preventive approach for the clinical management of patients undergoing cisplatin treatment. (
  • B and C ) mRNA levels of Il1b ( B ) and Ccl2 ( C ) in DRGs 8 days after the start of cisplatin treatment. (
  • Cisplatin is a common treatment choice for mesothelioma, often used in combination with other drugs. (
  • Combining cisplatin with other medications has been a basic treatment approach for decades. (
  • Cisplatin resistance in these cells correlated with increases in the antioxidant glutathione, yet treatment with buthionine sulphoximine, an inhibitor of glutathione synthesis, had no effect on resistance, suggesting that the increase in glutathione was not directly involved in cisplatin resistance. (
  • There are multiple resistance mechanisms induced by cisplatin treatment, even in the same cell type. (
  • Cisplatin-resistant cell lines are often more sensitive to another chemotherapeutic drug paclitaxel (H69CIS200), or are able to be sensitised to cisplatin with paclitaxel pre-treatment (H69-CP). (
  • The understanding of this sensitisation by paclitaxel using cell models of cisplatin resistance will lead to improvements in the clinical treatment of cisplatin resistant tumours. (
  • The new findings help explain why cisplatin is so toxic to the inner ear, and why hearing loss gets worse after each treatment, can occur long after treatment, and is more severe in children than adults. (
  • In most areas of the body, cisplatin is eliminated within days or weeks after treatment, but in the inner ear, the drug remains much longer. (
  • By looking at inner ear tissue of mice after the first, second, and third cisplatin treatment, researchers saw that cisplatin remained in the mouse inner ear much longer than in most other body tissues, and that it builds up with each successive treatment. (
  • They also studied inner ear tissue donated by deceased adult patients who had been treated with cisplatin, and observed that cisplatin is retained in the inner ear many months or years after treatment. (
  • Aminoglycoside (AG) antibiotics are widely used to prevent life-threatening infections, and cisplatin is used in the treatment of various cancers, but both are ototoxic and result in loss of sensory hair cells from the inner ear. (
  • Cisplatin is a widely used chemotherapeutic agent for the treatment of solid tumours. (
  • A serious complication of cisplatin treatment is permanent hearing loss. (
  • These findings have the potential to influence treatment modifications for cisplatin therapy and may improve safety in children. (
  • We administered PCG to 25 patients with advanced UC after failure of first-line cisplatin-based regimen between 2004 and 2010 at Saitama Red Cross Hospital, which is one of regional cancer treatment centers designnated by the Ministry of Health, Labour and Welfare of Japan since 2005 and is able to provide standard cancer care for regional patients. (
  • In this work we questioned whether the synthetic steroid mifepristone, which as monotherapy inhibits the growth of ovarian cancer cells, is capable of preventing repopulation of ovarian cancer cells if given after a round of lethal cisplatin-paclitaxel combination treatment. (
  • Four days after treatment the lethality of cisplatin-paclitaxel was evidenced by reduced number of cells, increased hypodiploid DNA content, morphological features of apoptosis, DNA fragmentation, and cleavage of caspase-3, and of its downstream substrate PARP. (
  • Male germ cell tumor (GCT) is a highly curable malignancy, which exhibits exquisite sensitivity to cisplatin treatment. (
  • We also demonstrate that cisplatin treatment induce de novo promoter hypermethylation in vivo. (
  • In addition, we show that the acquired cisplatin resistance in vitro alters the expression of specific genes and the highly resistant cells fail to reactivate gene expression after treatment to demethylating and histone deacetylase inhibiting agents. (
  • Blood and urine will be collected at specified time points before and after cisplatin during the first infusion and an infusion later during cancer treatment. (
  • Here we found that in basal-like PDAC cells, the combination of HSP90 inhibition and cisplatin treatment resulted in a synergistic reduction of cell viability, increased DNA damage and chromosome fragmentation. (
  • Our study suggests that PDAC cells show a distinct response towards cisplatin treatment and that combination of cisplatin with the HSP90 inhibitor onalespib is able to overcome cisplatin resistance in basal-like PDAC cells. (
  • Chemotherapy with cisplatin and pemetrexed improves survival in malignant pleural mesothelioma, and immune checkpoint inhibitors are an emerging treatment in this disease. (
  • The current treatment of PC consists of perioperative systemic chemotherapy and cytoreductive surgery, followed by intra-abdominal flushing with solutions of chemotherapeutics such as cisplatin and oxaliplatin. (
  • Purpose: Our previous study demonstrated the benefit of cumulative dose of cisplatin during the whole treatment on locally advanced nasopharyngeal carcinoma (NPC) treated with various chemotherapy strategies. (
  • The purpose of this study is to identify the subgroup of locally advanced NPC who benefits from higher dose of cisplatin, and to clarify whether cumulative dose of cisplatin during the whole treatment brings survival benefit to those treated with concurrent chemoradiotherapy (CCRT). (
  • Despite adequate first-line treatment, nearly one third of patients relapse and almost half develop cisplatin-resistant disease, which is often fatal. (
  • The treatment of cisplatin-resistant disease is challenging and prognosis remains poor. (
  • Here, we provide an overview of current and potential new treatment options including combination chemotherapy, high-dose chemotherapy and molecular targeted therapies, for patients with cisplatin-resistant ovarian germ cell tumors. (
  • In another group of tests, AIQ and PJ34 treatment began 12 and 24 h following the cisplatin. (
  • Gemcitabine plus cisplatin is now considered a first-line treatment for bladder cancer. (
  • Gemcitabine is used in combination with cisplatin for the treatment of advanced or metastatic bladder cancer. (
  • Cisplatin was considered the best treatment option before the advent of the antifolate agents, Dr. Berghmans commented. (
  • In the second trial presented at a press conference by Dr. Berghmans, first-line treatment with raltitrexed plus cisplatin was associated with a progression-free survival of 5.3 months, compared with 4 months for treatment with cisplatin alone ( P = .06). (
  • Cisplatin plus pemetrexed is the best treatment we've got for mesothelioma," Dr. Berghmans asserted. (
  • One patient died due to infectious complications during treatment with cisplatin and gemcitabine. (
  • Cisplatin is chemotherapy used for solid tumor treatment like lung , bladder , head and neck , ovarian and testicular cancers . (
  • KEMPINAS, W. G. Paternal treatment with cisplatin impairs reproduction of adult male offspring in rats. (
  • Optimal assessment methods and criteria for reporting hearing outcomes in children who receive treatment with cisplatin are uncertain. (
  • Eligible participants were 1 to 30 years, with planned cisplatin-containing treatment. (
  • The drug in question is cisplatin, widely used for cancer treatment for more than 40 years. (
  • Researchers also think that long term follow-up of those treated with cisplatin is necessary to see what effect aging has on hearing loss, meaning thorough hearing assessments are important before, during and after treatment. (
  • Cisplatin may cause severe allergic reactions, especially if you have received more than one dose of cisplatin injection. (
  • A child treated with cisplatin may need a hearing test before receiving the first dose. (
  • Peripheral neurotoxicity is a frequent dose-limiting side effect of the chemotherapeutic agent cisplatin. (
  • Thirty-six rats were administered intraperitoneally (i.p.) single dose cisplatin 10 mg/kg and divided in to 3 groups. (
  • Cisplatin-induced peripheral neuropathy is a frequent adverse effect leading to a dose reduction or the early cessation of chemotherapy, thereby potentially impacting patient survival [ 3 ]. (
  • Since cisplatin-induced neurotoxicity is the major dose-limiting adverse effect of cisplatin, there are numerous studies dealing with this issue [ 9 ]. (
  • Who benefited most from higher cumulative dose of cisplatin among patients with locally advanced nasopharyngeal carcinoma treated by intensity-modulated radiation therapy? (
  • Ou X, Xu T, He X, Ying H, Hu C. Who benefited most from higher cumulative dose of cisplatin among patients with locally advanced nasopharyngeal carcinoma treated by intensity-modulated radiation therapy? (
  • The median cumulative dose of cisplatin of 300mg/m 2 was chose to be the cutoff value of low and high dose subgroups. (
  • Cumulative dose of cisplatin were demonstrated an independent prognostic factors for DMFS (HR=0.524, 95% CI 0.340-0.806) and OS (HR=0.577, 95% CI 0.373-0.893) for the entire cohort upon MVA. (
  • Similarly, in the subgroup of T3-4N2-3, higher dose of cisplatin was associated with higher OS (80.3% vs. 52.3%, p=0.032). (
  • Cumulative dose of cisplatin was an independent prognostic factor for DMFS (HR=0.483, 95%CI 0.292-0.798) and OS (HR=0.429, 95%CI 0.258-0.715) for patients with T1-4N2-3 disease upon MVA. (
  • However, the benefit of higher dose of cisplatin was not observed in the subgroup of T3-4N0-1. (
  • For patients receiving CCRT (n=278), those treated with higher dose of cisplatin had a significantly higher DMFS (87.7% vs. 75.4%, p=0.004). (
  • Cumulative dose of cisplatin was associated with a lower risk of distant metastasis (HR=0.427, 95% CI 0.228-0.801) for patients treated with CCRT upon MVA. (
  • The third study was carried out in nude rats with implanted HT-29 tumors, and the Src inhibitor was administered as a cotreatment with a lower dose of cisplatin. (
  • In the third study, little hearing loss was induced because of the use of a lower dose of cisplatin. (
  • It was discovered that for every 100 mg/m 2 increase in cumulative dose of cisplatin, there was a 3.2 decibel (dB) impairment in age-adjusted overall hearing thresholds. (
  • Further, as experimental verification of microarray data, the cytotoxicity of the cisplatin (CDDP) was examined in hMT-3 and mock cells by MTT and clonogenic assays. (
  • The study hypothesis is that genetic variants in genes involved in drug metabolism and transport can contribute to increased susceptibility to hearing loss in pediatric oncology patients treated with cisplatin. (
  • METHODS: We retrospectively analyzed 84 patients treated with cisplatin combination chemotherapy for thoracic malignancies. (
  • PUBLIC HEALTH RELEVANCE: This project will result in molecular level characterization of the interaction between cisplatin, a widely prescribed anticancer drug, and copper transporters. (
  • PRIMARY OBJECTIVES: I. To compare overall survival (OS) in patients with untreated, advanced biliary cancers treated with gemcitabine hydrochloride (gemcitabine) and cisplatin (GC) versus those treated with gemcitabine, cisplatin, and nab-Paclitaxel (GCN). (
  • We analysed the response of a panel of seven PDAC cell lines against the chemotherapeutic agent cisplatin, determining two clearly separated response categories, cisplatin-sensitive and resistant cells. (
  • Oxidative stress, DNA damage, and inflammatory cytokines play major role in the mechanism of cisplatin-induced cytotoxicity [ 10 ]. (
  • Prepared DXA derivatives (M-w = 10-185 kDa) have been conjugated to cisplatin and the M-w of the carrier found to have a significant impact on cisplatin release rates, in vitro cytotoxicity, and migrastatic potential. (
  • The cytotoxicity of cisplatin correlates with cellular arrest in the G2 phase of the cell cycle. (
  • You might have cisplatin on its own or in combination with other cancer drugs or radiotherapy. (
  • The initial chemotherapy which consisted of four cycles of cisplatin and adriamycin alternative with ifosfamide and etoposide was provided. (
  • The survival with cisplatin-docexatel is better compared to cisplatin-etoposide, this applies to PFS as well. (
  • Many mechanisms of cisplatin resistance have been proposed from studies of cellular models of resistance including changes in cellular drug accumulation, detoxification of the drug, inhibition of apoptosis and repair of the DNA adducts. (
  • This suggests that increases in glutathione may contribute to cross-resistance to other drugs and radiation, but not directly to cisplatin resistance. (
  • Recent studies indicate that copper homeostatic proteins, particularly copper transport pumps and chaperones, may mediate cisplatin resistance. (
  • Our findings suggest that promoter hypermethylation of RASSF1A and HIC1 genes play a role in resistance of GCT, while the transcriptional inactivation of MGMT by epigenetic alterations confer exquisite sensitivity to cisplatin. (
  • The cisplatin-resistant cells can be linked to the basal-like subtype, which is characterised by even higher aggressiveness, lower survival rate and chemo-resistance. (
  • Cisplatin-resistant UC cell lines were generated to investigate underlying mechanisms and to develop new approaches for overcoming resistance. (
  • Interestingly, each cisplatin-resistant cell line contained an individual assortment of resistance mechanisms at multiple levels. (
  • Loss-of-function studies showed that CDC25A promoted cisplatin-resistance and paclitaxel-resistance and inhibited the drug-induced apoptosis in ovarian cancer MCS. (
  • 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. (
  • Clinical trials show that patients with mesothelioma live longer when given this combination than when receiving cisplatin alone, and the FDA approved it as a therapy for pleural mesothelioma in 2004. (
  • Cisplatin has also been tested in combination with the chemotherapy drug gemcitabine for mesothelioma patients. (
  • Combination chemotherapy with gemcitabine and cisplatin (GC) has been demonstrated to be equally effective and less toxic than M-VAC [3]. (
  • Materials and Methods: We evaluated the antitumor effects of necitumumab, a recombinant human IgG1 antibody targeting EGFR, in combination with cisplatin plus gemcitabine, pemetrexed, or paclitaxel in a panel of 9 subcutaneous tumor models of NSCLC established in nu/nu athymic mice. (
  • Results: Necitumumab in combination with cisplatin/gemcitabine was particularly effective, although interestingly, the mechanisms underlying these benefits were model dependent. (
  • In the first, 250 patients were randomized to either a combination of cisplatin plus raltitrexed or to cisplatin alone. (
  • Patients initially received gemcitabine 1000 mg/m 2 alone on days 1, 8 and 15 every 28-days for a total of six cycles (single agent cohort), and after protocol amendment a combination therapy with gemcitabine 1000 mg/m 2 and cisplatin 25 mg/m 2 on days 1 and 8 was administered every 21 days for a total of eight cycles (combined regimen cohort). (
  • The interim analysis met the predefined feasibility criteria and, from September 2010 on, the second group of 21 patients received the combination of cisplatin plus gemcitabine. (
  • Patients treated with the combination cisplatin-gemcitabine received an overall median RDI of 100% (IQR 50-100) for cisplatin and 100% (IQR 75-100) for gemcitabine respectively. (
  • CONCLUSIONS: We should consider avoiding administration of cisplatin to patients with CKD risk factors, particularly cardiac disease and NSAID use. (
  • Thus the researchers hope to use the results of the study to develop a way to protect hearing during the administration of cisplatin, rather than seek alternative treatments. (
  • They received intravenous paclitaxel (60 mg/m 2 ) and gemcitabine (1000 mg/m 2 ) on days 1 and 8, and cisplatin (70 mg/m 2 ) on day 2 of every 21-day course. (
  • developed a triplet first-line chemotherapy regimen of paclitaxel, gemcitabine, and cisplatin (PCG) and achieved an excellent response rate of 78% with median overall survival of 24 months [10]. (
  • This phase III trial studies how well gemcitabine hydrochloride and cisplatin given with or without nab-paclitaxel work in treating patients with newly diagnosed biliary tract cancers that have spread to other places in the body. (
  • Drugs used in chemotherapy, such as gemcitabine hydrochloride, cisplatin, and nab-paclitaxel, work in different ways to stop the growth of tumor cells, either by killing the cells, by stopping them from dividing, or by stopping them from spreading. (
  • It is not known if giving gemcitabine hydrochloride and cisplatin with or without nab-paclitaxel may work better at treating biliary tract cancers. (
  • ARM I: Patients receive nab-paclitaxel intravenously (IV) over 30 minutes, cisplatin IV over 60 minutes, and gemcitabine hydrochloride IV over 30 minutes on days 1 and 8. (
  • Seven days after receiving cisplatin-paclitaxel, cultures showed signs of relapse with escaping colonies that repopulated the plate in a time-dependent manner. (
  • Conversely, cultures exposed to cisplatin-paclitaxel followed by mifepristone not only did not display signs of repopulation following initial chemotherapy, but they also had their clonogenic capacity drastically reduced when compared to cells repopulating after cisplatin-paclitaxel. (
  • Neoadjuvant cisplatin and pemetrexed plus atezolizumab followed by surgical resection and maintenance atezolizumab met safety criteria, according to research presented today in OA13: Topics in Pleural Mesothelioma at the IASLC 2021 World Conference on Lung Cancer. (
  • We aimed to evaluate the activity of durvalumab, an anti-PD-L1 antibody, given during and after first-line chemotherapy with cisplatin and pemetrexed in patients with advanced malignant pleural mesothelioma. (
  • Also, nontreated cisplatin-injected rats showed significantly higher TNF- α and MDA levels and lower GSH level than control group. (
  • The best conjugate was four times more effective against malignant prostatic cell lines than free cisplatin and significantly inhibited the ovarian cancer cell migration. (
  • In the first two studies, cotreatment with the Src inhibitor reduced cisplatin-induced hearing loss significantly. (
  • We expect a paradigm shift in cisplatin chemotherapy based on the current study and future clinical trials, where honokiol is applied to reduce side effects including hearing loss. (
  • L. Richter, M. Buzzi and C. Dantas-Barbosa, " TP 53 Mutations and Chemotherapy Response to Neoadjuvant Metotrexate, Cisplatin and Adryamicin Chemotherapy in Resected Osteosarcoma," International Journal of Clinical Medicine , Vol. 4 No. 12A, 2013, pp. 44-50. (
  • The identification of biomarkers predicting and detecting AKI in children and adults treated with cisplatin can greatly inform future clinical investigations and practices. (
  • Injected Cis-pARG-HA NPs showed enhanced antitumor activity in a rat model of PC, compared to injection of the free cisplatin drug. (
  • Therefore, this study demonstrates that nanoparticles carrying chemotherapeutics can be synergistically combined with the PIPAC technique for IP therapy of disseminated advanced ovarian tumors, while this synergistic effect was not observed for the administration of free cisplatin. (
  • Nervous system problems may occur up to several weeks after you receive cisplatin, and these effects may not be reversible. (
  • How often and how many times you receive cisplatin will depend on the type of cancer you have. (
  • ARM II: Patients receive cisplatin IV over 60 minutes and gemcitabine hydrochloride IV over 30 minutes on days 1 and 8. (
  • Patients: Three hundred adults and 300 children planned to receive cisplatin therapy. (
  • Cisplatin was adopted as primary chemotherapy schedule in the 1970s in association with cyclophosphamide [ 5 ]. (
  • Cisplatin is used together with other cancer drugs to treat bladder cancer , testicular cancer , or ovarian cancer . (
  • Moreover, we also demonstrate that the antitumoral properties of cisplatin were not altered by istradefylline in tumor-bearing mice and could even be potentiated. (
  • In this study, we developed cisplatin-loaded polyarginine-hyaluronic acid nanoscale particles (Cis-pARG-HA NPs) with high colloidal stability, marked drug loading efficiency, unimpaired biological activity, and tumor-targeting ability. (
  • Excitingly, PARP-1 in addition has been implicated in the chemoresistance of cancers cells to cisplatin [28, 29] and PARP inhibition displays synergistic chemosensitivity of triple-negative breasts cancer tumor cell lines to gemcitabine and cisplatin [30]. (
  • With this research we looked into the part of PARP-1 in cisplatin-induced kidney damage utilizing a well-established mouse style of cisplatin-induced nephropathy [6, 31C40] and the consequences of PARP inhibitors only or in conjunction with Riociguat cisplatin on viability of tumor cells. (
  • 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. (
  • Patients with advanced cancer, previously untreated, were given 60 mg/m 2 cisplatin plus 60 mg/m 2 adriamycin by monthly intravenous injections. (
  • Because cisplatin targets fast-growing cells, it kills cancer cells and healthy cells that grow and divide rapidly. (
  • Cisplatin causes cancer cells to die by binding to and distorting DNA, triggering cell death. (
  • When first introduced in 1978, many considered cisplatin to be a cure for testicular cancer. (
  • Cisplatin is often combined with other drugs because, as a single agent, it may be effective for a limited period of time before the cancer becomes resistant to the drug. (
  • Cisplatin and similar platinum-based drugs are prescribed for an estimated 10 to 20 percent of all cancer patients, according to the NIH. (
  • The NIH's National Cancer Institute supported research that led to the 1965 discovery of cisplatin and continued development leading to its success as an essential weapon in the battle against cancer. (
  • Objective: To observe the effect of Curcumin in enhancing chemosensitivity of drug-resistant ovarian cancer cell line to cisplatin and investigate its mechanism. (
  • The majority of patients with advanced ovarian germ cell cancer are treated by cisplatin-based chemotherapy. (
  • It is believed that taking cisplatin with black cohosh can decrease the effectiveness of medicine for treating cancer. (
  • Researchers examined the cumulative effects of cisplatin-based chemotherapy on the hearing of testicular cancer survivors through in-depth testing of their ability to hear sounds at different frequencies. (
  • Although it has been in use for more than four decades and is currently one of the most commonly used ototoxic medications used to treat cancer, information about cisplatin-related hearing loss in cancer survivors is limited at this point, as it is just beginning to be studied. (
  • Complicating matters is the fact that cisplatin, despite its association with hearing loss, has been extremely successful in treating testicular cancer in particular. (
  • Researchers also emphasize that although this particular study was focused on testicular cancer patients, the results could apply to anyone with an adult-onset cancer who is treated with cisplatin-based chemotherapy. (
  • Adjuvant chemotherapy with gemcitabine with or without cisplatin was well tolerated and resulted in promising survival of the patients. (
  • Patients with locoregional, pathologically high-risk HNSCC recur frequently despite adjuvant cisplatin-radiation therapy (CRT). (
  • What is the most important information I should know about cisplatin (Platinol, Platinol (Restricted Access), Platinol-AQ)? (
  • What should I discuss with my healthcare provider before receiving cisplatin (Platinol, Platinol (Restricted Access), Platinol-AQ)? (
  • Boric acid improves the behavioral, electrophysiological and histological parameters of cisplatin-induced peripheral neuropathy in rats. (
  • This study was conducted to investigate the preventive effect of oxytocin (OT) on cisplatin-induced neurotoxicity in rats. (
  • Adult male Wistar rats treated with cisplatin demonstrated significant hearing loss , assessed by auditory brainstem responses (ABRs), hair cell loss and loss of ribbon synapse . (
  • Conclusion: Present investigation revealed that HAEPR resulted in attenuation of Cisplatin-induced renal damage in rats. (
  • Three studies were carried out to determine whether this compound has otoprotective activity in rats treated with cisplatin. (
  • To assess the DNA-damaging effect of Auger e- released as close as possible to DNA without chemical damage, we radio-synthesized no-carrier-added (n.c.a.) [189, 191Pt]cisplatin and evaluated both its in vitro properties and DNA-damaging effect. (
  • Patients received four cycles of neoadjuvant cisplatin and pemetrexed plus atezolizumab (CPA), resection, then radiation (EPP cases only), followed by one year of maintenance atezolizumab. (
  • Chart review 3 months after cisplatin therapy end will be conducted to document kidney health and survival. (
  • October 7, 2008 (Berlin, Germany) - Investigators announced the findings from phase 3 studies, which found that cisplatin plus an antifolate - either pemetrexed or raltitrexed - increase survival in patients with mesothelioma nearly 3-fold. (
  • Progression-free survival was 5.7 months in the cisplatin-plus-pemetrexed group and 3.9 months in the cisplatin-monotherapy group, a difference that was highly statistically significant ( P = .001), Dr. Berghmans said. (
  • On the other hand, pathophysiological mechanisms of cisplatin-induced neurotoxicity include oxidative damage, inflammation, mitochondrial dysfunction, DNA damage, and apoptotic cell death in the nervous system [ 11 , 12 ]. (
  • In treating mesothelioma, combinations are often recommended because cisplatin alone has a low response rate on mesothelioma tumors. (
  • Background: Cisplatin, a chemotherapy used to treat solid tumors, causes acute kidney injury (AKI), a known risk factor for chronic kidney disease and mortality. (
  • Methods: Patients will be recruited before their first cycle of cisplatin. (
  • Further, cisplatin efflux by export transporter seemed compromised upon HSP90 inhibition, as the platinum-DNA adduct formation was increased upon HSP90 inhibition. (
  • Endoscopic findings (A, B) and computed tomography images (C, D) before (A, C) and after (B, D) seven courses of modified docetaxel, cisplatin and capecitabine (DCX) (mDCX). (
  • Computed tomography images before (A, C) and after (B, D) four courses of modified docetaxel, cisplatin and capecitabine (DCX) (mDCX). (
  • Seventeen biopsies of osteosarcoma patients receiving primary metotrexate, cisplatin and adryamicin chemotherapy followed by surgery were analyzed. (
  • The platinum in cisplatin can cause kidney damage in some patients, especially those with previous kidney problems. (