Oxaliplatin/5fluorouracil-based chemotherapy was active and well tolerated in heavily pretreated patients with ovarian carcinoma

Rosa, Daniela D.; Awada, Ahmad; Mano, Max S.; Selleslags, Jean; Lebrun, Fabienne; Gil, Thierry; Piccart, Martine

doi:10.1007/s00404-008-0592-9

Cited by 14 publications

(18 citation statements)

References 28 publications

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“…However, a recent combination chemotherapy with 5FU and oxaliplatin has brought about a remarkable improvement of the long-term survival rates of inoperable colorectal cancer patients (1). Consequently, this combination chemotherapy with 5FU and oxaliplatin has also been applied to recurrent ovarian cancer patients after standard chemotherapy with paclitaxel and carboplatin (2,3). Since 5FU-combination chemotherapies have been reapplied to various cancer patients in addition to colorectal cancer patients, 5FU-resistance may become a large clinical problem in future cancer chemotherapies.…”

Section: Introductionmentioning

confidence: 99%

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Establishment and characterization of monoclonal 5-fluorouracil-resistant cell lines derived from human endometrial adenocarcinoma

Tanaka

Bai²,

Toujima³

2010

Int J Oncol

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Abstract. To investigate acquired 5-fluorouracil (5FU)-resistance in cancer cells, we established four monoclonal 5FU-resistant cell lines from human endometrial adenocarcinoma cells by long-term 5FU-exposure cultures and limiting dilution cultures. The established subclones exhibited 5-25 times greater 5FU-resistance than the parent cells, and showed suppression of 5FU-induced DNA fragmentation. All four 5FU-resistant subclones were 25-125 times more resistant to SN38, 4-hydroxy-cyclophosphamide, paclitaxel and etoposide than the parent cells while none of the four subclones showed resistance to mitomycin. Two of the four subclones showed no resistance to pirarubicin and bleomycin. Although all four 5FU-resistant subclones were 5-25 times more resistant to anti-Fas IgM than the parent cells, the resistance levels to anti-Fas IgM of the individual subclones did not coincide with the strengths of their multidrug resistance. Karyotyping analyses revealed that the parent cells and the three 5FU-resistant subclones examined had normal 46XX karyotypes. These results indicate that the cell death signals induced by mitomycin, pirarubicin and bleomycin are distinctly different from the Fas-mediated apoptotic signals, that acquisition of 5FU-resistance can occur without any large chromosomal deletions or rearrangements, and that there are several possible molecular changes during the acquisition of 5FU-resistance. The established cell lines represent useful tools for investigating the mechanisms and treatments of acquired 5FU-resistance.

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Section: Introductionmentioning

confidence: 99%

“…Combination chemotherapy with 5FU and oxaliplatin was reported to be effective for recurrent ovarian cancer patients after TC therapy (2,3). Therefore, 5FU-resistance may become a large clinical problem for endometrial and ovarian cancer patients in the near future.…”

Section: Introductionmentioning

confidence: 99%

Establishment and characterization of monoclonal 5-fluorouracil-resistant cell lines derived from human endometrial adenocarcinoma

Tanaka

Bai²,

Toujima³

2010

Int J Oncol

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“…Four studies have demonstrated reasonable efficacy with an acceptable toxicity profile of FOLFOX (5FU/leucovorin + oxaliplatin) in platinum resistant, heavily pre-treated EOC [85][86][87][88] (Table 6). Again, these studies were all in the second-line or beyond setting and included only a handful of mEOC patients, so it is difficult to draw conclusions.…”

Section: Fu/leucovorin and Oxaliplatin (Folfox)mentioning

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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“…New generations of oral fluoropyrimidine such as S-1, which inhibit the degradation of 5-FU and capecitabine have been developed and put into use in the treatment of several solid tumors (Schoffski, 2004). 5-FU and 4-HPR showed positive responses in combination with platinum based drugs or as a single agent in phase II trials respectively in ovary carcinoma (Rosa et al, 2008;Weiss, 1992;Garcia et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Ursolic acid benzaldehyde chalcone leads to inhibition of cell proliferation and arrests cycle in G1/G0 phase in ovarian cancer

Jia

Chen

et al. 2015

Bangladesh J Pharmacol

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<p>In the present study, the effect of ursolic acid benzaldehyde chalcone (UABC) on ovarian carcinoma cells was studied. The results revealed that ovarian carcinoma cells on UABC treatment increased Sub-G1 cell population, increased rate of cell apoptosis and morphological changes in mitochondrial membrane. In OVCAR 432 cells treatment with UABC increased the Sub-G1 cell population to 72.3% and growth inhibition rate of >72%. Treatment with 20 µM of UABC for 48 hours, led to an induction of apoptosis in 67.2% and induced morphological changes in OVCAR 432 cells. The Western blot results showed high concentration of cytochrome c in the cell cytosol after 48 hours of UABC treatment. Treatment of RMS-13 cells with UABC resulted in inhibition of GLI1, GLI2, PTCH1, and IGF2 genes. In addition, we found a significant reduction in hedgehog activity of RMS-13 cells after UABC treatment by means of a hedgehog-responsive reporter assay. Therefore, UABC can be a promising agent for the treatment of ovarian carcinoma.</p>

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Oxaliplatin/5fluorouracil-based chemotherapy was active and well tolerated in heavily pretreated patients with ovarian carcinoma

Cited by 14 publications

References 28 publications

Establishment and characterization of monoclonal 5-fluorouracil-resistant cell lines derived from human endometrial adenocarcinoma

Establishment and characterization of monoclonal 5-fluorouracil-resistant cell lines derived from human endometrial adenocarcinoma

Mucinous ovarian cancer: A therapeutic review

Ursolic acid benzaldehyde chalcone leads to inhibition of cell proliferation and arrests cycle in G1/G0 phase in ovarian cancer

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