Oxaliplatin/cisplatin (L-OHP/CDDP) combination in heavily pretreated ovarian cancer

Soulié, P; Bensmaine, Amine; Garrino, Cristina; Chollet, Philippe; Brain, Étienne; Fereres, M.; Jasmin, C; Musset, M; Misset, Jean-Louis; Cvitkovic, Esteban

doi:10.1016/s0959-8049(97)00122-6

Cited by 61 publications

(25 citation statements)

References 28 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: 81%

“…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: 81%

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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“…Of these platinum-based compounds, [SP-4-2-{1R-trans)]-(1,2-cyclohexanediamine-N,N9)[ethanedioata(2-)-O,O9]platinum (oxaliplatin), a novel compound containing a trans-1-(R,R)-1,2-diaminocyclohexane (DACH) carrier ligand, has recently been approved for the treatment of metastatic colorectal carcinoma in conjunction with fluoropyrimidines [2]. Oxaliplatin has shown in vitro and in vivo efficacy against many tumor cell lines and tumors including those that are resistant to cisplatin and carboplatin [1,[3][4][5]. In addition to its positive effects, oxaliplatin also shows several toxic effects.…”

Section: Introductionmentioning

confidence: 99%

Investigation of interaction between human hemoglobin A₀ and platinum anticancer drugs by capillary isoelectric focusing with whole column imaging detection

Lemma

Mandal

et al. 2008

J of Separation Science

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Original PaperInvestigation of interaction between human hemoglobin A 0 and platinum anticancer drugs by capillary isoelectric focusing with whole column imaging detection CIEF with whole column imaging detection (WCID) was used to investigate the interaction of platinum-based anticancer drugs, cis-platinum(II) diamine dichloride (cisplatin) and [SP-4-2-{1R-trans)]-(1,2-cyclohexanediamine-N,N9)[ethanedioata(2 -)-O,O9]platinum (oxaliplatin), with human hemoglobin A 0 (Hb). This technique facilitates the investigation and characterization of the formation of adducts between drugs and proteins. Cisplatin and oxaliplatin were mixed with the target protein at different concentrations (0:1, 1:1, 1:10, 1:50, and 1:100), and the reaction mixtures were incubated for 0, 0.5, 1, 12, 24, 48, and 72 h at 378C in a water-bath. The focused Hb -drug adduct profiles were imaged by WCID. At higher drug to protein molar ratios (for both oxaliplatin and cisplatin), the results exhibit significant changes in the peak shapes and heights, which may indicate the destabilization of the protein. However, the conformational change was less evident at lower molar ratios. In addition, a major pI shift was observed for the oxaliplatin reaction mixtures (for 1:10, 1:50, and 1:100 ratios). In comparison with previously reported findings obtained by other analytical methods, conclusions were drawn about the validity of CIEF as a simple and convenient method for the investigation of protein -drug interactions. These results may provide useful information for further understanding the activity and toxicity of these chemotherapeutic drugs and improving their clinical performance.

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“…In 25 patients with ovarian cancer, who had previously been heavily treated with cisplatin/carboplatin, oxaliplatin at a dose of 130 mg m-2 was combined with cisplatin at a dose of 100 mg m-2, each given every 3 weeks (Soulie et al, 1997). The results (shown in Table 1) indicate an overall response rate of 40%.…”

mentioning

confidence: 99%

Ongoing and unsaid on oxaliplatin: the hope

Cvitkovic

1998

Br J Cancer

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Summary Oxaliplatin, the first available diaminocyclohexane platinum, has clinical activity in colorectal and ovarian cancers. Its mechanism of action is thought to be similar to that of cisplatin, its main mechanism being the intrastrand DNA adduct between two adjacent guanins or two adjacent guanine and adenine adducts. Ongoing molecular pharmacological studies of the mechanism of action of cisplatin suggest that platinated adducts are recognized by proteins of the mismatch repair system, including the products of the hMLH1 and hMSH2 genes. DNA mismatch repair defects occur in a wide variety of sporadic human cancers, are the main genetic factor in hereditary non-polyposis colon cancer and a frequent de novo or acquired phenomenon in ovarian cancer and other solid tumours. Moreover, they have recently been reported to be a cause of resistance to cisplatin but not to oxaliplatin, as diaminocyclohexane platinum adducts do not appear to be recognized by the mismatch repair complex. These findings explain the oxaliplatin activity in some cisplatin-resistant tumours. In addition, the good safety profile of oxaliplatin makes it a drug of choice for combination therapy, and it has been shown to be synergistic with other cytotoxic agents, including 5-fluorouracil, cisplatin, carboplatin, topotecan, gemcitabine and CPT-11. The results of several ongoing trials are awaited, but available data demonstrate that oxaliplatin is highly effective in the treatment of advanced colorectal and ovarian cancers. Promising early results suggest that it is also efficacious in non-Hodgkin's lymphoma, breast and non-small-cell lung cancers. As a result of its mechanism of action, its favourable safety profile and the differential profile of its antitumoral activity, the full potential of oxaliplatin as an active, versatile antitumoral agent is yet to be fully explored.

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Oxaliplatin/cisplatin (L-OHP/CDDP) combination in heavily pretreated ovarian cancer

Cited by 61 publications

References 28 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

Investigation of interaction between human hemoglobin A₀ and platinum anticancer drugs by capillary isoelectric focusing with whole column imaging detection

Ongoing and unsaid on oxaliplatin: the hope

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Oxaliplatin/cisplatin (L-OHP/CDDP) combination in heavily pretreated ovarian cancer

Cited by 61 publications

References 28 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

Investigation of interaction between human hemoglobin A0 and platinum anticancer drugs by capillary isoelectric focusing with whole column imaging detection

Ongoing and unsaid on oxaliplatin: the hope

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Investigation of interaction between human hemoglobin A₀ and platinum anticancer drugs by capillary isoelectric focusing with whole column imaging detection