Single agent activity of oxaliplatin in heavily pretreated advanced epithelial ovarian cancer

Chollet, Philippe; Bensmaïne, M. A.; Brienza, S.; Deloche, Claire; Curé, Hervé; Caillet, H.; Cvitkovic, Esteban

doi:10.1093/oxfordjournals.annonc.a010500

Cited by 124 publications

(56 citation statements)

References 13 publications

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“…In our study of the H69 SCLC cells, oxaliplatin did not have activity against the cisplatin-resistant H69CIS200 cells and there are similar reports in ovarian carcinoma [40]. This also complements the clinical studies showing a lack of activity of oxaliplatin in cisplatin resistant ovarian carcinoma [17][18][19]. Our study questions the effectiveness of oxaliplatin in cisplatin resistant cancer and suggests that more research into the mechanisms of low-level platinum resistance is needed to resolve this issue.…”

Section: Discussionsupporting

confidence: 80%

“…Platinum pre-treated patients and clinical platinum resistance are not necessarily the same and different criteria are used in different clinical trails. When oxaliplatin was studied as a single agent in ovarian carcinoma where patients were divided into platinum resistant or platinum sensitive based on Markman's criteria [16], there was a clear drop in response rate to oxaliplatin in the cisplatin resistant patients [17][18][19]. This suggests that oxaliplatin's activity is reduced in cisplatin resistant cancer as this cohort failed to respond to oxaliplatin as a single agent.…”

Section: Introductionmentioning

confidence: 99%

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Oxaliplatin induces drug resistance more rapidly than cisplatin in H69 small cell lung cancer cells

Stordal

Davey

2005

Cancer Chemother Pharmacol

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Cisplatin produces good responses in solid tumours including small cell lung cancer (SCLC) but this is limited by the development of resistance. Oxaliplatin is reported to show activity against some cisplatin-resistant cancers but there is little known about oxaliplatin in SCLC and there are no reports of oxaliplatin resistant SCLC cell lines.Studies of drug resistance mainly focus on the cellular resistance mechanisms rather than how the cells develop resistance. This study examines the development of cisplatin and oxaliplatin resistance in H69 human SCLC cells in response to repeated treatment with clinically relevant doses of cisplatin or oxaliplatin for either 4 days or 2h. Treatments with 200ng/ml cisplatin or 400ng/ml oxaliplatin for 4 days produced sublines (H69CIS200 and H69OX400 respectively) that showed low level (approximately 2-fold) resistance after 8 treatments. Treatments with 1000ng/ml cisplatin or 2000ng/ml oxaliplatin for 2h also produced sublines, however these were not stably resistant suggesting shorter treatment pulses of drug may be more effective. Cells survived the first five treatments without any increase in resistance, by arresting their growth for a period and then regrowing. The period of growth arrest was reduced after the sixth treatment and the H69CIS200 and H69OX400 sublines showed a reduced growth arrest in response to cisplatin and oxaliplatin treatment suggesting that "regrowth resistance" initially protected against drug treatment and this was further upregulated and became part of the resistance phenotype of these sublines. Oxaliplatin dose escalation produced more surviving sublines than cisplatin dose escalation but neither set of sublines were associated with increased resistance as determined by 5-day cytotoxicity assays, also suggesting the involvement of regrowth resistance. The resistant sublines showed no change in platinum accumulation or glutathione levels even though the H69OX400 subline was more sensitive to buthionine sulfoximine treatment. The H69CIS200 cells were cross-resistant to oxaliplatin demonstrating that oxaliplatin does not have activity against low level cisplatin resistance. Relative to the H69 cells, the H69CIS200 and H69OX400 sublines were more sensitive to paclitaxel and taxotere suggests the taxanes may be useful in the treatment of platinum resistant SCLC. These novel cellular models 3 of cisplatin and oxaliplatin resistant SCLC will be useful in developing strategies to treat platinum-resistant SCLC.

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Section: Discussionsupporting

confidence: 80%

Section: Introductionmentioning

confidence: 99%

Oxaliplatin induces drug resistance more rapidly than cisplatin in H69 small cell lung cancer cells

Stordal

Davey

2005

Cancer Chemother Pharmacol

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“…Oxaliplatin has a more manageable toxicity profile than cisplatin, with no renal toxicity and a lower incidence of haematological and gastrointestinal toxicities. It lacks the nephrotoxicity of cisplatin and causes less myelotoxicity than carboplatin, the leading cisplatin analog, and it may be active in cisplatin-and carboplatin-resistant tumours (Chollet et al, 1996;Raymond et al, 1998b). The main toxicity associated with oxaliplatin is a generally reversible peripheral neuropathy (Raymond et al, 1998a).…”

mentioning

confidence: 99%

Phase II study of gemcitabine plus oxaliplatin as first-line chemotherapy for advanced non-small-cell lung cancer

et al. 2005

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This phase II study evaluated the response rate and tolerability of gemcitabine -oxaliplatin chemotherapy in non-small-cell lung cancer (NSCLC) patients. Chemonaive patients with stage IIIB or IV NSCLC received gemcitabine 1000 mg m À2 on days 1 and 8, followed by oxaliplatin 130 mg m À2 on day 1. Cycles were repeated every 21 days for up to six cycles. From February 2002 to May 2004, 60 patients were enrolled into the study in seven Italian institutions. We observed one complete response (1.7%) and 14 partial responses (23.3%), for an overall response rate of 25.0% (95% confidence interval, 14.7 -37.9%). The median duration of response was 5.9 months (range 1.5 -17.1 months). With a median follow-up of 6.7 months, median time to progressive disease and overall survival were 2.7 (range 1.9 -3.4 months) and 7.3 months (range 7.2 -8.6 months), respectively. The main grade 3 -4 haematological toxicities were transient neutropenia in 11.7% and thrombocytopenia in 8.3% of the patients. Nausea/vomiting was the main grade 3 -4 nonhaematological toxicity, occurring in 10.0% of the patients. Two (3.3%) patients developed grade 3 neurotoxicity. Our results show that gemcitabine -oxaliplatin chemotherapy is active and well tolerated in patients with advanced NSCLC, deserving further study, especially for patients not eligible to receive cisplatin.

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“…In combination with 5FU/leucovorin, it represents the preferential first-line regimen in the management of CRC in both adjuvant [81] and metastatic [82] settings. With respect to EOC, phase II studies with single agent oxaliplatin have reported an overall response rate (ORR) of 5.6-17% and 42-46% with single agent oxaliplatin in platinum resistant and platinum sensitive disease respectively [83,84].…”

Section: Oxaliplatinmentioning

confidence: 99%

Mucinous ovarian cancer: A therapeutic review

Wen

Rush

Rickett

et al. 2016

Critical Reviews in Oncology/Hematology

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Highlights Mucinous epithelial ovarian cancer (mEOC) is a rare chemo-resistant subtype of ovarian cancer with distinct epidemiology, pathology and natural history.  mEOC can often masquerade as metastatic mucinous tumours from the gastrointestinal (GI) tract.  Molecularly, in contrast to high-grade serous ovarian cancer (HGSOC), mEOC are far less defined by p53 mutations and instead commonly harbour KRAS and HER 2 mutations.  The current gold standard of 1 st line platinum/taxane doublet chemotherapy, is more tailored towards HGSOC and generally ineffective for mEOC.  This review summarises the limited evidence for using GI style chemotherapeutic agents in treating mEOC and explores novel therapeutic possibilities such as targeting HER2, VEGF and Src. AbstractMucinous ovarian cancer represents approximately 3% of epithelial ovarian cancers (EOC).Despite this seemingly low prevalence, it remains a diagnostic and therapeutic conundrum that has resulted in numerous attempts to adopt novel strategies in managing this disease.Anecdotally, there has been a prevailing notion that established gold standard systemic regimens should be substituted for those utilised in cancers such as gastrointestinal (GI) malignancies; tumours that share more biological similarities than other EOC subtypes. This review summarises the plethora of small studies which have adopted this philosophy and influenced the design of the multinational GOG142 study, which was ultimately terminated due to poor accrual. To date, there is a paucity of evidence to support delivering 'GI style' chemotherapy for mucinous ovarian cancer over and above carboplatin-paclitaxel doublet therapy. Hence there is an urge to develop studies focused on targeted therapeutic agents driven by refined mutational analysis and conducted within the context of harmonised international collaborations.3

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Single agent activity of oxaliplatin in heavily pretreated advanced epithelial ovarian cancer

Cited by 124 publications

References 13 publications

Oxaliplatin induces drug resistance more rapidly than cisplatin in H69 small cell lung cancer cells

Oxaliplatin induces drug resistance more rapidly than cisplatin in H69 small cell lung cancer cells

Phase II study of gemcitabine plus oxaliplatin as first-line chemotherapy for advanced non-small-cell lung cancer

Mucinous ovarian cancer: A therapeutic review

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