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• W2063485703 abstract "Hany Elsaleh and colleagues (May 20, p 1745)1Elsaleh H Joseph D Frieu F Zeps N Spry N Iacopetta B Association of tumour site and sex with survival benefit from adjuvant chemotherapy in colorectal cancer.Lancet. 2000; 355: 1745-1750Summary Full Text Full Text PDF PubMed Scopus (513) Google Scholar studied patients with Dukes' C colorectal cancer—23 with microsatellite instability (MSI) and 249 with microsatellite stable (MSS) tumours—all of whom were treated with fluorouracil. They postulate that the better survival seen in the patients with MSI is a result of the effect of the fluorouracil adjuvant chemotherapy. However, this interpretation could be misleading. Deficiency of DNA mismatch repair is a common feature of MSI cancers, recognised by their high rate of spontaneous frameshift mutations within microsatellite sequences and their resistance to cytotoxic drugs, including fluorouracil.2Carethers JM Chauhan DP Fink D et al.Mismatch repair proficiency and in vitro response to 5-fluorouracil.Gastroenterology. 1999; 117: 123-131Summary Full Text Full Text PDF PubMed Scopus (385) Google Scholar An alternative explanation could be related to the fact that most MSS colorectal cancers have multiple genetic abnormalities in the tumour suppressor pathway consisting of multiple losses of heterozygosity on chromosomes 5q, 17p (in the p53 region), and 18q as well as a predominance of ras mutations. All these genetic abnormalities are significantly less frequently observed in MSI colorectal cancers. Thus, the worse survival of the 249 MSS colorectal cancer patients may be better explained in terms of the alteration of the fluorouracil response as a result of disruption of the p53 function. Cells with targeted p53 deletion have been found to be resistant to fluorouracil apoptosis. Cells with one disrupted p53 allele display a sensitivity between that of parental cells and cells with both alleles disrupted, suggesting a tight control of fluorouracil sensitivity by p53.3Bunz F Hwang PM Torrance Ch et al.Disruption of p53 in human cancer cells alters the responses to therapeutic agents.J Clin Invest. 1999; 104: 263-269Crossref PubMed Scopus (916) Google Scholar A far better survival for a subgroup of MSI colorectal cancers was originally inversely correlated with the lack of loss of heterozygosity4Thibodeau SN Bren G Schaid D Microsatellite instability in cancer of the proximal colon.Science. 1993; 260: 816-819Crossref PubMed Scopus (2776) Google Scholar and not associated with adjuvant chemotherapy effect (the survival curves shown in the last graph of figure 5 article by Elsaleh and colleagues are similar to those shown in figure 2 of the paper by Thibodeau and colleagues.4Thibodeau SN Bren G Schaid D Microsatellite instability in cancer of the proximal colon.Science. 1993; 260: 816-819Crossref PubMed Scopus (2776) Google Scholar) Pharmacogenetically speaking, fluorouracil is an inhibitor of thymidylate synthase, which catalyses the methylation of deoxyuridine to thymidylate, a DNA precursor. Response to treatment and survival from colorectal cancer has been associated with the thymidylate synthase mRNA concentrations, thymidine phosphorylase, and the dihydropyrimidine dehydrogenase. The three genes involved can be used to predict fluorouracil response and to customise adjuvant chemotherapy by using other available drugs, such as CPT-11, for patients expected to be fluorouracil-resistant.5Salonga D Danenberg KD Johnson M et al.Colorectal tumors responding to 5-fluorouracil have low gene expression levels of dihydropyrimidine dehydrogenase, thymidylate synthase, and thymidine phosphorylase.Clin Cancer Res. 2000; 6: 1322-1327PubMed Google Scholar Elsaleh and colleagues use the BAT- 26 marker to establish MSI status, but no explanation for the use of this marker is given in the text. A set of microsatellite markers is usually recommended to establish the degree of MSI, and a panel of five microsatellites has been validated; a high frequency of MSI is defined if two or more of the five markers show instability. The investigators have used a mononucleotide repeat (BAT-26) that is quasi-monomorphic, but its reliability as a sole marker has not yet been validated." @default.
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• W2063485703 date "2000-09-01" @default.
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• W2063485703 title "Tumour site, sex, and survival in colorectal cancer" @default.
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• W2063485703 doi "https://doi.org/10.1016/s0140-6736(05)73438-3" @default.
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