Association between excision repair cross-complementation group 1 polymorphism and clinical outcome of platinum-based chemotherapy in patients with epithelial ovarian cancer

Kang, Sokbom; Ju, Woong; Kim, Jae Weon; Park, Noh Hyun; Song, Yong Sang; Kim, Seung Cheol; Park, Soo‐Jin; Kang, Soon Beom; Lee, Hyo Pyo

doi:10.1038/emm.2006.38

Cited by 82 publications

(76 citation statements)

References 14 publications

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“…Consistent with previous studies regarding the C/C genotype and its relationship with poor treatment response (38), these authors found that ovarian cancer patients harboring C/C genotypes were less responsive to chemotherapy and maintained a higher risk for disease progression and death in contrast to those harboring C/T or T/T genotypes. Findings of Smith et al showed that ovarian cancer patients with a high ERCC-1 expression or the C/C genotype at codon 118 may benefit from a platinum/ paclitaxel combination, whereas patients with a low ERCC-1 expression or the C/T or T/T genotype may respond well to platinum without paclitaxel.…”

Section: Mthfr C677t Polymorphism and Methotrexatesupporting

confidence: 87%

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‘Genetic profiling’ and ovarian cancer therapy (Review)

et al. 2011

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Abstract. High variability observed among ovarian cancer patients in response to the same therapy and the related toxicity may be correlated to gene polymorphisms and genetic alterations affecting the metabolism of drugs commonly used to treat this tumor. Recent studies have shown a correlation between the polymorphisms characterizing GSTM1-T1 detoxifying enzymes and poor outcome in advanced ovarian cancer patients treated with platinum/paclitaxel-based chemotherapy. Multidrug resistance 1 (mdr-1) polymorphisms were found to be associated with resistance to paclitaxel treatment. Polymorphisms of MRP2, a protein involved in methotrexate, cisplatin and irinotecan active metabolite glucuronide transport, negatively affect platinum-based chemotherapy response. A similar occurrence has been observed with CYP1A1 Ile462Val and ercc1 C118T polymorphisms while patients who were carriers of MTHFR C677T polymorphism had a better response to methotrexate therapy, but an elevated risk of toxicity. Biological therapy with Bevacizumab, the anti-vascular endothelial growth factor has been shown to be less efficient in ovarian cancer patients carrying the polymorphism of the Interleukin-8 gene. Instead, polymorphisms in the XPD gene (Lys751Gln and Asp312Asn), a member of the nucleotide excision repair pathway, positively affects the response to therapy with carboplatin/paclitaxel. Therefore, the study of 'genetic profiling' is crucial to improving the clinician's ability to tailor effective therapy to the molecular profile of the patient while minimizing toxicities. This review describes clinical applications of the above genetic polymorphisms in ovarian cancer patients treated with platinum/paclitaxel-based chemotherapy.

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Section: Mthfr C677t Polymorphism and Methotrexatesupporting

confidence: 87%

“…Another study on ovarian cancer patients has stressed the association between the C/C genotype and increased resistance to platinum-based chemotherapy, consistent with a higher transcription activity of the AAC codon (38).…”

Section: Mthfr C677t Polymorphism and Methotrexatementioning

confidence: 90%

‘Genetic profiling’ and ovarian cancer therapy (Review)

et al. 2011

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“…It is possible that a decreased level of ERCC1 mRNA expression influences the repair efficiency of DNA damage, which then contributes to cancer susceptibility. Studies have also shown an association between the polymorphism and malignancies such as lung, ovarian and colorectal cancer (26)(27)(28)(29), although no previous association with cervical cancer has been shown. Our study showed that ERCC1 118C>T may be a potential risk factor for SCC.…”

Section: Cin Scc Cin Scc --------------------------------------------mentioning

confidence: 99%

Single nucleotide polymorphisms in DNA repair genes and risk of cervical cancer: A case-control study

et al. 2011

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Abstract. In this report, we describe a case control study in a Chinese population aimed at identifying possible associations between susceptibility to cervical cancer and single nucleotide polymorphisms in XRCC1 194C>T, XRCC1 280G>A, XRCC1 399G>A, ERCC2 751A>C , ERCC2 156C>A, ERCC1 118C>T, PARP1 762T>C , RAD51 135G>C and HER2 655A>G. The cases comprised 154 patients: 80 cervical squamous cell carcinomas (SCCs), 2 adenocarcinomas and 72 cervical intraepithelial neoplasias (CINs). A total of 177 healthy women were recruited as the controls. A significant association was found between ERCC1 118C>T and SCC in the additive genetic model [odds ratio (OR)=1.711; 95% confidence interval (CI), 1.089-2.880; p=0.021] and the dominant genetic model (OR=1.947; 95% CI, 1.056-3.590; p=0.033). Among women with a smoking family member, ERCC1 118C>T increased SCC risk in the additive model (OR=2.800; 95% CI, 1.314-5.968; p= 0.008). For women who had first intercourse before 22 years of age, XRCC1 280G>A was found to act as a protective factor for SCC under the additive model (OR=0.228; 95% CI, 0.058-0.900; p=0.035), while RAD51 135G>C was a risk factor for CIN (OR=4.246; 95% CI, 1.335-13.502; p=0.014). For women who had first intercourse after 22 years of age, the additive genetic model showed RAD51 135G>C (OR=0.359; 95% CI, 0.138-0.934; p=0.036) and HER2 655A>G (OR=0.309; 95% CI, 0.098-0.972; p=0.045) to be protective factors for SCC. XRCC1 399G>A increased CIN risk among women who first gave birth before the age of 22 in the additive genetic model (OR=4.459; 95% CI, 1.139-17.453; p=0.032). For those who first gave birth after age 22, ERCC1 118C>T was found to be a risk factor for SCC in the additive genetic model (OR=1.884; 95% CI, 1.088-3.264; p=0.024). A significant interaction was observed between RAD51 135G>C and age at first intercourse (p interaction =0.033 for SCC, p interaction =0.021 for CIN), as well with sexual partner number (p interaction =0.001 for SCC). The interaction between HER2 655A>G and age at first intercourse, ERCC2 156C>A and family smoking status and XRCC1 280G>A and alcohol consumption were significant, with p interaction =0.023 for SCC, p interaction =0.021 for CIN and p interaction =0.025 for SCC, respectively.

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“…We assume that these differences were due to the absence of larger studies. Which genotype is associated with higher mRNA levels and/or better prognosis with the patients that received platinum compound is still a controversial topic (21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31). Some reported environmental factors such as smoking interaction might modulate and mask the genetic effect of polymorphism (35)(36)(37).…”

Section: Responder/global -------------------------------------------mentioning

confidence: 99%

“…Since Yu et al, reported that ERCC1 mRNA levels were reduced in human ovarian cancer cells with a variant allele, and that those cells were inferior in recovery from platinum damage to cells with wild-type allele (21), several studies have assessed the relation between ERCC1 codon 118 polymorphism and sensitivity to a platinum agent in ovarian cancers, colorectal cancers, gastric cancers, and non-small cell lung cancers (22)(23)(24)(25)(26)(27)(28)(29)(30)(31). It is possible for ERCC1 codon 118 polymorphism to be a biomarker for assessing the sensitivity to a platinum-based therapy, although it is still a matter of controversy whether either a wild-type allele or a mutant-type allele affect the platinum resistance.…”

Section: Introductionmentioning

confidence: 99%

ERCC1 codon 118 polymorphism is a useful prognostic marker in patients with pancreatic cancer treated with platinum-based chemotherapy

Kamikozuru

Kuramochi²,

Hayashi³

et al. 2008

Int J Oncol

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Abstract. Excision repair cross-complementation 1 (ERCC1) has been reported to play a major role in the response to platinum-based therapies. It has recently been proposed that a synonymous polymorphism at codon 118 converting a common codon usage (AAC) to an infrequent one (AAT) may impair ERCC1 translation and to affect the response to cisplatin chemotherapy. We analyzed the association between this polymorphism and clinical outcome in 67 pancreatic cancer patients treated with cisplatin and S-1 or with S-1 alone. ERCC1 codon 118 polymorphism was analyzed using PCR-RFLP. Thirty-nine of the patients (58.2%) were homozygous for AAC codon, 7 (10.4%) were homozygous for AAT codon, and 21 (31.3%) were heterozygous. Among those treated with cisplatin and S-1, no significant difference in objective response rate was observed between genotypes. However, the patients with one or two AAT codons had a significantly longer progression-free survival (PFS) and overall survival (OS) than those homozygous for AAC allele (PFS: 338 days vs 106 days, p=0.006, OS: 763 days vs 415 days, p=0.030). In contrast, no significant difference in PFS or OS was observed between genotypes among the patients treated with S-1 alone. ERCC1 polymorphism may be a useful prognostic marker in patients with pancreatic cancer treated with platinum-based chemotherapy.

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Association between excision repair cross-complementation group 1 polymorphism and clinical outcome of platinum-based chemotherapy in patients with epithelial ovarian cancer

Cited by 82 publications

References 14 publications

‘Genetic profiling’ and ovarian cancer therapy (Review)

‘Genetic profiling’ and ovarian cancer therapy (Review)

Single nucleotide polymorphisms in DNA repair genes and risk of cervical cancer: A case-control study

ERCC1 codon 118 polymorphism is a useful prognostic marker in patients with pancreatic cancer treated with platinum-based chemotherapy

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