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 ...

The purposes of this study are to determine:. How standard gemcitabine plus cisplatin compares to fixed dose rate of gemcitabine plus cisplatin in the treatment of non-small cell lung cancer.. The safety of standard gemcitabine plus cisplatin and any side effects that might be associated with it as compared to a fixed dose rate of gemcitabine plus cisplatin. ...

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, ...

The cumulative incidence of locoregional failures at 3 years was 23% in the cetuximab group vs 9% in the cisplatin group (P = .0036; adjusted cause-specific HR = 2.49, P = .0045). The cumulative incidence of distant failures at 3 years was 9% in the cetuximab group vs 6% in the cisplatin group (P = .52; adjusted cause-specific HR = 1.45, P = .39).. Event-free survival at 3 years was 67% vs 85% (P = .0054; adjusted HR = 1.99, P = .0053). No significant difference in local control was observed between patients who received dose escalation to 73.1 Gy vs those receiving the standard radiotherapy dose.. Toxicity. Acute toxicity profiles differed between groups; nausea, vomiting, acute kidney injury, neutropenia, tinnitus, and dysphagia were significantly more common in the cisplatin group, and mucositis, skin reactions, and acneiform rash were significantly more common in the cetuximab group. Among late adverse events, pain and poor oral mucosa status was significantly more common in the cetuximab ...

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 ...

This is a multicentric randomized phase III trial comparing intensity-modulated radiotherapy plus concomitant cisplatin versus conventional radiotherapy plus concomitant cisplatin in patients with stage III-IV squamous cell carcinoma of oral cavity, oropharynx or hypopharynx. The main end points are the rate of locoregional control and the rate of xerostomia at 2 years.. The IMRT total dose is 75 Gy (50 Gy to PTV1 and T0 + 25 Gy (10 fractions) to PTV2). The conventional radiotherapy total dose is 70 Gy (50 Gy to PTV1 + 20 Gy (10 fractions) to PTV2). In both arms, the cervical nodes will receive 50 Gy (65 Gy in case of Np) by conventional radiotherapy (IMRT is allowed in the IRMT arm). In the two arms, patients will receive concomitant cisplatin (100 mg/m² D1, D21, D42). ...

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]).. ...

TY - JOUR. T1 - Amifostine does not protect against the ototoxicity of high-dose cisplatin combined with etoposide and bleomycin in pediatric germ-cell tumors. T2 - A Childrens Oncology Group study. AU - Marina, Neyssa. AU - Chang, Kay W.. AU - Malogolowkin, Marcio. AU - London, Wendy B.. AU - Frazier, A. Lindsay. AU - Womer, Richard B.. AU - Rescorla, Frederick. AU - Billmire, Deborah F.. AU - Davis, Mary M.. AU - Perlman, Elizabeth J.. AU - Giller, Roger. AU - Lauer, Stephen J.. AU - Olson, Thomas A.. PY - 2005/8/15. Y1 - 2005/8/15. N2 - BACKGROUND. High-dose cisplatin combined with etoposide and bleomycin (HD-PEB) improves event-free survival (EFS) in advanced pediatric germ-cell tumors (PGCT), but has significant ototoxicity. Amifostine appears to protect against toxicity. The authors combined amifostine with HDPEB and evaluated the efficacy and toxicity, specifically whether ototoxicity deccreased. METHODS. Eligibility criteria included age , 15 years and unresectable Stage III/IV ...

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

Concomitant platinum-based chemotherapy and radiotherapy (CT-RT) is the recommended treatment for unresectable locally advanced stage III non-small cell lung cancer (NSCLC). We conducted a phase II study to evaluate the efficacy and safety of fractionated oral vinorelbine with cisplatin as induction CT followed by CT-RT. Patients with stage III NSCLC received 2 induction cycles of intravenous vinorelbine 25 mg/m2 and cisplatin 80 mg/m2 on day 1 and oral vinorelbine 60 mg/m2 on day 8. Responding patients received 2 more cycles of cisplatin 80 mg/m2 on day 1 and oral vinorelbine 20 mg on days 1, 3 and 5 concomitantly with radiotherapy 2 Gy daily, 5 days/week for a total of 66 Gy. Seventy patients, median age 61 years, were enrolled. Overall response rate (ORR) was 50.0%; Disease Control Rate was 81.42%. Median PFS was 14.58 months [95% CI, 10.97-18.75]. Median OS was 17.08 months [95% CI, 13.57-29.57]. One-year and 2-year survival rates were 68.6% [95% CI, 57.7-79.4] and 37%. One patient had a grade 3

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, http://www.cancerresearchuk.org/health-professional/cancer-statistics/statistics-by-cancer-type/bladder-cancer, 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 ...

Patients with locally advanced esophageal cancer who are treated with trimodality therapy have a high recurrence rate. Preclinical evidence suggests that inhibition of cyclooxygenase 2 (COX2) increases the effectiveness of chemoradiation, and observational studies in humans suggest that COX-2 inhibition may reduce esophageal cancer risk. This trial tested the safety and efficacy of combining a COX2 inhibitor, celecoxib, with neoadjuvant irinotecan/cisplatin chemoradiation. This single arm phase 2 trial combined irinotecan, cisplatin, and celecoxib with concurrent radiation therapy. Patients with stage IIA-IVA esophageal cancer received weekly cisplatin 30 mg/m2 plus irinotecan 65 mg/m2 on weeks 1, 2, 4, and 5 concurrently with 5040 cGy of radiation therapy. Celecoxib 400 mg was taken orally twice daily during chemoradiation, up to 1 week before surgery, and for 6 months following surgery. Forty patients were enrolled with stage IIa (30 %), stage IIb (20 %), stage III (22.5 %), and stage IVA (27.5 %)

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 ...

For locally advanced or metastatic urothelial carcinoma, cisplatin-based chemotherapy is the standard regimen. Nevertheless, almost all responding patients experience recurrence within the first year. When patients who have received prior cisplatin-based therapy become resistant, combination therapy with gemcitabine and paclitaxel has been reported. Few published case reports have addressed the utility of paclitaxel/cisplatin/gemcitabine combination therapy as second-line chemotherapy for advanced or metastatic urothelial carcinoma. This is the first report describing paclitaxel/cisplatin/gemcitabine combination therapy for metastatic urothelial carcinoma arising in a transplanted renal allograft and leading to a successful outcome. We present a case of metastatic urothelial carcinoma of a renal allograft in a 32-year-old Japanese man with a history of kidney transplantation ten years prior. Because the patients serum creatinine increased, hemodialysis was resumed, and the surgical allograft was

Cisplatin is one of the most widely used chemical drugs for anticancer treatment. Recent studies have focused on the ability of cisplatin to retain the high mobility group box 1 (HMGB1) protein in cisplatin-DNA adducts, thereby preventing its release from the nucleus. Because HMGB1 is a powerful inflammatory mediator in many diseases, the aim of this study is to evaluate the therapeutic effect of cisplatin acute liver failure. In this study, low-dose cisplatin was administered to treat PMA-induced macrophage-like cells induced by PMA and rats with acute liver failure. We found that cell viability and liver injury were greatly improved by cisplatin treatment. The extracellular levels of HMGB1, TNF-α and IFN-γ were also significantly decreased by the administration of cisplatin. During inflammation, nuclear HMGB1 translocates from the nucleus to the cytoplasm. The administration of cisplatin reduced the cytoplasmic levels of HMGB1 and increased nuclear HMGB1 levels in vitro and in vivo. In conclusion,

Chemotherapy is a standard therapeutic regimen to treat triple-negative breast cancer (TNBC); however, chemotherapy alone does not result in significant improvement and often leads to drug resistance in patients. In contrast, combination therapy has proven to be an effective strategy for TNBC treatment. Whether metformin enhances the anticancer effects of cisplatin and prevents cisplatin resistance in TNBC cells has not been reported. Cell viability, wounding healing, and invasion assays were performed on Hs 578T and MDA-MB-231 human TNBC cell lines to demonstrate the anticancer effects of combined cisplatin and metformin treatment compared to treatment with cisplatin alone. Western blotting and immunofluorescence were used to determine the expression of RAD51 and gamma-H2AX. In an in vivo 4T1 murine breast cancer model, a synergistic anticancer effect of metformin and cisplatin was observed. Cisplatin combined with metformin decreased cell viability and metastatic effect more than cisplatin alone.

TY - JOUR. T1 - Time-dependent influence of procaine hydrochloride on cisplatin antitumor activity in P388 tumor bearing mice. AU - Viale, M.. AU - Vánnozzi, M. O.. AU - Mandys, V.. AU - Esposito, M.. PY - 2001. Y1 - 2001. N2 - In previous papers (1,2) we demonstrated that procaine hydrochloride may increase the therapeutic index of cisplatin by an improvement of its antitumor activity and a reduction of its nephrotoxicity. In the present study we investigated the relationship between the antitumor activity obtained by cisplatin associated with procaine hydrochloride and the relative time of administration of these two agents. When procaine hydrochloride (40 mg/Kg body wt) was administered 30 or 120 minutes before cisplatin (16 mg/kg) diluted in normal saline (i.e. clinical condition) it increased, although not significantly, its percent increase in life span (%ILS) and cure rate (%ILS: +292 and +217 vs +150; cure rate: 46.2% and 42.3% vs 23%, respectively), compared to cisplatin alone ...

TY - JOUR. T1 - Weekly Cisplatin during cranial irradiation for malignant melanoma metastatic to brain. AU - Stewart, David J.. AU - Feun, Lynn G.. AU - Maor, Moshe. AU - Leavens, Milam. AU - Burgess, M. Andrew. AU - Benjamin, Robert S.. AU - Bodey, Gerald P.. N1 - Copyright: Copyright 2007 Elsevier B.V., All rights reserved.. PY - 1983/3. Y1 - 1983/3. N2 - Because Cisplatin potentiates the effect of radiotherapy in animal tumor systems and because Cisplatin is capable of causing regressions of human malignant melanomas, a study was initiated in patients with malignant melanoma metastatic to brain to investigate the feasibility of administering Cisplatin once a week during cranial irradiation. Cisplatin 40 mg/m2/week (three doses) was given LV. to 18 patients during whole brain irradiation, 3 000 rads in 12 fractions over 2 1/2 weeks. Eleven patients also received Cisplatin 120 mg/m2 every three weeks, starting three weeks after cranial irradiation. Median survival was ten weeks, and only one of ...

Antiestrogens are currently used for treating breast cancer patients who have estrogen receptor-positive tumors. However, patients with advanced disease will eventually develop resistance to the drugs. Therefore, compounds effective on antiestrogen-resistant tumors will be of great importance for future breast cancer treatment. In this study, we have investigated the effect of the chemotherapeutic compound cisplatin using a panel of antiestrogen-resistant breast cancer cell lines established from the human breast cancer cell line MCF-7. We show that the antiestrogen-resistant cells are significantly more sensitive to cisplatin-induced cell death than antiestrogen-sensitive MCF-7 cells and we show that cisplatin induces cell death by activating both the caspase and lysosomal death pathways. The antiestrogen-resistant cell lines express lower levels of antiapoptotic Bcl-2 protein compared with parental MCF-7 cells. Our data show that Bcl-2 can protect antiestrogen-resistant breast cancer cells from

TY - JOUR. T1 - Evaluation of the continuous infusion of etoposide plus cisplatin in metastatic breast cancer a collaborative north central cancer treatment group/mayo clinic phase ii study. AU - Krook, James E.. AU - Loprinzi, Charles L.. AU - Schaid, Daniel J.. AU - Kardinal, Carl G.. AU - Mailliard, James A.. AU - Pfeifle, Delano M.. AU - Ellison, Neil M.. AU - Reuter, Nicholas F.. AU - Nelimark, Robert A.. N1 - Copyright: Copyright 2016 Elsevier B.V., All rights reserved.. PY - 1990/2/1. Y1 - 1990/2/1. N2 - A prospective clinical trial was done to evaluate the efficacy and toxicity of cisplatin plus etoposide (VP‐16) in patients with breast cancer who failed one previous chemotherapy regimen for advanced disease or relapsed within 12 months of adjuvant chemotherapy. Partial responses occurred in 11 of 44 evaluable patients (25%; 95% confidence interval (CI), 13% to 40%). The median time to disease progression in responding patients was 4 months (range, 3 to 6+ months), whereas the median ...

TY - JOUR. T1 - Establishment of cisplatin-resistant ovarian yolk sac tumor cells and investigation of the mechanism of cisplatin resistance using this cell line. AU - Shibata, Kiyosumi. AU - Umezu, Tomokazu. AU - Sakurai, Maiko. AU - Kajiyama, Hiroaki. AU - Yamamoto, Eiko. AU - Ino, Kazuhiko. AU - Nawa, Akihiro. AU - Kikkawa, Fumitaka. PY - 2011/3. Y1 - 2011/3. N2 - Background: Cisplatin is used as a key drug for ovarian yolk sac tumor (YST), but relapse may occur. Details of the molecular mechanism responsible for cisplatin resistance remain unclear. Methods: We established cisplatin-resistant ovarian YST cells (NOY1-CR) from parent NOY1. To characterize these cells, we examined cross-resistance to other anticancer drugs. Then, cDNA microarray analysis was performed to quantify gene expression in NOY1 and NOY1-CR cells. The expression of several potential genes related to drug resistance was compared with parent cells by real-time PCR and Western blotting. Knockdown experiments using small ...

Cancer chemotherapy drugs, such as cisplatin, potently produce nausea and vomiting. Acute effects of these treatments are partly controlled by antiemetic drugs, but the delayed effects (|24 h), especially nausea, are more difficult to treat. It is unknown what brain pathways produce this delayed sickness. Our prior data show that brain Fos expression is increased for at least 48 h after cisplatin treatment in the rat, a nonvomiting species. Here, we extend these observations by using house musk shrews (Suncus murinus), a species with an emetic response. Compared with saline injection, cisplatin treatment (30 mg/kg ip) induced Fos expression in hindbrain areas known to play a role in the generation of emesis, the dorsal motor nucleus (DMN), the area postrema, and the nucleus of the solitary tract (NTS), for up to 48 h. Cisplatin also stimulated Fos expression in the parabrachial nucleus (PBN) of the midbrain and the central nucleus of the amygdala (CeA) for at least 48 h after treatment. When animals

To determine the efficacy of the addition of ifosfamide to cisplatin plus etoposide (VIP), or vinblastine (VeIP), in patients with recurrent germ cell tumors. DESIGN: Nonrandomized, prospective phase II trial. SETTING: Tertiary referral university hospital. PATIENTS: Fifty-six of fifty-eight entered patients with measurable and progressive recurrent germ cell tumors of testicular (46 patients), ovarian (1 patient), and extragonadal (9 patients) origin were evaluable for response after not being cured with cisplatin, vinblastine, and etoposide regimens. INTERVENTIONS: Patients were administered cisplatin (20 mg/m2 body surface area daily for 5 days), ifosfamide (1.2 g daily for 5 days), plus either etoposide (75 mg daily for 5 days) or vinblastine (0.11 mg/kg body weight on days 1 and 2). In addition, vigorous intravenous hydration therapy with normal saline (100 to 125 mL/h) was administered during the treatment course. Uroepithelial protective agents, N-acetylcysteine (orally) or mesna ...

WHITEHORN, H et al. High prevalence of cisplatin-induced ototoxicity in Cape Town, South Africa. SAMJ, S. Afr. med. j. [online]. 2014, vol.104, n.4, pp.288-291. ISSN 2078-5135.. BACKGROUND: Cisplatin is administered as the first-line treatment of soft-tissue cancers. It has a reported cure rate of up to 85%, but is associated with a high incidence of ototoxicity, characterised by irreversible bilateral hearing loss and affecting 23 - 50% of adults who receive the drug. OBJECTIVE: To determine the incidence of cisplatin-induced ototoxicity at Groote Schuur Hospital (GSH), Cape Town, South Africa. METHODS: A retrospective cross-sectional study of cisplatin-receiving cancer patients attending GSH between January 2006 and August 2011. RESULTS: A total of 377 patients were recorded as receiving cisplatin therapy during the study period. A 300% increase in new cisplatin-receiving patients receiving audiological monitoring was observed between 2006 and 2010. However, only patients with all clinical ...

TY - JOUR. T1 - Phase I trial of high-dose tamoxifen in combination with cisplatin in patients with lung cancer and other advanced malignancies. AU - Perez, Edith A.. AU - Gandara, David R.. AU - Edelman, Martin J.. AU - ODonnell, Robert. AU - Lauder, Ignacio J.. AU - DeGregorio, Michael. PY - 2003/3/18. Y1 - 2003/3/18. N2 - Background. Tamoxifen has been reported to enhance the antitumor activity of cisplatin in preclinical models by modulation of protein kinase C signal transduction and apoptosis-related pathways. Methods. We conducted a phase I study of high-dose oral tamoxifen in combination with intravenous cisplatin, with two objectives: 1) to determine tolerability, and 2) to determine the daily tamoxifen dose required to achieve serum levels equivalent to in vitro concentrations reported to enhance cisplatin cytotoxicity in preclinical models. Tamoxifen was administered days one through seven at escalating daily doses of 160mg/m2 (n = 5), 200mg/m2 (n = 6), and 250 mg/m2 (n = 4) by ...

Long noncoding RNAs (lncRNAs) play critical roles in tumour progression and metastasis. Emerging evidence indicates that the lncRNA X inactive-specific transcript (XIST) is dysregulated in several tumor types, including non-small cell lung cancer (NSCLC). However, in NSCLC and other cancers the oncogenic mechanism of XIST remains incompletely understood. Here, we confirmed that XIST is upregulated in human NSCLC specimens, and is especially overexpressed in tumors previously treated with cisplatin (cis-diamminedichloroplatinum(II); DDP). In vitro, XIST knockdown inhibited NSCLC cell growth and promoted DDP chemosensitivity by stimulating apoptosis and pyroptosis. Moreover, XIST’s oncogenic effects and ability to promote DDP chemoresistance were largely related to its binding to the TGF-β effector SMAD2, which inhibited its translocation to the nucleus and prevented the transcription of p53 and NLRP3, crucial regulators of apoptosis and pyroptosis, respectively. Using DDP-resistant NSCLC

TY - JOUR. T1 - Cisplatin and TNF-α downregulate transcription of Bcl-xL in murine malignant mesothelioma cells. AU - Fox, S.A.. AU - Kusmiaty, D.. AU - Loh, S.. AU - Dharmarajan, Arunasalam. AU - Garlepp, M.J.. PY - 2005. Y1 - 2005. N2 - Malignant mesothelioma (MM) is an aggressive and highly chemo-resistant tumour. In this study, we examined cisplatin-induced apoptosis in mouse models of this disease and investigated the role of constitutive and inducible expression of apoptosis related genes in this process. All of the four mouse MM cell lines examined expressed Bax, Bcl-xL, c-Myc, and caspase-3 but not Bcl-2. Cisplatin-induced apoptosis characterised by DNA fragmentation and cell death while caspase-3/7 was activated in 3 of 4 cell lines. Quantitation of basal gene expression showed significant differences but there was no correlation between single genes and cisplatin sensitivity. In the AC29 and AB1 models, both cisplatin and TNF-alpha downregulated Bcl-xL gene expression, indicating that ...

Abstract Background: Pineal hormone melatonin (MEL) is a versatile molecule with diverse physiological roles ranging from circadian entrainment to anti-cancer effects. Clinical trials indicated that a co-application of cisplatin and melatonin improved the 1-year survival rate. Also, Futugami (2001) claimed melatonin enhances the sensitivity of an ovarian cancer cell line to cisplatin. Objective: Here we study the anti-cancer effects of a co-application of cisplatin (CDDP, 1pM -10 mM - log10 scale) and melatonin (1pM - 100μM) on MCF-7 cells. Methods: Cell viability was assessed through MTT assays and trypan blue exclusion tests. Results: 1) a) CDDP causes concentration-dependent growth inhibition of MCF-7 cells at high concentrations (1-100 μM) over 24 and 48 hrs with an IC50 of 99.6 ± 5μM (24 hrs) b) Over a period of 6 days, 1uM CDDP causes significant (52.35 ± 0.64% of control) growth inhibition 2) MEL does not significantly inhibit MCF-7 cell growth over 24 hr and 6 day time points. 3)

TY - JOUR. T1 - S-1 plus leucovorin and oxaliplatin versus S-1 plus cisplatin as first-line therapy in patients with advanced gastric cancer (SOLAR). T2 - a randomised, open-label, phase 3 trial. AU - Kang, Yoon Koo. AU - Chin, Keisho. AU - Chung, Hyun Cheol. AU - Kadowaki, Shigenori. AU - Oh, Sang Cheul. AU - Nakayama, Norisuke. AU - Lee, Keun Wook. AU - Hara, Hiroki. AU - Chung, Ik Joo. AU - Tsuda, Masahiro. AU - Park, Se Hoon. AU - Hosaka, Hisashi. AU - Hironaka, Shuichi. AU - Miyata, Yoshinori. AU - Ryu, Min Hee. AU - Baba, Hideo. AU - Hyodo, Ichinosuke. AU - Bang, Yung Jue. AU - Boku, Narikazu. PY - 2020/8. Y1 - 2020/8. N2 - Background: S-1 plus leucovorin and oxaliplatin showed promising efficacy for treatment of advanced gastric cancer in a randomised phase 2 study. We aimed to evaluate the efficacy and safety of oral TAS-118 (S-1 plus leucovorin) and oxaliplatin versus S-1 plus cisplatin in patients with advanced gastric cancer. Methods: We did a randomised, open-label, phase 3 trial in ...

Background: Lung cancer is the most common cancer in males worldwide. The principal mode of treatment inthe early stage of non-small cell lung cancer (NSCLC) is surgery. However, five-year survival is only about 15%for all stages. The aim is to investigate the effect of daily low dose cisplatin concurrently with radiation therapyin advanced NSCLC patients with poor performance status. Materials and Methods: Ten patients diagnosed asinoperable Stage IIIB NSCLC with comorbid disease were assessed retrospectively in Bezmialem Vakif University,Faculty of Medicine, Department of Radiation Oncology, between 2011 to 2013. ECOG performance status wasbetween 3 and 4. Cisplatin was administered at 6mg/m2 daily, for 5 days a week concurrently with radiotherapyusing 160-200 cGy daily fractions, 54 Gy being the lowest and 63 Gy being the highest dose. Results: Completeresponse at the primary tumour site was obtained in 20% patients. Grade I esophagitis was seen 70 percent ofpatients, and the grade II haematological

View more ,Background: Trimodality therapy (TMT) with neoadjuvant chemoradiotherapy (nCRT) using concurrent carboplatin plus paclitaxel (CP) followed by surgery is the standard of care for locoregional esophageal or gastroesophageal junction (GEJ) cancers. Alternatively, nCRT with cisplatin plus fluorouracil (CF) can be used. Definitive chemoradiotherapy (dCRT) with CP or CF can be used if surgery is not planned. In the absence of comparative trials, we aimed to evaluate outcomes of CP and CF in the settings of TMT and dCRT. Methods: A single-site, retrospective cohort study was conducted at the Princess Margaret Cancer Centre to identify all patients who received CRT for locoregional esophageal or GEJ cancer. Overall survival (OS) and disease-free survival (DFS) were assessed using the Kaplan-Meier method and multivariable Cox regression model. The inverse probability treatment weighting (IPTW) method was used for sensitivity analysis. Results: Between 2011 and 2015, 93 patients with esophageal ...

Dr. Chris Carter, project manager and university lecturer at the Strathclyde Institute of Pharmacy and Biosciences, with Professor Alex Mullen and dr. Valeria Ferro discovered that a common chemotherapy drug is used to treat malignant pleural mesothelioma and lung cancer more effectively when administered. evaporated state. The chemotherapy drug cisplatin is an important drug for the treatment of mesothelioma, the chemotherapy drugs used to treat mesothelioma by intravenous drip. This remedy becomes effective after a few hours. the effect will be reduced. However, the Scottish research team has discovered that if Cisplatin is administered by inhalation instead of intravenous drip, the drug begins to work faster and more effectively on the cancerous tissue. ...

TY - JOUR. T1 - [A case report-highly advanced gastric cancer leading to perforation during neoadjuvant chemotherapy with docetaxel, cisplatin and S-1].. AU - Mihara, Koki. AU - Egawa, Tomohisa. AU - Kemmochi, Takeshi. AU - Irino, Tomoyuki. AU - Okamura, Akihiko. AU - Inaba, Yusaku. AU - Eto, Eiichi. AU - Segami, Kenki. AU - Ito, Yasuhiro. AU - Hayashi, Shinobu. AU - Nagashima, Atsushi. PY - 2011/11. Y1 - 2011/11. N2 - A 70-year-old man was found to have advanced gastric cancer with a deep ulcer and multiple lymph-node metastases. Although the tumor was resectable, we predicted that the patient would have a poor outcome. We therefore administered neoadjuvant chemotherapy with docetaxel, cisplatin, and S-1 to improve the prognosis before curative resection. On day 15 of chemotherapy, sudden abdominal pain occurred, and we performed an emergency surgery for a diagnosis of panperitonitis due to gastric cancer perforation. The defect in the gastric wall was about 2 cm in diameter and was located in ...

Patients and Methods Six hundred sixty-seven patients with stage I to IV CCC of the ovary were randomly assigned to receive irinotecan 60 mg/m2 on days 1, 8, and 15 plus cisplatin 60 mg/m2 on day 1 (CPT-P group) every 4 weeks for six cycles or paclitaxel 175 mg/m2 plus carboplatin area under the curve 6.0 mg/mL/min on day 1 every 3 weeks for six cycles (TC group). The primary end point was progression-free survival. Secondary end points were overall survival, overall response rate, and adverse events ...

Phase II trial of gemcitabine [Gemzar], cisplatin, and sunitinib in patients with advanced/metastatic urothelial carcinoma will assess the efficacy and

Background. The addition of cyclo-oxygenase-2 (COX-2) inhibitors and prolonged constant infusion (PCI) of gemcitabine to treatment for advanced non-small-cell lung cancer (NSCLC) might improve treatment efficacy. We aimed to assess whether the addition of rofecoxib or PCI gemcitabine could improve overall survival compared with first-line treatment with cisplatin plus gemcitabine given by standard infusion. Methods. Patients with stage IV or IIIb (with supraclavicular nodes or pleural effusion) NSCLC who were under 70 years of age and who had performance status 0 or 1 were eligible for this multicentre, prospective, open-label, randomised phase III trial with 2×2 factorial design. Patients were randomly assigned to one of four treatment groups: group A,gemcitabine 1200 mg/m2 in a 30-min intravenous infusion on days 1 and 8 and intravenous cisplatin 80 mg/m2 on day 1, every 21 days for six cycles; group B, the same treatments as group A plus oral rofecoxib 50 mg/day until disease progression; ...

Platinum resistance is a major cause of treatment failure in ovarian cancer. We previously identified matrix metalloproteinase 9 (MMP-9) as a potential therapeutic target of chemoresistant disease. A2780cis (cisplatin-resistant) and A2780 (cisplatin-sensitive) ovarian carcinoma cell lines were used. The cytotoxic effect of MMP-9/MMP-2 inhibitor, (2R)-2-[(4-Biphenylsulfonyl) amino]-3 phenylpropionic acid (C21H19NO4S) alone or in combination with cisplatin was determined using high content screening. Protein expression was examined using immunohistochemistry and ELISA. Co-incubation of cisplatin and an MMP-9/MMP-2 inhibitor, (2R)-2-[(4-Biphenylsulfonyl) amino]-3 phenylpropionic acid (C21H19NO4S) resulted in significantly greater cytotoxicity as compared to either treatment alone in a cisplatin resistant MMP-9 overexpressing cell line; A2780cis. In addition, pre-incubating with MMP-9i prior to cisplatin further enhances the cytotoxic effect. No significant difference was observed in MMP-9 protein in tissue

The worlds first wiki where authorship really matters. Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts.

Of 224 patients entered on this study, 30 were ineligible for a variety of reasons, leaving 194 evaluable patients. Early in the study, the dose of the combination regimen was reduced by 20% (1 day) because of toxicity. The investigational arms were balanced for age, grade, and Gynecologic Oncology Group performance status. Percentages of adverse effects reported in 191 patients receiving chemotherapy included (ifosfamide/cisplatin-ifosfamide) grade 3 or 4 granulocytopenia (36/60), grade 3 or 4 anemia (8/17), grade 3 or 4 central nervous system toxicity (19/14), and grade 3 or 4 peripheral neuropathy (1/12). Treatment may have contributed to the deaths of 6 patients treated with full doses of ifosfamide and cisplatin for 5 days. The proportion of patients responding to ifosfamide alone versus ifosfamide-cisplatin therapy was (0.36 versus 0.54) overall, 0.47 versus 0.61 for pelvic, 0.21 versus 0.54 for lung, and 0.33 versus 0.40 for other metastatic sites of measurable disease. The relative ...

Metastatic urothelial carcinoma remains a disease that is associated with few therapeutic options, poor prognosis and short-term survival. Worldwide, an estimated 429,800 of new cases of urinary bladder cancer and 165,100 deaths occurred in 2012 [1].. Cisplatin-containing combination therapy is standard-of-care for metastatic patients, with a median overall survival (OS) of 12.5-15 months and a long-term disease free survival in about 15% of patients [2-5]. Unfortunately, approximately 50% of patients are unfit for cisplatin-containing chemotherapy and may only be palliated with carboplatin-based regimens, without a statistically significant improvement in OS or progression-free survival (PFS) [2, 6].. Therapies blocking the PD-1/PD-L1 pathway (e.g. pembrolizumab, nivolumab and atezolizumab) have shown encouraging responses in patients with metastatic urothelial carcinoma, with an overall response rate of 15-26% [6-10]. This has resulted in the recent FDA approval of nivolumab and atezolizumab ...

Trade Name: Platinol®, Platinol®-AQ. For which conditions is this drug approved? The FDA has approved cisplatin for the following conditions: metastatic testicular cancer in combination with other chemotherapy agents following appropriate surgery and/or radiation therapy; metastatic ovarian cancer in combination with other chemotherapy agents following appropriate surgery and/or radiation therapy, or as a single agent in metastatic ovarian cancer that has stopped responding to other standard chemotherapy agents; and advanced bladder cancer that is not suitable for surgery and/or radiation. It is important for patients to remember that physicians have the ability to prescribe medication for conditions other than those for which the drug has been approved by the FDA. Patients who have received a prescription of this drug for a condition other than which it is approved may wish to discuss this issue with their physician.. What is the mechanism of action? Cisplatin belongs to a group of drugs ...