Journal articles on the topic 'Ovarian cancer, cisplatin, dose intensity'
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1
Levin, L., and W. M. Hryniuk. "Dose intensity analysis of chemotherapy regimens in ovarian carcinoma." Journal of Clinical Oncology 5, no. 5 (May 1987): 756–67. http://dx.doi.org/10.1200/jco.1987.5.5.756.
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The relationship between outcome and dose intensity was analyzed for first-line chemotherapy of advanced ovarian cancer using a particular CHAP (cyclophosphamide, hexamethylmelamine, Adriamycin [Adria Laboratories, Columbus, OH], cisplatin) regimen as the standard. Previously described techniques were used to calculate the average dose intensity of regimens containing one, two, three, or all four drugs of CHAP, relative to the standard. The average relative dose intensity, especially the relative dose intensity of cisplatin, correlated significantly with clinical response and with median survival time (MST) of the entire group (not just the remitters). There was a distinct advantage for multiagent regimens over single alkylating agents and especially for multiagent regimens containing cisplatin. Survival correlated with response rate (of multiagent regimens). This analysis suggests that dose intensity is a determinant of treatment outcome. Prospective randomized trials would be required to test whether, and to what extent, dose intensity determines outcome independently of total amount of drug given, performance status, or other factors. If dose intensity does determine outcome, methods of increasing it should be tested in an attempt to improve treatment results.
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McGuire, W. P., W. J. Hoskins, M. F. Brady, H. D. Homesley, W. T. Creasman, M. L. Berman, H. Ball, J. S. Berek, and J. Woodward. "Assessment of dose-intensive therapy in suboptimally debulked ovarian cancer: a Gynecologic Oncology Group study." Journal of Clinical Oncology 13, no. 7 (July 1995): 1589–99. http://dx.doi.org/10.1200/jco.1995.13.7.1589.
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PURPOSE We report a prospective randomized trial in women with advanced ovarian cancer to evaluate the importance of chemotherapy dose-intensity on survival, progression-free survival (PFS), and response. PATIENTS AND METHODS A total of 485 patients with epithelial ovarian cancer and residual masses more than 1 cm following surgery (stage III presentation) or any stage IV presentation were randomly assigned to receive either standard therapy (cyclophosphamide 500 mg/m2 and cisplatin 50 mg/m2 intravenously every 3 weeks for eight courses) or intense therapy (cyclophosphamide 1,000 mg/m2 and cisplatin 100 mg/m2 intravenously every 3 weeks for four courses). Dose modification was rigidly controlled to maintain intensity. Clinical and pathologic responses were assessed, when appropriate, as well as PFS interval and survival. RESULTS A total of 458 patients met all eligibility criteria and were assessed for survival and PFS. The dose-intensive group received the same total dose of cyclophosphamide and cisplatin, but 1.97 times greater dose-intensity than the standard group. Clinical and pathologic response rates; response duration, and survival were similar in both groups of patients. Hematologic, gastrointestinal, febrile episodes, septic events, and renal toxicities were significantly more common and severe in the dose-intensive group. CONCLUSION A doubling of the dose-intensity in the treatment of bulky ovarian epithelial cancers led to no discernible improvement in patient outcome and was associated with more severe toxicity. This study provides no evidence to support the hypothesis that modest increases in dose-intensity without increasing total dose are associated with significant improvement in overall survival or PFS.
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Conte, P. F., M. Bruzzone, F. Carnino, A. Gadducci, R. Algeri, A. Bellini, F. Boccardo, et al. "High-dose versus low-dose cisplatin in combination with cyclophosphamide and epidoxorubicin in suboptimal ovarian cancer: a randomized study of the Gruppo Oncologico Nord-Ovest." Journal of Clinical Oncology 14, no. 2 (February 1996): 351–56. http://dx.doi.org/10.1200/jco.1996.14.2.351.
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PURPOSE The aim of the study was to compare high-versus low-dose cisplatin in combination with cyclophosphamide and epidoxorubicin as primary chemotherapy for suboptimal stage III and IV ovarian cancer. PATIENTS AND METHODS One hundred forty-five patients were randomized to receive six courses of cisplatin 50 or 100 mg/m2 plus epidoxorubicin 60 mg/m2 and cyclophosphamide 600 mg/m2. The two treatment arms were well balanced; all patients had greater than 2 cm and 37.2% had greater than 5 cm of residual disease; 29.6% had stage IV disease. RESULTS Patients in the high-dose arm received a double dose-intensity and double total dose of cisplatin. The high-dose regimen induced significantly more episodes of leukopenia (47.8% v 32.8%, P = .05), thrombocytopenia (21.7% v 3.2%, P = .003), anemia (37.6% v 12.5%, P = .002), nephrotoxicity (six v one patient), and neurotoxicity (30.4% v 6.3%, P = .002). There were no significant differences in efficacy in terms of clinical response rate (high-dose 57.5% v low-dose 61.1%), pathologic complete response (CR) (9.6% v 18.1%), median survival times (29 v 24 months), and median progression-free survival (18 v 13 months). CONCLUSION This study shows that doubling the dose-intensity and total dose of cisplatin in combination with epidoxorubicin and cyclophosphamide has significant toxic effects and does not improve clinical outcome in patients with suboptimal ovarian cancer.
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Gandara, D. R., W. A. Nahhas, M. D. Adelson, S. M. Lichtman, E. S. Podczaski, S. Yanovich, H. D. Homesley, P. Braly, P. S. Ritch, and S. R. Weisberg. "Randomized placebo-controlled multicenter evaluation of diethyldithiocarbamate for chemoprotection against cisplatin-induced toxicities." Journal of Clinical Oncology 13, no. 2 (February 1995): 490–96. http://dx.doi.org/10.1200/jco.1995.13.2.490.
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PURPOSE Diethyldithiocarbamate (DDTC) blocks cisplatin-induced toxicities in animal models without inhibiting antitumor effects. DDTC chemoprotection was tested in a randomized, multicenter, double-blind comparison versus placebo (PB) in patients with lung or ovarian cancer. Primary end points were nephrotoxicity, ototoxicity, neuropathy, and completion of therapy. PATIENTS AND METHODS Between April 1990 and February 1992, 221 patients were registered with small-cell lung cancer (SCLC), non-small-cell lung cancer (NSCLC), or ovarian cancer. Cisplatin (100 mg/m2) and cyclophosphamide (in ovarian cancer) or etoposide (in lung cancer) were administered with either DDTC (1.6 g/m2 over 4 hours) or PB intravenously, every 4 weeks for a planned six cycles. RESULTS At an interim safety analysis, data were available for 195 patients from the combined lung and ovarian cancer populations (PB, 99 patients; DDTC, 96 patients). Withdrawal for chemotherapy-induced toxicities occurred in 9% of PB-treated patients and 23% of DDTC-treated patients (P = .008). The mean cisplatin delivered dose-intensity (DDI) was 23 mg/m2/wk on both arms. However, the mean cisplatin cumulative dose delivered (CDD) was 379 mg/m2 on the PB arm, compared with 247 mg/m2 on the DDTC arm (P = .0001). At the time of interim analysis, 28% of PB-treated patients had completed all six cycles of therapy, compared with only 6% of DDTC-treated patients (P < .001). Although, clinical hearing loss, neuropathy, emesis, and myelosuppression were equivalent in the two treatment arms, DDTC-treated patients had more nephrotoxicity as determined by changes in serum creatinine concentration. Toxicities related to DDTC infusion included transient hypertension, flushing, and hyperglycemia. DDTC did not compromise response rates in either tumor type. CONCLUSION This study did not demonstrate a significant chemoprotective effect against cisplatin-induced toxicities with the DDTC dose schedule tested. Patients who received DDTC received lower cumulative doses of cisplatin, but were more likely to be withdrawn from treatment early due to chemotherapy-related toxicities.
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Gore, M., P. Mainwaring, R. A'Hern, V. MacFarlane, M. Slevin, P. Harper, R. Osborne, et al. "Randomized trial of dose-intensity with single-agent carboplatin in patients with epithelial ovarian cancer. London Gynaecological Oncology Group." Journal of Clinical Oncology 16, no. 7 (July 1998): 2426–34. http://dx.doi.org/10.1200/jco.1998.16.7.2426.
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PURPOSE We have examined the role of an increase in cisplatin dose-intensity in patients with advanced epithelial ovarian cancer by means of single-agent carboplatin therapy. PATIENTS AND METHODS Two hundred twenty-seven patients were randomized to treatment and eligible for analysis. The dose of carboplatin was calculated according to the Calvert formula. One hundred seventeen patients received carboplatin at an area under the concentration time curve (AUC) of 6 for six courses, administered every 28 days, and 110 patients received carboplatin at an AUC of 12 for four courses, administered every 28 days. Patients were eligible provided they had not received prior chemotherapy or radiotherapy and had International Federation of Gynecology and Obstetrics stages II to IV or relapsed stage I epithelial ovarian cancer. RESULTS The planned total-dose increase was 33% for the patients treated with carboplatin AUC 12, but the received percentage total-dose increase was 20%. There were no differences in progression-free or overall survival between the two treatment arms; the overall survival rate at 5 years was 31% and 34% of patients treated at AUCs 6 and 12, respectively. There was significantly more toxicity associated with carboplatin AUC 12, which resulted in more treatment delays and/or dose reductions (52% v 18%; P < .001). CONCLUSION We have shown that carboplatin can be delivered at an AUC of 12 for four courses without granulocyte colony-stimulating factor support, although significant hematologic toxicity occurs. Nonhematologic toxicities were not clinically significant. Carboplatin offers an opportunity to intensify cisplatin therapy, but a greater than two-fold increase in dose-intensity probably needs to be achieved before significant effects on survival will be produced and hematologic support will be required.
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Von Hoff, D. D., G. M. Clark, G. R. Weiss, M. H. Marshall, J. B. Buchok, W. A. Knight, and C. F. LeMaistre. "Use of in vitro dose response effects to select antineoplastics for high-dose or regional administration regimens." Journal of Clinical Oncology 4, no. 12 (December 1986): 1827–34. http://dx.doi.org/10.1200/jco.1986.4.12.1827.
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Several preclinical and clinical studies have documented that dose or dose intensity of chemotherapeutic agents are important factors for response of patients' tumors. This finding has prompted empiric trials of certain chemotherapeutic agents in high-dose or regional administration treatment regimens. The present study was performed to identify agents that would be particularly good candidates for high-dose or regional administration regimens against particular types of tumors. Using a human tumor cloning technique, we constructed dose in vitro response lines for ten different chemotherapeutic agents against seven different histologic types of malignancies. Slopes of the lines indicated the agents with the greatest increases of in vitro response per increment in dose of the agent. Tumors against which the agents gave the steepest dose response lines included lymphoma, head and neck cancer, ovarian cancer, and small-cell lung cancer, while the dose response lines for non-small-cell lung cancer, breast cancer, and colon cancer were quite flat. Suggestions for clinical trials based on these findings include the use of high-dose melphalan for patients with lymphoma, head and neck, and ovarian cancer; the use of mitoxantrone in high-dose regimens for patients with breast cancer; high-dose cisplatin regimens for patients with small-cell lung cancer; high-dose bleomycin regimens for patients with non-small-cell lung and head and neck cancer; and regional perfusion of liver metastases from colorectal cancer with cisplatin. Prospective testing of high-dose or regional administration regimens suggested by this new model should indicate its use for prediction of the best agent to use in high-dose regimens against a particular tumor type.
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Kudelka, A. P., D. Tresukosol, C. L. Edwards, R. S. Freedman, C. Levenback, P. Chantarawiroj, C. Gonzalez de Leon, et al. "Phase II study of intravenous topotecan as a 5-day infusion for refractory epithelial ovarian carcinoma." Journal of Clinical Oncology 14, no. 5 (May 1996): 1552–57. http://dx.doi.org/10.1200/jco.1996.14.5.1552.
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PURPOSE To determine the efficacy and toxicity of topotecan administered as a 5-day intravenous infusion in patients with advanced ovarian cancer refractory to cisplatin-based chemotherapy. PATIENTS AND METHODS Thirty patients with advanced epithelial ovarian cancer refractory to cisplatin-based chemotherapy received intravenous infusions of topotecan 1.5 mg/m2 delivered over 30 minutes each day for 5 days. A course was repeated every 21 days. The patient eligibility requirements included age > or = 18 years, Zubrod score < or = 2, measurable disease, adequate hepatic and renal function, neutrophil count > or = 1,500/microL, platelet count > or = 100,000/microL, and anticipated survival > or = 3 months. RESULTS Twenty eight patients were assessable for response and toxicity. All patients were assessable for survival. The major toxicity from administration of topotecan at this dose schedule was myelosuppression; 21 patients required dose reductions. Four patients had neutropenic fever that required hospitalization, and seven patients required platelet transfusions. Maculopapular pruritic exanthema occurred in 20% of patients; gastrointestinal side effects were mild. No deaths were reported on the study. At dose levels of 1.5, 1.25, and 1.0 mg/m2, 61%, 31%, and 25% of patients, respectively, required dose reductions. Of 28 assessable patients, four (14%; 95% confidence interval [CI], 4% to 34%) achieved a partial response (PR) at a median of 1.4 months and lasting 8.9 months, and 17 had stable disease (SD). The overall median survival time was 10.0 months (95% CI, 8.1 to 13.5). CONCLUSION Topotecan shows modest clinical activity against cisplatin-refractory ovarian cancer, although the dose-intensity is compromised by the depth of the granulocyte nadir and the duration of granulocytopenia. Further studies of topotecan may necessitate a reevaluation of optimal dose schedule, with the possible incorporation of multilineage cytokines, and its activity in taxane-resistant tumors.
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Creemers, G. J., G. Bolis, M. Gore, G. Scarfone, A. J. Lacave, J. P. Guastalla, R. Despax, et al. "Topotecan, an active drug in the second-line treatment of epithelial ovarian cancer: results of a large European phase II study." Journal of Clinical Oncology 14, no. 12 (December 1996): 3056–61. http://dx.doi.org/10.1200/jco.1996.14.12.3056.
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PURPOSE Topotecan is a topoisomerase I inhibitor with preclinical activity against various tumor types. We conducted a large multicenter phase II study with topotecan in ovarian cancer in patients who had failed to respond to one prior cisplatin-based chemotherapeutic regimen. PATIENTS AND METHODS Topotecan 1.5 mg/m2/d was administered intravenously by 30-minute infusion for 5 days repeated every 3 weeks. As the cisplatin-free interval relates to response in subsequent treatment, patients were stratified in subgroups, ie, cisplatin-refractory, cisplatin-resistant, and cisplatin-sensitive. RESULTS One-hundred eleven patients entered the study. Nineteen patients were considered to be ineligible; 92 patients were assessable for response. A total of 552 courses were given (median, four per patient; range, one to 17). The major toxicities were leukocytopenia and neutropenia, which were grade 3 to 4 in 54.2% and 69.1% of courses, respectively, but with only 4.3% of these being grade 4 neutropenia plus fever or infectious complications. Prophylactic granulocyte colony-stimulating factor (G-CSF) was given in 20.5% of courses to maintain dose-intensity. Other relatively frequent side effects were alopecia (82%), nausea (36.4%), and vomiting (17.5%). The overall response rate was 16.3%, with one complete response (CR) and 14 partial responses (PRs). In the cisplatin-refractory, cisplatin-resistant, and cisplatin-sensitive strata, the response rates were 5.9%, 17.8%, and 26.7%, respectively. The median duration of time of documented response was 21.7 weeks (range, 4.6 to 41.9). CONCLUSION Topotecan in a daily-times-five schedule is an effective regimen as second-line treatment in ovarian cancer. Further investigations of topotecan in ovarian cancer, including first-line use and combination with other active agents, are indicated.
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Bolis, G., G. Favalli, S. Danese, F. Zanaboni, G. Mangili, C. Scarabelli, S. Tateo, et al. "Weekly cisplatin given for 2 months versus cisplatin plus cyclophosphamide given for 5 months after cytoreductive surgery for advanced ovarian cancer." Journal of Clinical Oncology 15, no. 5 (May 1997): 1938–44. http://dx.doi.org/10.1200/jco.1997.15.5.1938.
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PURPOSE To compare the efficacy of a treatment with cisplatin plus cyclophosphamide given for 5 months and a short treatment with cisplatin alone in advanced ovarian cancer, we conducted a multicenter randomized clinical trial. PATIENTS AND METHODS Eligibility criteria were as follows: first diagnosis of histologically confirmed invasive epithelial ovarian cancer of International Federation of Gynecology and Obstetric (FIGO) stage III-IV, age younger than 75 years, and Eastern Cooperative Oncology Group (ECOG) performance status 0, 1, or 2. Within 28 days of cytoreductive surgery, eligible women were randomly assigned treatment with weekly cisplatin 50 mg/m2 for nine courses or cisplatin 75 mg/m2 plus cyclophosphamide 750 mg/m2 every 21 days for six courses. RESULTS A total of 607 women were entered onto the study. There was no difference in the response to treatment. Pathologic complete response (CR) was documented in 63 of the weekly cisplatin cases and 70 of the cisplatin plus cyclophosphamide group (chi 1(2) = 1.43; P = .23). The median follow-up time was 3 years. There were 151 and 148 deaths in the weekly cisplatin and cyclophosphamide plus cisplatin arms, respectively. Survival curves were similar in the two groups, with a 3-year percent survival estimate of 44.1 (SE = 3.4) in the weekly cisplatin and 44.6 (SE = 3.4) in the cisplatin plus cyclophosphamide group (log-rank test chi 1(2) = 0.004; P = .96). CONCLUSION This study found that 2-month monochemotherapy treatment with cisplatin was as effective as 5-month polychemotherapy including cisplatin at a similar doses but different dose-intensity plus cyclophosphamide.
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Shibata, K., F. Kikkawa, M. Mika, Y. Suzuki, H. Kajiyama, K. Ino, and S. Mizutani. "Neoadjuvant chemotherapy for FIGO stage III or IV ovarian cancer: Survival benefit and prognostic factors." International Journal of Gynecologic Cancer 13, no. 5 (2003): 587–92. http://dx.doi.org/10.1136/ijgc-00009577-200309000-00003.
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The survival benefit of neoadjuvant chemotherapy (NAC) was assessed in patients with FIGO stage III or IV ovarian cancer, and the prognostic value of various therapeutic factors was determined. In patients treated for stage III or IV ovarian malignancies at the Department of Obstetrics and Gynecology of Nagoya University or related institutions between 1987 and 1996, 119 had a histologic diagnosis of serous cystadenocarcinoma. For this group, the long-term outcome was compared between 96 patients receiving conventional adjuvant chemotherapy following standard surgery and 23 patients treated with NAC, both followed by a second cytoreductive surgery. In a total of 29 patients with all histologic types of malignancy, the tumor response to NAC and survival were analyzed on the basis of histology, chemotherapy regimen, residual tumor size after the second cytoreductive operation, and the dose intensity of cisplatin. The long-term outcome (5-year survival rate) was better in patients treated with conventional adjuvant chemotherapy than in patients receiving NAC, although the difference was not significant. Overall survival did not differ significantly in relation to tumor histology or chemotherapy regimen. With respect to residual tumor size after the second surgery, patients with a residual tumor ≦ 2 cm in diameter had a significantly better prognosis than those with a residual tumor >2 cm. A better prognosis was also associated with a higher dose intensity of cisplatin, and patients treated at ≧ 18 mg/m2/week survived significantly longer than those receiving <18 mg/m2/week.
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Lévi, F., M. Benavides, C. Chevelle, F. Le Saunier, F. Bailleul, J. L. Misset, C. Regensberg, J. M. Vannetzel, A. Reinberg, and G. Mathé. "Chemotherapy of advanced ovarian cancer with 4'-O-tetrahydropyranyl doxorubicin and cisplatin: a randomized phase II trial with an evaluation of circadian timing and dose-intensity." Journal of Clinical Oncology 8, no. 4 (April 1990): 705–14. http://dx.doi.org/10.1200/jco.1990.8.4.705.
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The efficacy and toxicity of the new anthracycline, 4'-0-tetrahydropyranyl doxorubicin (THP) (50 mg/m2 intravenous [IV] bolus) in association with cisplatin (100 mg/m2 IV as a 4-hour infusion) was assessed in 31 patients with advanced ovarian carcinoma. Twenty-eight patients were assessable for toxicity among whom 25 were assessable for response (International Federation of Gynecology and Obstetrics [FIGO] stage IIIa, four patients; IIIb, 15 patients; IV, six patients). Nine patients had received prior treatment. Patients were randomized to receive schedule (sch) A (THP at 6 hours, then cisplatin from 16 to 20 hours) or sch B (THP at 18 hours, then cisplatin from 4 to 8 hours). Sch A was hypothesized as less toxic since THP was best tolerated in the late rest span and cisplatin near the middle of the activity span in experimental studies. The rate of clinical complete response (CR) was 52%, that of partial response (PR) was 12%, and the overall clinical response rate (CR plus PR) was 64% (sch A, 73%; sch B, 57%). Median progression-free survival and survival times were, respectively, 10 and 19 months. Of 12 patients in clinical CR evaluated at second-look laparotomy, four had a pathological CR (33%), and three had microscopic residual disease (MD). The overall rate of pathological CR was 16%. Sch A was associated with less neutropenia (P = .10), thrombocytopenia (P less than .01), anemia (P less than .01), and renal toxicity (P less than .05) than sch B. Of four patients withdrawn for toxicity, three were on sch B (one death). Mean dose intensities (DIs) of THP and cisplatin, respectively, decreased by 30% and 47% over the five initial courses. Such decrease was significantly more pronounced for sch B than for sch A in previously untreated patients (P from 2-way analysis of variance [ANOVA] less than .01). THP-cisplatin is active against advanced ovarian cancer, and its toxicities can be significantly decreased by dosing THP in the early morning and cisplatin in the late afternoon as compared with THP in the evening and cisplatin the next morning.
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Fennelly, D., C. Aghajanian, F. Shapiro, C. O'Flaherty, M. McKenzie, C. O'Connor, W. Tong, L. Norton, and D. Spriggs. "Phase I and pharmacologic study of paclitaxel administered weekly in patients with relapsed ovarian cancer." Journal of Clinical Oncology 15, no. 1 (January 1997): 187–92. http://dx.doi.org/10.1200/jco.1997.15.1.187.
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PURPOSE Paclitaxel has shown significant activity in advanced ovarian cancer. In vitro studies with paclitaxel have suggested that fractionated brief infusion schedules may be more effective than the standard 24-hour infusion. We commenced a phase I evaluation of escalating-dose paclitaxel (40, 50, 60, 80, 100 mg/m2) administered weekly as a 1-hour infusion in patients with recurrent ovarian cancer. All patients had received prior paclitaxel and cisplatin therapy. All patients received standard premedication. PATIENTS AND METHODS Eighteen patients are assessable on this phase I study. The mean age was 54 years (range, 48 to 74). The median number of prior chemotherapy regimens was three (range, two to five). The mean paclitaxel-free interval was 10.1 months (range, 1 to 24). RESULTS A total of 194 cycles of therapy were administered, with a mean of 10 (range, one to 12) per patient. No mucositis or grade III neuropathy was seen. Alopecia occurred in one out of 18 assessable patients. The mean neutrophil nadir was 4.0 x 10(9)/L. At the top dose level (100 mg/m2) delivered, dose-intensity was 90.75% of that planned and greater than two fold the standard dose-intensity. Partial responses were seen in four of 13 assessable patients (30%). Two patients with progression of disease on standard three-week paclitaxel schedules switched to a weekly schedule with demonstrated response. Increasing paclitaxel dose correlated with measured area under the curve (AUC) (R2 = .614). Dose-limiting toxicity was reached at 100 mg/m2 with two of three patients experiencing a treatment delay, thus defining a maximum-tolerated dose of 80 mg/m2 in this group of heavily pretreated patients on this weekly schedule. CONCLUSION (1) Paclitaxel administered as a 1-hour infusion is well tolerated; (2) this schedule of administration does not result in cumulative myelosuppression; and (3) this schedule of administration results in dose-intensive paclitaxel delivery with a favorable toxicity profile.
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Suzuki, T., M. Morishita, M. Matsuura, T. Fujimoto, R. Tanaka, E. Ito, Y. Ebina, and T. Saito. "A phase I study of modified irinotecan (CPT-11) plus cisplatin (CDDP) [m-IP] against paclitaxel/carboplatin [TC] -resistant and recurrent ovarian cancer." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 13015. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.13015.
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13015 Background: CPT-11/CDDP is effective regimen for ovarian cancer. Particularly against ovarian cancer resistant to prior chemotherapy, a 40% response rate was reported (Sugiyama T Cancer Letters, 1998). However, every 4 weeks treatment with CPT-11 day 1, 8, and 15, administration on day 15 was skipped in about 60% due to toxicity, and the relative dose intensity of IP was 66.7% in non-small cell lung cancer (Saito H Am J Clin Oncol 2006). We planed Phase I study, in consideration of the effect of prior chemotherapy in TC-resistant ovarian cancer, a modified CPT-11 (day 1, 8) and CDDP (day 1) for every 4 weeks treatment (m-IP). The aim of this study conducted to examine the dose limiting toxicity (DLT), to evaluate the maximum tolerated dose (MTD), and define the recommended dose (RD) for a phase II study. Methods: Patients with TC-resistant ovarian cancer having a PS 0–1, age 30–75 years, normal organ functions, and written informed consent. CPT-11 was administered intravenously over 90 minutes on day 1 and day 8, plus CDDP was day 1, repeated every 4 weeks. The dose escalation schedule was defined: Doses of CPT-11/CDDP (mg/m2) were 60/60 at level 1, 70/60 at level 2 and 70/70 at level 3. DLT were determined as Grade 4 hematological toxicity and = Grade 3 non-hematological toxicity occurred, and when dosing on day 8 was delayed for more than 8 days due to toxicity. Results: Nine patients were enrolled (level 1/2/3: 3/3/3). DLTs, at level 1 and 2, no patients developed. At level 3, grade 3 nausea and vomiting and delayed treatment on day 8 due to anorexia, were observed in all of 3 patients. Therefore, MTD was determined to be level 3 and RD was determined to be level 2 (CPT-11: 70mg/m2, CDDP: 60mg/m2). Major =Grade 3 toxicities observed were leukopenia, neutropenia, nausea, and vomiting. No Grade 4 hematological toxicities were observed. Diarrhea was mild. Antitumor effect at RD was observed in 1 patient with CR, 1 patient with PR and 1 patient with PD. Conclusions: The MTD of m-IP was CPT-11 70mg/m2 and CDDP 70mg/m2 (level 3), the RD was CPT-11 70mg/m2 and CDDP 60mg/m2 (level 2). Preliminary response are promissing associated with tolerable toxicity for TC-resistant and recurrent ovarian cancer. A Phase II study is currently conducted. No significant financial relationships to disclose.
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Grem, J., P. O'Dwyer, P. Elson, N. Simon, D. Trump, M. Frontiera, G. Falkson, and S. Vogl. "Cisplatin, carboplatin, and cyclophosphamide combination chemotherapy in advanced-stage ovarian carcinoma: an Eastern Cooperative Oncology Group pilot study." Journal of Clinical Oncology 9, no. 10 (October 1991): 1793–800. http://dx.doi.org/10.1200/jco.1991.9.10.1793.
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Cyclophosphamide (CTX) 600 mg/m2, carboplatin 280 mg/m2, and cisplatin 50 mg/m2 were administered on day 1 every 4 weeks to 41 previously untreated ovarian cancer patients with residual disease greater than 2.0 cm after primary laparotomy. Of 22 patients with measurable disease treated with up to eight cycles of therapy, the overall clinical response rate was 73% (exact 95% confidence interval [CI], 50% to 89%), with 50% complete response (CR). Six of 11 clinical CR (cCR) patients underwent surgical restaging; three pathologic CRs (pCRs) and three pathologic partial responses (pPRs) with residual disease less than 2.0 cm were documented. Fourteen patients had nonmeasurable but assessable disease; the clinical response rate was 57% (Cl, 29% to 82%) with two (14%) CRs. Second-look surgery was performed in one of the two cCR patients; a pPR was documented. Five patients with nonassessable disease were stable during chemotherapy; two underwent surgery and had pCRs. The median time to treatment failure (TTF) was 14.8 months, and median survival for the 41 patients is 26.7 months. Overall, 37% of the patients had progression-free intervals of at least 2 years, and 27% have survival times in excess of 3 years. Hematologic toxicity was substantial but manageable, with 58% and 66% experiencing a granulocyte nadir less than 500/microL and a platelet nadir less than 50,000/microL, respectively. One treatment-associated fatality occurred as a result of leukopenic sepsis and renal failure in the setting of progressive disease and ureteral obstruction. Mild to moderate nausea and vomiting occurred in most patients, but none experienced severe ototoxicity or peripheral neuropathy. Over all courses, 73% of the projected dose intensity of CTX and carboplatin and 86% of cisplatin were delivered. Since granulocytopenia and thrombocytopenia were dose-limiting, the addition of colony-stimulating factors that support both myeloid and megakaryocyte precursors may permit further dose intensification.
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Dittrich, Ch, P. Sevelda, H. Salzer, A. Obermair, P. Speiser, G. Breitenecker, M. Schemper, and A. Kaider. "Erratum to “Lack of impact of platinum dose intensity on the outcome of ovarian cancer patients: 10-year results of a prospective randomised phase III study comparing carboplatin–cisplatin with cyclophosphamide-cisplatin”." European Journal of Cancer 40, no. 4 (March 2004): 627. http://dx.doi.org/10.1016/j.ejca.2003.09.001.
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Burg, M. E., J. T. Janssen, P. B. Ottevanger, L. G. Kerkhofs, F. Valster, J. M. Stouthard, W. Onstenk, F. Termorshuizen, and J. Verweij. "Multicenter randomized phase III trial of 3-weekly paclitaxel/platinum (PC3w) versus weekly paclitaxel/platinum (PCw) induction therapy followed by PC3w maintenance therapy in advanced epithelial ovarian cancer (EOC)." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): 5538. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.5538.
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5538 Background: Response rates (RR) up to 50% were found with PCw in platinum resistant EOC. We compared the efficacy of first-line PCw induction therapy to PC3w. Methods: 270 patients (pts) with FIGO stage II-IV, Performance status (PS) 0–2 were randomly assigned to 3 x PC3w (P 175mg/m2 with either cisplatin [Cis] 75mg/m2 or carboplatin [Car] AUC 6) or 6 x PCw (P 90mg/m2 with either Cis 70mg/m2 or Car AUC 4, day 1,8,15 and day 29,36,43) followed by up to 6 cycles PC3w in both arms. Pts were stratified for FIGO stage, PS, tumor size and center. Primary endpoints were progression free survival (PFS) and overall survival (OS). Secondary endpoints were RR and toxicity. A total of 225 events were needed to detect a 10–13% absolute difference in PFS/OS with a power of 84% (one-sided). Results: 267 pts (134 TC-3w and 133 TCw) were eligible (3 pts wrong tumor type). Pt characteristics were well balanced; median age 58 years, serous 62%, residual disease >1cm 66%, FIGO stage II 7%, III 64%, IV 29%. Median dose-intensity for PC3w was: P 58(47–58) and Cis 25(22.5–25) mg/m2/w, Car 2(1.6–2) AUC/w, for PCw: P 60(36–60) and Cis 44.7(30–44.7) mg/m2/w and for Car 2.7(1,6–2,7) AUC/w. After a median follow-up of 39 months (m) (range 0.03 - 93.3m) 206 pts (77%) had progressed and 164 pts (61%) had died. Median PFS was 18m for TC3w and 19m for TCw, 5-year PFS was 20% and 18%, respectively (logrank test: p = 0.63). Median OS was 44m for TC3w and 45m for TCw, 5-year OS was 36% and 37%, respectively (logrank test: p = 0.87). RR after induction therapy in 176 pts with measurable disease was 72% for TC3w and 74% for TCw (p = 0.68). TCw was well tolerated. Grade 3/4 toxicity for TC3w vs. TCw was respectively, platelets 1.75% vs.1.55% (ns), WBC 5.5% vs. 8.7 (p = <0.0001), granulocytes 16.7% vs. 11.7% (p = <0.001) and delay 3% vs. 9% of the cycles. TCw induced less grade 2/3 muscular and joint pain (TC3w 6.3% and 3.5% vs. TCw 0.3% and 0.8% of the cycles) and less neurotoxicity (TC3w 6% vs. 1.6% of the pts in TCw). The other toxicities were similar in frequency and severity in both arms. Conclusions: TCw was well tolerated and had less granulocytopenia, neurotoxicity, and muscular and joint pain but did not yield benefit in terms of OS, PFS or RR. No significant financial relationships to disclose.
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Soćko, Renata. "Etoposide. Documentation of proposed values of occupational exposure limits (OELs)." Podstawy i Metody Oceny Środowiska Pracy 36, no. 2(100) (June 30, 2019): 73–98. http://dx.doi.org/10.5604/01.3001.0013.2532.
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Etoposide at room temperature is a solid present in the form of a white or yellow-brown crystalline powder. It is an anticancer drug with cytotoxic and anti-mitotic activity, used to treat patients with testicular cancer, acute myelogenous leukemia, lung cancer, non-small-cell lung cancer, adrenal cortex cancer, gastric cancer, hepatoblastoma, acute lymphoblastic leukemia and brain tumors. It is also recommended for the treatment of Ewing sarcoma and Kaposi's sarcoma associated with AIDS. This cytostatic is available in capsules taken by food and in concentrate for solution for infusion. Occupational exposure to etoposide occurs during its manufacture, confectioning, packaging and use in everyday treatment practices of hospital wards. The monograph, along with the proposal for a hygiene standard for etoposide, was developed as a continuation of work on the determination of the value of hygiene standards for cytostatics. According to the National Consultant's report in the field of nursing in 2010 (incomplete data, covering only 12 voivodeship), the number of nurses employed in oncology facilities totaled 5077. On the basis of data from the Central Register of Data on Exposure to Carcinogenic or Mutagenic Substances, Mixtures, Agents or Technological Process in Poland exposure to etoposide in Poland in the last three years has been growing. In 2015, 414 people were exposed to the substance. This substance has not been officially classified in the European Union. Most manufacturers of etoposide importers classify it for carcinogenic activity to category 1.B with risk phrase: May cause cancer and acute toxicity after oral exposure to category 4. The main effect of the toxicity of etoposide as a medicine is suppression of bone marrow function, which results in neutropenia, granulocytopenia and thrombocytopenia, leukopenia, an increase in the number of megaloblasts in the bone marrow and gastrointestinal symptoms (eg nausea, vomiting with mild to moderate intensity) , bronchospasm, inflammation of mucous membranes, feelings of disgust in the mouth, baldness and secondary leukemia. According to the IARC, there is limited evidence of carcinogenicity of etoposide in animals, but there is sufficient evidence of carcinogenicity of etoposide in humans when combined exposure to cisplatin and bleomycin. In IARC, etoposide was classified as probably carcinogenic to humans (Group 2.A.), and in combination with cisplatin and bleomycin as a carcinogen for humans (Group 1). The genotoxic activity of etoposide has been demonstrated in studies performed on human and animal material in vitro without metabolic activation. Etoposide caused the occurrence of chromosomal aberrations in both humans and experimental animals, increased sister chromatid exchange, double-strand break in DNA and the micronucleus formation. In experimental animal studies (mice, rats, rabbits), etoposide was teratogenic and embryotoxic. In women treated with etoposide, transient ovarian dysfunction is reported. The effect of etoposide on ovarian function, however, did not depend on the dose, but on the patient's age. In addition, spontaneous births were reported in women treated with etoposide. In some cases, the embryotoxic effects of the drug have been demonstrated. There were no congenital malformations in children whose mothers were treated with etoposide alone or in combination with other cytostatics, as well as in children of men treated with etoposide. The critical effect of the action of etoposide as a drug is bone marrow suppression. The lowest therapeutic dose of the drug was found at 2.37 mg/kg/day. In Poland, the maximum permissible concentrations of etoposide in the work environment have not yet been established. The following data was taken into account when determining the NDS of etoposide: - occupational exposure levels established by etoposide manufacturers for this substance amount to 0.0003 or 0.0007 mg/m3; - available results of human and animal studies do not allow to determine the dose-effect relationship; - due to the genotoxic, carcinogenic, teratogenic and reproductive effects of etoposide, NIOSH assumed that the OEL should be set at a level below 0.01 mg/m3; - according to the classification proposed by the group operating within the framework of the "Global strategy of risk management", etoposide should be in category 4, ie substances for which the OEL value in the work environment should be in the range of 0.001 mg/m3 ÷ 0.01 mg/m3. The MAC value of etoposide was proposed at the level of the equivalent concentration to 0.1% of the lowest therapeutic dose used in humans (2.37 mg/kg), similar to other cytostatics (eg N-hydroxyurea, fluorouracil). An additional uncertainty factor "F" was adopted at level 10 related to the long-term effects of exposure, i.e. genotoxic, carcinogenic and reprotoxic effects of the substance. The MAC of the inhalable fraction of etoposide was set at 0.0017 mg/m3. There are no substantive basis to establish the value of the short- -term (STEL) and permissible concentrations in biological material (DSB) for etoposide. Based on quantitative data characterizing skin absorption of etoposide, which has a molecular weight of 588.56 and its poor solubility in water, it has been found that the substance is characterized by a low ability to penetrate the skin. Due to the observed embryotoxicity in humans and teratogenic and embryotoxic etoposide in experimental animals, the substance was marked with the letters "Ft" - a substance harmful for reproduction. In addition, the labeling recommended by the manufacturers of "Carc 1.B" that indicated that it is a carcinogenic substance of category 1.B.
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Ozols, Robert F. "Ovarian Cancer: Is Dose Intensity Dead?" Journal of Clinical Oncology 25, no. 27 (September 20, 2007): 4157–58. http://dx.doi.org/10.1200/jco.2007.12.1723.
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Ozols, R. F., Y. Ostchega, G. Curt, and R. C. Young. "High-dose carboplatin in refractory ovarian cancer patients." Journal of Clinical Oncology 5, no. 2 (February 1987): 197–201. http://dx.doi.org/10.1200/jco.1987.5.2.197.
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Thirty previously treated refractory ovarian cancer patients, all of whom received prior therapy with cisplatin, were treated in a phase II trial with high-dose carboplatin (800 mg/m2 per cycle with cycles administered every 35 days). Patients were treated with high-dose carboplatin when they were no longer responding to prior therapy or had relapsed after an initial response. Objective responses were achieved in eight of 30 patients (27%) while ten patients had minor responses or stable disease. No responses were observed from high-dose carboplatin in patients who had progressive disease during prior therapy with a cisplatin-based regimen. The primary toxicity of high-dose carboplatin was myelosuppression with a median WBC nadir of 0.6 and a median platelet nadir of 6,500 after the first cycle of therapy. Myelosuppression was not particularly cumulative as 78% of patients were able to receive either 100% or 75% of the projected dose even with the fourth cycle of high-dose carboplatin. The gastrointestinal (GI) toxicity of carboplatin was mild and there was no clinically apparent nephrotoxicity or neurotoxicity. These results demonstrate that: there is marked cross-resistance between cisplatin and carboplatin, and high-dose carboplatin may be a potential alternative to high-dose cisplatin in the treatment of ovarian cancer patients.
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Wiltshaw, E., B. Evans, G. Rustin, E. Gilbey, J. Baker, and G. Barker. "A prospective randomized trial comparing high-dose cisplatin with low-dose cisplatin and chlorambucil in advanced ovarian carcinoma." Journal of Clinical Oncology 4, no. 5 (May 1986): 722–29. http://dx.doi.org/10.1200/jco.1986.4.5.722.
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Sixty-one patients with FIGO stage III ovarian carcinoma and 30 patients with stage IV ovarian carcinoma were randomized to receive either high-dose cisplatin (100 mg/m2) or low-dose cisplatin (20 mg/m2) and chlorambucil. Overall response rates were similar in both arms, with 68% and 49% of stage III patients and 61% and 72% of stage IV patients responding to high-dose cisplatin and the combination, respectively. There was a strong trend for better survival in stage III (P less than .05) but not in stage IV patients treated with cisplatin alone. The toxicity suffered by patients treated with high-dose cisplatin was severe, and in 15 patients cisplatin therapy was stopped because of unacceptable toxicity.
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Ozols, Robert F., Brent C. Behrens, Yechiam Ostchega, and Robert C. Young. "High dose cisplatin and high dose carboplatin in refractory ovarian cancer." Cancer Treatment Reviews 12 (September 1985): 59–65. http://dx.doi.org/10.1016/0305-7372(85)90019-2.
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&NA;. "High-dose cisplatin of no benefit in ovarian cancer." Inpharma Weekly &NA;, no. 1029 (March 1996): 18. http://dx.doi.org/10.2165/00128413-199610290-00034.
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Ghersi, Davina, MaheshK B. Parmar, David Guthrie, Chris Williams, and D. J. Dodwell. "High versus low dose cisplatin in epithelial ovarian cancer." Lancet 340, no. 8820 (September 1992): 678–79. http://dx.doi.org/10.1016/0140-6736(92)92221-z.
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Ozols, R. F., Y. Ostchega, C. E. Myers, and R. C. Young. "High-dose cisplatin in hypertonic saline in refractory ovarian cancer." Journal of Clinical Oncology 3, no. 9 (September 1985): 1246–50. http://dx.doi.org/10.1200/jco.1985.3.9.1246.
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Nineteen previously treated refractory ovarian cancer patients, including 17 who had received standard-dose cisplatin regimens, were treated in a phase II trial with high-dose cisplatin (40 mg/m2 daily for five days with cycles administered every 28 to 35 days). Objective responses were achieved in 6/19 (32%) patients while eight patients had minor responses or stable disease. The median duration of survival from the start of salvage chemotherapy was 12 months for all patients, and 16 months for responding patients. The dose-limiting toxicity was peripheral neuropathy with 37% of patients having severe paresthesias or ataxia. These results indicate that the dose of cisplatin may be an important factor in improving survival in ovarian cancer patients.
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Morgan, Robert D., Andrew R. Clamp, Cong Zhou, Geoff Saunders, Nerissa Mescallado, Richard Welch, Claire Mitchell, Jurjees Hasan, and Gordon C. Jayson. "Dose-dense cisplatin with gemcitabine for relapsed platinum-resistant ovarian cancer." International Journal of Gynecologic Cancer 29, no. 2 (January 23, 2019): 341–45. http://dx.doi.org/10.1136/ijgc-2018-000067.
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IntroductionStandard of care treatment for women who develop relapsed ovarian cancer includes sequential platinum- and/or paclitaxel-based chemotherapy, with reducing disease-free intervals. Once platinum resistance develops, treatment options become limited and dose-dense regimens may be offered. We report the efficacy and safety of dose-dense cisplatin with gemcitabine chemotherapy for relapsed platinum-resistant ovarian cancer.MethodsA retrospective analysis of all patients with relapsed, platinum-resistant ovarian, primary peritoneal or fallopian tube cancer treated with cisplatin 35 mg/m2 of body surface area by intravenous infusion with gemcitabine 1000 mg/m2 of body surface area by intravenous infusion on days 1 and 8 of every 21-day treatment cycle between 1 January 2009 and 1 June 2017.ResultsNinety-four eligible patients had received a median of three (range one–eight) prior lines of cytotoxic therapy for relapsed ovarian cancer. Sixty patients (64%) had received ≥ 1 prior dose-dense chemotherapy regimen. Dose-dense cisplatin with gemcitabine was associated with a median progression-free survival (PFS) of 4.4 months (95% CI 3.6 to 5.3) and overall survival of 7.6 months (95% CI 5.6 to 9.6). The median PFS for dose-dense cisplatin with gemcitabine as first- (n = 34), second- (n = 42), and third-line or later (n = 18) dose-dense therapy was 4.2 (95% CI 3.2 to 5.2), 5.0 (95% CI 3.5 to 6.5), and 4.2 (95% CI 3.3 to 5.1) months respectively. The RECIST objective response rate for first-, second-, and third-line dose-dense cisplatin with gemcitabine was 23%, 14 %, and 7 % respectively. The most common grade 3 – 4 adverse events were thrombocytopenia (20%), anemia (18%), and neutropenia (14%).DiscussionDose-dense cisplatin with gemcitabine provides modest efficacy whether it is used as a first- or subsequent line of dose-dense chemotherapy to treat relapsed platinum-resistant ovarian cancer and the toxicity is manageable with supportive measures.
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Jakobsen, A., K. Bertelsen, J. E. Andersen, H. Havsteen, P. Jakobsen, K. A. Moeller, K. Nielsen, E. Sandberg, and I. Stroeyer. "Dose-effect study of carboplatin in ovarian cancer: a Danish Ovarian Cancer Group study." Journal of Clinical Oncology 15, no. 1 (January 1997): 193–98. http://dx.doi.org/10.1200/jco.1997.15.1.193.
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PURPOSE To elucidate the effect of a doubled carboplatin dose-intensity in epithelial ovarian cancer in combination with a fixed dose of cyclophosphamide. PATIENTS AND METHODS A total of 222 patients with epithelial ovarian cancer stages II to IV were included in the study. Following surgery, patients were randomly assigned to receive carboplatin at an area under the concentration-versus-time curve (AUC) of 4 (AUC4) or carboplatin at an AUC of 8 (AUC8) and cyclophosphamide 500 mg/m2 given every 4 weeks for six courses. The AUC was calculated according to Calvert's formula. In 123 patients, the carboplatin AUC was also measured based on a single-sample method and the results were compared with the calculated AUC. The end points of the trial were complete pathologic remission (CPR) and crude survival. RESULTS Approximately 50% of patients in both arms underwent second-look surgery. The frequency of CPR was 32% and 30%, respectively. The survival curves showed no significant difference (P = .84). The dose-intensity of cyclophosphamide was almost identical in the two arms, whereas that of carboplatin was different. In the AUC8 arm, the dose-intensity was 1.86 times that of the AUC4 arm. The results also demonstrated good agreement between the calculated and the measured AUC in most patients. Bone marrow toxicity was significantly higher in the AUC8 arm. CONCLUSION A doubling of the carboplatin dose-intensity did not result in any significant improvement of pathologic remission or survival. Calvert's formula can be used to give a fairly accurate estimate of the carboplatin AUC. Bone marrow toxicity increased with higher dose-intensity, and a further increase of dose is only feasible with growth-factor or stem-cell support.
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Cavaletti, G., L. Marzorati, G. Bogliun, N. Colombo, M. Marzola, M. R. Pittelli, and G. Tredici. "Cisplatin-lnduced peripheral neurotoxicity is dependent on total-dose intensity and single-dose intensity." Cancer 69, no. 1 (January 1, 1992): 203–7. http://dx.doi.org/10.1002/1097-0142(19920101)69:1<203::aid-cncr2820690133>3.0.co;2-1.
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Neijt, Jan P. "The challenge of dose-intensity in ovarian cancer." Annals of Oncology 4, no. 5 (May 1993): 349–50. http://dx.doi.org/10.1093/oxfordjournals.annonc.a058512.
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Torri, V., EL Korn, and R. Simon. "Dose intensity analysis in advanced ovarian cancer patients." British Journal of Cancer 67, no. 1 (January 1993): 190–97. http://dx.doi.org/10.1038/bjc.1993.33.
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Thigpen, J. T. "Dose-intensity in ovarian carcinoma: hold, enough?" Journal of Clinical Oncology 15, no. 4 (April 1997): 1291–93. http://dx.doi.org/10.1200/jco.1997.15.4.1291.
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Hrushesky, W. J., R. V. Roemeling, P. A. Wood, T. R. Langevin, P. Lange, and E. Farley. "High-dose intensity systemic therapy of metastatic bladder cancer." Journal of Clinical Oncology 5, no. 3 (March 1987): 450–55. http://dx.doi.org/10.1200/jco.1987.5.3.450.
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Forty-three consecutively diagnosed patients with widely metastatic transitional cell carcinoma of the bladder (TCCB) were treated with a high-dose intensity, chronobiologically timed combination of doxorubicin and cisplatin, followed by Cytoxan (Mead Johnson Pharmaceuticals, Evansville, IN), 5-fluorouracil (5-FU), and cisplatin maintenance for up to 2 years. Fifty-seven percent of the 35 evaluable patients with widespread metastatic cancer responded objectively. Twenty-three percent had complete disappearance of all cancer. Median survival from first treatment for complete responders (CRs) was more than 2 years, and 1 year for partial responders (PRs). Three of the CRs were alive without evidence of cancer more than 2 years after stopping all therapy. High-dose intensity combination chemotherapy can induce durable CRs of widespread bladder cancer.
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Chen, Huaping, Charles N. Landen, Yuanyuan Li, Ronald D. Alvarez, and Trygve O. Tollefsbol. "Enhancement of Cisplatin-Mediated Apoptosis in Ovarian Cancer Cells through Potentiating G2/M Arrest and p21 Upregulation by Combinatorial Epigallocatechin Gallate and Sulforaphane." Journal of Oncology 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/872957.
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Advanced-stage ovarian cancer is characterized by high mortality due to development of resistance to conventional chemotherapy. Novel compounds that can enhance the efficacy of conventional chemotherapy in ovarian cancer may overcome this drug resistance. Consumption of green tea (epigallocatechin gallate, EGCG) and cruciferous vegetables (sulforaphane, SFN) is inversely associated with occurrence of ovarian cancer and has anticancer effects through targeting multiple molecules in cancer cells. However, the effects of EGCG and SFN combinational treatment on ovarian cancer cells and on efficacy of cisplatin to these cells are unknown. In this study, EGCG or SFN was used to treat both cisplatin-sensitive (A2780) and cisplatin-resistant (A2780/CP20) ovarian cancer cells alone or in combination with cisplatin. We found that EGCG and SFN combinational treatment can reduce cell viability of both ovarian cancer cell lines time- and dose-dependently. Furthermore, EGCG and SFN combinational treatment can enhance cisplatin-induced apoptosis and G2/M phase arrest, thereby enhancing the efficacy of cisplatin on both cisplatin-sensitive and cisplatin-resistant ovarian cancer cells. EGCG and SFN combinational treatment upregulated p21 expression induced by cisplatin in cisplatin-sensitive ovarian cancer cells, while p27 expression was not regulated by these treatments. Collectively, these studies provide novel approaches to overcoming cisplatin chemotherapy resistance in ovarian cancer.
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Nichols, C. R., S. D. Williams, P. J. Loehrer, F. A. Greco, E. D. Crawford, J. Weetlaufer, M. E. Miller, A. Bartolucci, L. Schacter, and L. H. Einhorn. "Randomized study of cisplatin dose intensity in poor-risk germ cell tumors: a Southeastern Cancer Study Group and Southwest Oncology Group protocol." Journal of Clinical Oncology 9, no. 7 (July 1991): 1163–72. http://dx.doi.org/10.1200/jco.1991.9.7.1163.
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Between 1984 and 1989, 159 patients presenting with advanced germ cell cancer were entered on a randomized clinical trial comparing the efficacy and toxicity of etoposide and bleomycin and either standard-dose cisplatin (20 mg/m2 daily for 5 days) or high-dose cisplatin (40 mg/m2 daily for 5 days). Of the 159 patients, 153 were assessable for toxicity and response. As expected, patients receiving the high-dose cisplatin regimen experienced significantly more neurotoxicity, ototoxicity, nausea and vomiting, and myelo-suppression. Four patients (3%) died related to therapy. Despite the toxicity encountered, dose intensity was maintained. Overall, 84% of patients in the high-dose arm received 80% or more of the projected dose of cisplatin, etoposide, and bleomycin; and 90% of patients on the standard-dose arm received 80% or more of the projected dose. Of the 76 eligible patients randomized to receive the high-dose cisplatin regimen, 52 (68%) became disease-free with chemotherapy alone or with subsequent resection of residual teratoma or cancer. Of the 77 patients randomized to the standard-dose arm, 56 (73%) became disease-free with chemotherapy alone or with surgery. Median follow-up is now 24 months. Eleven patients (three high-dose and eight standard-dose) relapsed from disease-free status. Overall, 74% of patients receiving the high-dose cisplatin regimen are alive, and 63% are continuously free of disease. Of the patients receiving the standard-dose cisplatin regimen, 74% are alive, and 61% are continuously free of disease. This randomized prospective trial in advanced germ cell cancer achieved dose intensity of the most active single agent in this disease. This dose intensity did not translate into an improved survival or cure. We conclude that dose escalation of cisplatin beyond standard doses results in excess toxicity with no accompanying therapeutic benefit.
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De Giorgi, Ugo, Chiara Casadei, Alice Bergamini, Laura Attademo, Gennaro Cormio, Domenica Lorusso, Sandro Pignata, and Giorgia Mangili. "Therapeutic Challenges for Cisplatin-Resistant Ovarian Germ Cell Tumors." Cancers 11, no. 10 (October 17, 2019): 1584. http://dx.doi.org/10.3390/cancers11101584.
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The majority of patients with advanced ovarian germ cell cancer are treated by cisplatin-based chemotherapy. 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. There are limited data on the efficacy of specific chemotherapeutic regimens, high-dose chemotherapy with autologous progenitor cell support and targeted therapies. The inclusion of patients in clinical trials is strongly recommended, especially in clinical trials on the most frequent male germ cell tumors, to offer wider therapeutic opportunities. 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.
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Ma, Yen-Ying, Hao Lin, Jau-Sung Moh, Kuang-Den Chen, I.-Wen Wang, Yu-Che Ou, Ying-Shu You, and Chia-Chi Lung. "Low-dose LBH589 increases the sensitivity of cisplatin to cisplatin-resistant ovarian cancer cells." Taiwanese Journal of Obstetrics and Gynecology 50, no. 2 (June 2011): 165–71. http://dx.doi.org/10.1016/j.tjog.2011.01.022.
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McCullough, Emilee, Aditya V. Shreenivas, Stephanie Spitzer, Michelle Schroeder, Aniko Szabo, David Friedland, and Stuart J. Wong. "Impact of statin type and intensity on cisplatin-related hearing loss." Journal of Clinical Oncology 40, no. 28_suppl (October 1, 2022): 192. http://dx.doi.org/10.1200/jco.2022.40.28_suppl.192.
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192 Background: Ototoxicity is a common and treatment-limiting side effect of cisplatin. Rates of permanent hearing loss due to cisplatin treatment range from 40 to 80% and are associated with considerable morbidity and negative impact on quality of life. Currently, there are no FDA-approved therapies for preventing hearing loss caused by cisplatin. HMG-CoA reductase inhibitors (statins) are of interest due to putative pleiotropic effects, decreasing inflammation and oxidative stress. Some preclinical and retrospective studies have shown reduction in cisplatin-related hearing loss with concurrent administration of statins. Objectives: This study's primary objective was to evaluate the impact of statin use on cisplatin-related hearing loss rates measured by change in Chang Grade (CG). Chang criteria was chosen as it allows for evaluation of hearing loss severity without the need for word recognition. This study also assessed the effect of statin dose intensity, cisplatin dose, and concurrent use of ototoxins on cisplatin-induced hearing loss. Methods: We performed a retrospective chart review of adult patients who received cisplatin within a single health care network between March 2010 and December 2020. Patients were included in this IRB-approved analysis if they had baseline and follow-up audiograms prior to and after cisplatin treatment. Each patient had data collected on primary cancer location, cumulative cisplatin dose, chemotherapy regimen, concurrent radiation treatment to the head and neck area, and ototoxin use. In addition, data on the type of statin used, its dose intensity were collected when applicable. Multivariable analysis of change in CG (primary outcome) was performed using logistic regression with generalized estimating equations. Results: A total of 367 patients were included in this study, of which 87 were using statins and 280 were not using statins concurrently during cisplatin treatment. Median age of study population was 63 and there was a male predominance (67%). Change in CG did not differ between statin users and non-statin users (p = 0.36). In the multivariable analysis, adjusting for statin use and age, hearing loss was predicted by cisplatin dose (OR 1.19 per 100mg; 1.09-1.30; p < 0.001) and use of radiation therapy (OR = 2.04, 95% CI: 1.34-3.10, p < 0.001). Statin intensity did not have a significant effect on the change in CG when evaluating low-intensity (p = 0.34), moderate intensity (p = 0.77) or high-intensity (p = 0.44) compared to no statin use. Type of statin use and concurrent use of ototoxins also did not have a significant impact on the changes in CG. Conclusions: To our knowledge this is one of the largest retrospective analyses of statin’s impact on cisplatin related hearing loss. Our study found no difference in changes in CG hearing loss between statin users vs non-statin users. As expected, total cisplatin dose (mg) and concurrent radiation treatment remain important predictors of hearing loss.
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Zhang, Tingting, Chenxin Xu, Peisen Zheng, Xiaoxian Zhang, Chenyu Qiu, Fengjiao Wu, Jundixia Chen, et al. "Glaucocalyxin B Attenuates Ovarian Cancer Cell Growth and Cisplatin Resistance In Vitro via Activating Oxidative Stress." Oxidative Medicine and Cellular Longevity 2022 (February 25, 2022): 1–12. http://dx.doi.org/10.1155/2022/6324292.
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Ovarian cancer is one of the fatal gynecological cancers around the world. Cisplatin is the first-line chemotherapy drug for the clinical treatment of ovarian cancer. However, many patients with ovarian cancer are still suffering from resistance to cisplatin. Therefore, the new drug combinations or treatment strategies for ovarian cancer are urgently needed. Glaucocalyxin B (GLB), a diterpenoid isolated from the aerial parts of Rabdosia japonica, has shown antitumor activity in some tumors. However, the mechanisms by which GLB inhibits ovarian cancer remain unclear. In the present study, we showed that GLB potently inhibits ovarian cancer cell growth in a dose-dependent manner. Furthermore, we found that GLB has a notably synergistic antitumor effect with cisplatin. Mechanistically, we found that GLB enhances the sensitivity of ovarian cancer cells to cisplatin via increasing reactive oxygen species (ROS) levels, the phosphorylation of c-Jun N-terminal kinase (JNK), and DNA damage. Interestingly, a synergistic inhibitory effect of GLB with cisplatin was also observed in the cells which were resistance to cisplatin. Together, these data suggest that GLB can sensitize ovarian cancer cells to cisplatin by increasing ROS levels.
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Gandara, D. R., J. Crowley, R. B. Livingston, E. A. Perez, C. W. Taylor, G. Weiss, J. R. Neefe, L. F. Hutchins, R. W. Roach, and S. M. Grunberg. "Evaluation of cisplatin intensity in metastatic non-small-cell lung cancer: a phase III study of the Southwest Oncology Group." Journal of Clinical Oncology 11, no. 5 (May 1993): 873–78. http://dx.doi.org/10.1200/jco.1993.11.5.873.
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PURPOSE To test the concept that cisplatin dose-intensity is important in the treatment of non-small-cell lung cancer (NSCLC), the Southwest Oncology Group (SWOG) performed a randomized trial comparing standard-dose cisplatin (SDCP) 50 mg/m2 days 1 and 8 on a 28-day cycle for eight cycles, high-dose cisplatin (HDCP) 100 mg/m2 days 1 and 8 for four cycles, and high-dose cisplatin plus mitomycin (HDCP-M) 8 mg/m2 day 1. To isolate the effects of dose-intensity versus total dose, the planned cumulative cisplatin dose was 800 mg/m2 in each arm. PATIENTS AND METHODS Between July 1988 and April 1990, 356 patients were enrolled and 323 were eligible and assessable. All patients had metastatic, measurable disease, were chemotherapy-naive, and had a performance status (PS) of 0 to 2. RESULTS Confirmed complete plus partial response rates were SDCP, 12%; HDCP, 14%; and HDCP-M, 27% (P < .05). Complete responses were uncommon (HDCP, 3%; HDCP-M, 4%) and were observed only in the high-dose arms. Progressive disease occurred more frequently in the SDCP arm (57%) compared with HDCP (38%) or HDCP-M (34%) (P < .05). However, there were no significant differences in median survival times (SDCP, 6.9 months; HDCP, 5.3 months; HDCP-M, 7.2 months; P = .53). The mean delivered dose-intensity for cisplatin was significantly greater in the high-dose arms: HDCP 41 mg/m2/wk and HDCP-M 39 mg/m2/wk, versus SDCP 23 mg/m2/wk (P = .05). The high-dose arms resulted in an increased incidence of ototoxicity, emesis, and myelosuppression, but similar degrees of renal toxicity and neuropathy compared with SDCP. CONCLUSION This study does not confirm evidence of a steep clinical dose-response curve for cisplatin in NSCLC at the cisplatin dose-intensities achieved. The addition of mitomycin increases the response rate, but does not improve survival. Continued evaluation of new agents in this disease is warranted.
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Fanning, James, and Robert D. Hilgers. "High-Dose Cisplatin Carboplatin Chemotherapy in Primary Advanced Epithelial Ovarian Cancer." Gynecologic Oncology 51, no. 2 (November 1993): 182–86. http://dx.doi.org/10.1006/gyno.1993.1269.
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Wilding, G., R. Caruso, T. S. Lawrence, Y. Ostchega, E. J. Ballintine, R. C. Young, and R. F. Ozols. "Retinal toxicity after high-dose cisplatin therapy." Journal of Clinical Oncology 3, no. 12 (December 1985): 1683–89. http://dx.doi.org/10.1200/jco.1985.3.12.1683.
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Because of increasing complaints of visual dysfunction, 13 patients with refractory or recently diagnosed ovarian carcinoma were evaluated for possible cisplatin-induced ophthalmologic toxicity. All patients had received high-dose cisplatin (200 mg/m2 in five divided daily doses) over two to four cycles. Eight patients (62%) developed symptoms of blurred vision and three (23%) also developed altered color perception. Retinal toxicity in the form of cone dysfunction was documented by electroretinography and color vision testing in 11 patients. Three patients were studied prospectively. Two patients who developed cone dysfunction had normal ophthalmologic exams before the initiation of chemotherapy or after one cycle of cisplatin, suggesting a causal relationship between cisplatin therapy and subsequent retinal abnormalities. Though visual acuity improved off therapy, color vision abnormalities persisted as long as 16 months beyond therapy.
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Kaye, S. B., J. Paul, J. Cassidy, C. R. Lewis, I. D. Duncan, H. K. Gordon, H. C. Kitchener, et al. "Mature results of a randomized trial of two doses of cisplatin for the treatment of ovarian cancer. Scottish Gynecology Cancer Trials Group." Journal of Clinical Oncology 14, no. 7 (July 1996): 2113–19. http://dx.doi.org/10.1200/jco.1996.14.7.2113.
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PURPOSE In 1992, we reported the first results of a randomized study in ovarian cancer, comprising two doses of cisplatin and indicated a significant difference (P = .0008) in median survival. Four years later, we now describe the results of this trial. PATIENTS AND METHODS After a median follow-up of 4 years and 9 months, 115 of 159 cases of advanced ovarian cancer, originally randomized to receive six cycles of cyclophosphamide 750 mg/m2 and either a high dose (HD) of 100 mg/m2 cisplatin or a low dose (LD) of 50 mg/m2 (LD) cisplatin, have now died. RESULTS The overall survival for HD and LD patients is 32.4% and 26.6%, respectively, and the overall relative death rate is 0.68 (P = .043). This represents a reduction in overall benefit with longer follow-up compared with the first 2 years (relative death rate of 0.52). Toxicity, particularly neurotoxicity, is still evident in the fourth year (10/31 on HD compared with 1/24 on LD). CONCLUSION Our recommended dose of cisplatin in combination schedule is therefore 75 mg/m2, representing the optimal balance between efficacy and toxicity.
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Meng, Fanliang, Guigin Sun, Mei Zhong, Yanhong Yu, and Molly Brewer. "Anticancer efficacy of the combination of low-dose cisplatin and trichostatin A or 5-aza-2’-deoxycytidine in ovarian cancer cells." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): e15563-e15563. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e15563.
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e15563 Background: We investigated the combination of low dose cisplatin with histone deacetylase inhibitor trichostatin A and methyl transferase inhibitor 5-aza-2’-deoxycytidine to determine if these agents could improve the sensitivity of ovarian cancer cell lines to cisplatin. The goal was to improve efficacy and decrease the toxicity of conventional chemotherapy in human ovarian cancer. Methods: Two chemoresistant ovarian cancer cell lines HEY, SKOV3 and one immortalized cell line IOSE were were treated with increasing doses of each drug alone and in combination to determine optimal cytotoxicity at the lowest dose. Markers of adhesion, metastasis, proliferation, self renewal, and measures of epigenetic regulation were measured. Spheroids, treated with single and combination drugs, were measured for cell viability. SCID mice were injected with pretreated cells and with untreated cells and then treated sequentially. Results: TSA or 5-aza-2’-deoxycytidine combined with Cisplatin had a marked reduction in E-cadherin and N-cadherin (adhesion and migration), proliferation protein Akt and Akt-1, self-renewal markers Oct4/Nanog/Sox2, and the drug transporter ABCG2. DNA methylase, DNMT3a/3b, histone deacetylase HDAC1/2 and histone demethylase LSD1, measures of epigenetic regulation, were suppressed with combined treatment. Histone methylation markers H3K4 and H3K9 were regulated differentially, with the trimethyled-H3K9 significantly suppressed, suggesting bivalent chromatin regulation. Cisplatin/TSA suppressed spheroid formation, growth, and viability. Cisplatin/TSA suppressed tumorigenesis in SCID mice when cells were pretreated. Animals treated after tumor formation with epigenetic modifiers followed by cisplatin achieved significant tumor regression, suggesting that both approaches enhance anticancer effects. Conclusions: Our research suggests the combination of low dose cisplatin with epigenetic modifiers administered together or sequentially may be promising treatments for ovarian cancer with reduced toxicity and may reverse platinum resistance.
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Basu, D. "Cisplatin etoposide in heavily pretreated relapsed ovarian cancer." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 15061. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.15061.
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15061 Background: Ovarian Cancer is chemo sensitive but recurrence rate is high and patients who are platinum refractory have a poor outcome. Methods: 14 patients with histologically confirmed epithelial ovarian cancer that had relapsed after 3rd line chemotherapy (with platinum combination). Chemotherapy protocol - Cisplatin IVI 50 mg/m2 days 1,8 & 15, Etoposide PO 50 mg Days 1–15; Regime Cisplatin/oral Etoposide repeat 28 days total cycles 2, then oral Etoposide if appropriate. Toxicity Profile: Haematological - neutropenia WHO grade 3 in 20% requiring dose reduction, 64% experienced at least one haematological toxicity; Neutropenic sepsis in 14% of patients but no fatalities. Non-haematological: was mild; Nausea & vomiting - Grade I - II, 86%; Neurotoxicity - Grade I - II, 26%; Nephrotoxicity - Grade I - II, 18%; Fatigue - common, 70%. Results: CA 125 response in 82%; Clinical response with symptom control in 86%; Progression free survival median 6.1 months; Duration of response: 3 months to 18 months (median of 9 months); Stable disease in 7 patients, partial response in 4, complete response occurred in no patients, progression of disease in 2 patients; one patient unable to complete treatment. Conclusion: Chemotherapy for relapsed and heavily pre-treated ovarian cancer is essentially palliative. Symptomatic platinum sensitive patients have a favourable response to rechallenge. Cisplatin-etoposide has considerable activity with tolerable toxicity profile even in platinum refractory patients. Complete information about chances of response and adverse effects should be discussed with all relapsed patients. No significant financial relationships to disclose.
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Murphy, Madison, Grace Martin, Zahra Mahmoudjafari, Cory Bivona, Dennis Grauer, and David Henry. "Intraperitoneal paclitaxel and cisplatin compared with dose-dense paclitaxel and carboplatin for patients with stage III ovarian cancer." Journal of Oncology Pharmacy Practice 26, no. 7 (January 16, 2020): 1566–74. http://dx.doi.org/10.1177/1078155219899460.
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Introduction Patients diagnosed with stage III ovarian cancer are at high risk of recurrence and optimal adjuvant therapy is often debated. There is limited literature that directly compares intraperitoneal paclitaxel and cisplatin with dose-dense paclitaxel and carboplatin. Objectives The primary objective was to compare progression-free survival, overall survival, and tolerability of adjuvant intraperitoneal paclitaxel and cisplatin to dose-dense paclitaxel and carboplatin in stage III ovarian cancer patients. Methods A retrospective, IRB-approved, single center chart review was conducted reviewing adult patients with stage III ovarian cancer undergoing adjuvant intraperitoneal therapy or dose-dense therapy between 2010 and 2018. Results Eighty-two patients were included in the final analysis; 44 in the intraperitoneal group and 38 in the dose-dense group. Intraperitoneal therapy was not associated with a longer progression-free survival (35.4 vs. 31.1 months; P = 0.97). The duration of overall survival did not differ between intraperitoneal and dose-dense (56.3 vs. 54.5 months; P = 0.55). Dose reductions were less frequent with intraperitoneal than dose-dense (11.36% vs. 31.58%; P = 0.02). No difference in treatment delays (45.5% vs. 65.8%; P = 0.07), dose cancellations (59.1% vs. 57.9%; P = 0.91), supportive care additions (95.5% vs. 84.2%; P = 0.09), or therapy discontinuation (59.1% vs. 39.5%; P = 0.07) between groups was noted. Conclusions Intraperitoneal therapy with paclitaxel and cisplatin, as compared with dose-dense paclitaxel and carboplatin, did not prolong progression-free or overall survival in the adjuvant setting among stage III ovarian cancer patients. A trend towards decreased tolerability was noted with intraperitoneal therapy.
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Li, Yanyi, Ying Shan, Yingchun Duan, Cui Jiang, Jisaihan A, and Yuko Ohno. "Synergetic effect of poly (ADP-ribosyl) polymerase (PARP) inhibitor and cisplatin on ovarian cancer." Tropical Journal of Pharmaceutical Research 21, no. 7 (August 19, 2022): 1403–9. http://dx.doi.org/10.4314/tjpr.v21i7.7.
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Purpose: To investigate the effect of the combination of poly (ADP-ribosyl) polymerase (PARP) inhibitor, talazoparib (BMN673), and cisplatin on the proliferation and apoptosis of ovarian cancer cells in vitro, and on xenograft tumors of ovarian cancer cells in vivo.
Methods: Cell viability was determined by CCK-8 assay, while cell proliferation and cell cycle were assessed using colony formation assay and flow cytometry, respectively. Cell apoptosis was evaluated by flow cytometry and TUNEL assays. Western blot assay was used to measure the expression levels of proliferation- and apoptosis-related proteins.
Results: The PARP inhibitor, BMN673, produced a dose-dependent synergistic effect with cisplatin (p < 0.05). Compared with when cisplatin or BMN673 was used alone, the combination of cisplatin and BMN673 significantly inhibited the growth of transplanted tumors (p < 0.05). Immunohistochemical analysis showed that cisplatin and BMN673 treatment increased the number of cells positive for TUNEL, but reduced the population of cells positive for Ki67.
Conclusion: Thus, BMN673 and cisplatin are synergistic against ovarian cancer cells, and therefore, should be subjected to further investigations, including clinical trials, to determine the potentials of the combination for the management of ovarian carcinoma.
Keywords: PARP inhibitor; Ovarian cancer; Xenografted tumor; Cisplatin
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Bertelsen, K. "489 A dose intensity study of carboplatin in ovarian cancer." European Journal of Cancer 31 (November 1995): S104—S105. http://dx.doi.org/10.1016/0959-8049(95)95743-p.
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Yun, Jeong Sup, Ha Jeong Kim, Sung Kyoo Jang, Ki Hyung Kim, and Man Soo Yoon. "Combination Chemotherapy with High Dose Cisplatin - Cyclophosphamide in Primary Epithelial Ovarian Cancer." Korean Journal of Gynecologic Oncology and Colposcopy 12, no. 1 (2001): 12. http://dx.doi.org/10.3802/kjgoc.2001.12.1.12.
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Ochiai, Kazunori, Satoshi Takakura, Seiji Isonishi, Hiroshi Sasaki, and Yoshiteru Terashima. "Maximal Cytoreductive Surgery and High Dose Cisplatin Chemotherapy for Advanced Ovarian Cancer." Asia-Oceania Journal of Obstetrics and Gynaecology 19, no. 4 (May 24, 2010): 375–81. http://dx.doi.org/10.1111/j.1447-0756.1993.tb00396.x.
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Zhao, Lili, Shihai Liu, Donghai Liang, Tao Jiang, Xiaoyan Yan, Shengnan Zhao, Yuanwei Liu, Wei Zhao, and Hongsheng Yu. "Resensitization of cisplatin resistance ovarian cancer cells to cisplatin through pretreatment with low‐dose fraction radiation." Cancer Medicine 8, no. 5 (April 2, 2019): 2442–48. http://dx.doi.org/10.1002/cam4.2116.
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Richardson, D. L., K. Kim, L. G. Seamon, D. M. O'Malley, L. A. Eaton, D. E. Cohn, L. J. Copeland, and J. M. Fowler. "Combination gemcitabine and cisplatin for recurrent ovarian cancer." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 16037. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.16037.
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16037 Background: Recent evidence suggests gemcitabine combined with a platinum drug is active in recurrent ovarian cancer. In an effort to decrease dose-limiting myelosuppression associated with gemcitabine plus carboplatin, cisplatin can be substituted for carboplatin. Our objective is to describe a single institutional experience with day 1 and day 15 (D1/15) gemcitabine (1000 mg/m2) and cisplatin (30 mg/m2) for the treatment of recurrent ovarian cancer. Methods: A retrospective chart review was performed of all patients with recurrent epithelial ovarian, fallopian tube, and primary peritoneal cancer who were treated with gemcitabine and cisplatin from 8/2001 through 8/2006 at a single institution. Sixty-seven patients met inclusion criteria. Results: The median number of prior chemotherapy regimens was 2 (range 1–6). The median platinum-free treatment interval was 10 months (range 0–40). While 34 (51%) patients were platinum sensitive, 24 (36%) patients were platinum resistant, and 9 patients (13%) were platinum refractory. Patients were treated with a median of 6 cycles (range 1–31) of gemcitabine plus cisplatin. Fifteen (22%) patients had a complete clinical response with a median progression free survival (PFS) of 16 months (range 5–40); 15 (22%) patients had a partial clinical response (median PFS 6 months, range 2–15). Stable disease was noted in 19 patients, with a median PFS of 24 months (range 4–36). Three (38%) out of eight patients with refractory ovarian cancer had a complete clinical response, and 1 patient had a partial response. Non-hematologic toxicities were most common, occurring in 23% of the patient population (neuropathy, fatigue and pain). Grade 3 and 4 hematologic toxicities were rare, occurring in less than 10% of patients. Conclusions: Gemcitabine plus cisplatin (D1/15) is a well tolerated and active regimen in patients with recurrent ovarian cancer, regardless of previous response to platinum-based chemotherapy. No significant financial relationships to disclose.