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Review

Fluoropyrimidine resistance in colon cancer

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Pages 409-416 | Published online: 10 Jan 2014

References

  • Bertino JR. Kamofsky Memorial Lecture: ode to methotrexate. j Clin. Oncol 11, 5–14(1993).
  • Gorlick R, Bertino JR. Drug resistance in colon cancer. Semin. Oncol 26, 606–611 (1999).
  • Boring CC, Squires TS, Tong T Cancer statistics 1993. 43, 7–26 (1993).
  • Cohen AM, Shank B, Friedman MA. Colorectal cancer. In: Cancer Principles and Practice of Oncology Devita VT, Hellman S, Rosenberg SA (Eds), Lippincott-Raven, Philadelphia, PA, USA, 895–964, (1989).
  • Goker E, Gorlick R, Bertino JR. Resistance mechanisms to antimetabolites. In: Drug Resistance in the Treatment of Cancer Pinedo HM, Giaccone G (Eds), Cambridge University Press, Cambridge, MA, USA, 1-13(1998).
  • Grem JL. Fluorinated pyrimidines. In: Cancer Chemotherapy and Biotherapy Chabner BA, Longo DL (Eds), Lippincott-Raven, Philadelphia, PA, USA, 180–224 (1996).
  • Will CL, Dolnick BJ. 5-Fluorouracil inhibits dihydrofolate reductase precursormRNA processing and/or nuclear mRNAstability in methotrexate-resistant KB cells.Biol. Chem. 264, 21413–21421 (1989).
  • •5-Fluorouracil treatment increases the levels of precursor mRNA relative to mRNA levels suggesting the drug affects RNA processing or stability.
  • Kinsella AR, Smith D, Pickard M et al. Resistance to chemotherapeutic antimetabolites: a function of salvage pathway involvement and cellular response to DNA damage. Br. Cancer75, 935–945 (1997).
  • Sobrero, AF, Aschele C, Bertino JR. Fluorouracil in colorectal cancer — a tale of two drugs: implications for biochemical modulation. Clin. Oncol 15, 368–381 (1997).
  • ••Discussed that 5-FU mechanisms of actionand resistance depends on whether it is given as a bolus or a continuous infusion.
  • Jenh CH, Geyer PK, Baskin F et al. Thymidylate synthase gene amplification in fluorodeoxyuridine-resistant mouse cell lines. Mal Pharmacol 28, 80–85 (1985).
  • Copur S, Aiba K, Drake JC et al. Thymidylate synthase gene amplification in human colon cancer cell lines resistant to 5-fluorouracil. Biochem. Pharmacol 49,1419–1426 (1995).
  • Clark JL, Berger SH, Mittelman A et al Thymidylate synthase overproduction gene amplification in a colon tumor resistant to fluoropyrimidine chemotherapy. Cancer Treat. Rep. 71, 261–265 (1987).
  • Lenz HJ, Leichman CG, Danenberg KID et al Thymidylate synthase mRNA level in adenocarcinoma of the stomach: a predictor for primary tumor response and overall survival." Clin. Dna. 14, 176–182 (1996).
  • Leichman L, Lenz HJ, Leichman CG et al Quantitation of intratumoral thymidylate synthase expression predicts for resistance to protracted infusion of 5-fluorouracil and weekly leucovorin in disseminated colorectal cancers: Preliminary report from an ongoing trial. Eur. J. Cancer 31A, 1306–1310 (1995).
  • Johnston PG, Lenz HJ, Leichman CG et al. Thymidylate synthase gene and protein expression correlate and are associated with response to 5-fluorouracil in human colorectal and gastric tumors. Cancer Res. 55, 1407–1412 (1995).
  • •One of several early and influential studies that demonstrated both low TS mRNA and protein expression were associated with response to 5-FU chemotherapy.
  • Johnston PG, Fisher ER, Rockette HE et al The role of thymidylate synythase expression in prognosis and outcome of adjuvant chemotherapy in patients with rectal cancer. Clin. Oncol 12, 2640–2647 (1994).
  • Yamachika T, Nakanishi H, Inada K et al. A new prognostic factor for colorectal carcinoma, thymidylate synthase and its therapeutic significance. Cancer 82, 70–77 (1998).
  • Leichman L, Lenz HJ, Leichman CG et al. Quantitation of intratumoral thymidylate synthase expression predicts for disseminated colorectal response and resistance to protracted infusion of fluorouracil and weekly leucovorin. j Clin. Dried 15, 3223–3229 (1997).
  • Lenz HJ, Hayashi K, Salonga D et al p53 point mutations and thymidylate synthase messenger RNA levels in disseminated colorectal cancer: an analysis of response and survival. Clin. Cancer Res. 4, 1243–1250 (1998).
  • Aschele C, Debernarclis D, Casazza S et al Immunohistochemical quantitation of thymidylate synthase expression in colorectal cancer metastases predicts for clinical outcome to fluorouracil-based chemotherapy. Clin. Oncol 17, 1760–1767 (1999).
  • Gorlick R, Metzger R, Danenberg KD et al Higher levels of thymidylate synthase gene expression are observed in pulmonary as compared to hepatic metastases of colorectal adenocarcinoma. j Clin. Oncol 16, 1465–1469 (1998).
  • •Study demonstrated that the pulmonary metastases of colorectal cancer have higher levels of TS than hepatic metastases explaining their lack of response to 5-FU.
  • Cascinu S, Aschele C, Barni S et al. Thymidylate synthase protein expression in advanced colon cancer: correlation with the sites of metastasis and the clinical response to leucovorin-modulated bolus 5-fluorouracil. Clin. Cancer Res. 5, 1996–1999 (1999).
  • Baneijee D, Gorlick R, Liefshitz A et al. Levels of E2F-1 expression are higher in lung metastasis of colon cancer as compared with hepatic metastasis and correlate with levels of thymidylate synthase. Cancer Res. 60, 2365–2367 (2000).
  • •Suggests that the E2F-1 transcription factor may be regulating the levels of TS expression in colon cancer.
  • Chu E, Voeller D, Koeller DM et al Identification of an RNA binding site for human thymidylate synthase. Proc. Natl Acad. Sci. USA 90, 517–521 (1993).
  • Kitchens ME, Forsthoefel AM, Rafique Z, Spencer HT, Berger FG. Ligand-mediated induction of thymidylate synthase occurs by enzyme stabilization. Implications for autoregulation of translation. J. Biol. Chem. 274, 12544–12547 (1999).
  • ••Suggests that 5-FU modulates IS proteinlevels in the absence of transcription by altering protein stability rather than through regulation of translation, which had been believed previously.
  • Pullarkat ST, Stoehlmacher J, Ghaderi V et al. Thymidylate synthase gene polymorphism determines response and toxicity of 5-FU chemotherapy. Pharmacogenomics 1, 65–70 (2001).
  • •A polymorphism exists in the IS promoter having either double or triple tandem repeats and it is associated with the toxicity and response patients have following 5-FU chemotherapy.
  • Ju J-F, Baneijee D, Lenz H-J et al. Restoration of wild type p53 activity in p53-null HL-60 cells confers multidrug sensitivity. Clin. Cancer Res. 4, 1315–1322 (1998).
  • Lowe SW Bodis S, McClatchey A et al p53 status and the efficacy of cancer therapy in vivo. Science 266, 807–810 (1994).
  • Livingstone LR, White A, Sprouse J et al Altered cell cycle arrest and gene amplification potential accompany loss of wild type p53. Ce1170, 923–935 (1992).
  • Yin Y, Tainsky MA, Bischoff FZ. Wild type p53 restores cell cycle control and inhibits gene amplification in cells without mutant p53 alleles. Ce1170, 937–948 (1992).
  • Goker E, Waltham M, Kheradpour A et al Amplification of the dihydrofolate reductase gene is a mechanism of acquired resistance to methotrexate in patients with acute lymphocytic leukemia and is correlated with p53 gene mutations. Blood 86, 677–684 (1995).
  • Pritchard DM, Watson AJM, Potten CS et al. Inhibition by uridine but not thymidine of p53-dependent intestinal apoptosis initiated by 5-fluorouracil: evidence for the involvement of RNA perturbation. Proc. Natl Acad. Sci. USA 94, 1795–1799 (1997).
  • Harwood FG, Frazier MW Krajewski S et al. Acute and delayed apoptosis induced by thymidine deprivation correlates with expression of p53 and p53-regulated genes in colon carcinoma cells. Oncogene 12, 2057-2067 (1996).
  • O'Connor PM, Jackman J, Bae I et al Characterization of the p53 tumor suppressor pathway in cell lines of the National Cancer Institute anticancer drug screen and correlations with the growth-inhibitory potency of 123 anticancer agents. Cancer Res. 57, 4285–4300 (1997).
  • Kastrinakis WV, Ramchurren N, Rieger KM et al Increased incidence of p53 mutations is associated with hepatic metastases in colorectal neoplastic progression. Oncogenell, 647–652 (1995).
  • Flamini G, Curigliano G, Ratto C et al. Prognostic significance of cytoplasmic p53 overexpression in colorectal cancer. An immunohistochemical analysis. Eur. Cancer32A, 802–806 (1996).
  • Belluco C, Guillem JG, Kemeny N et al. p53 nuclear protein overexpression in colorectal cancer: a dominant predictor of survival in patients with advanced hepatic metastases. j Clin. Oncol 14, 2696–2701 (1996).
  • •Demonstrates that the presence of p53 alterations determined imrnunohistochemically is a strong predictor of survival in patients with colorectal cancer who have hepatic metastases.
  • Cascinu S, Catalano V, Aschele C et al. Immunohistochemical determination of p53 protein does not predict clinical response in advanced colorectal cancer with low thymidylate synthase expression receiving a bolus 5-fluorouracil-leucovorin combination. Ann. Oncol 11, 1053–1056 (2000).
  • •Demonstrated that p53 status measured by imrnunohistochemistry did not correlate with response to 5-FU in patients with advanced colorectal cancer. This contradicts the findings of the prior cited studies.
  • Nevins JR. E2E A link between the Rb tumor suppressor protein and viral oncoproteins. Science 258, 424–429 (1992).
  • Gorlick R, Goker E, Trippett T, Waltham M, Banerjee D, Bertino JR. Intrinsic and acquired resistance to methotrexate in acute leukemia. N Engl. I Med. 335, 1041–1048 (1996).
  • Dyson N. The regulation of E2F by pRB-family proteins. Genes Dev. 12, 2245–2262 (1998).
  • Muller H, Helm n K. The E2F transcription factors: key regulators of cell proliferation. Biochim. Biophys. Acta 1470, M1—M12 (2000).
  • DeGregori J, Kowalik U, Nevins JR. Cellular targets for activation by the E2F1 transcription factor include DNA synthesis-and G15-regulatory genes. Mal Cell. Biol. 15, 4215–4224 (1995).
  • Banerjee D, Schnieders B, Fu JZ, Adhikari D, Zhao S-C, Bertino JR. Role of E2F-1 in chemosensitivity. Cancer Res. 58, 4292–4296 (1998).
  • ••Demonstrates that elevated levels of E2F-1result in 5-FU resistance through increased IS expression as well as collateral sensitivity to irinotecan.
  • Kasahara M, Takahashi Y, Nagata U et al Thymidylate synthase expression correlates closely with E2F1 expression in colon cancer. Clin. Cancer Res. 6, 2707–2711 (2000).
  • Zhang SY, Shao S-C, Johnson DG, Klein-Szanto AJP E2F-1 gene transfer enhances invasiveness of human head and neck carcinoma cell lines. Cancer Res. 60, 5972–5976 (2000).
  • Mulkins MA, Heidelberger C. Biochemical characterization of fluoropyrimidine-resistant murine leukemic cell lines. Cancer Res. 42, 965–973 (1982).
  • Wang F-S, Aschele C, Sobrero A et al Decreased folylpolyglutamate synthetase expression: a novel mechanism of fluorouracil resistance. Cancer Res. 53, 3677–3680 (1993).
  • Sobrero AF, Moir RD, Bertino JR et al Defective facilitated diffusion of nucleotides, a primary mechanism of resistance to 5-fluoro-2 --deoxyuridine in the HCT-8 human carcinoma. Cancer Res. 45, 3155–3160 (1985).
  • Aschele C, Sobrero A, Faderan M, Bertino JR. Novel mechanism(s) of resistance to 5-fluorouracil in human colon cancer (HCT-8) sublines following exposure to two different clinically relevant dose schedules. Cancer Res. 52, 1855–1864 (1992).
  • •Demonstrates that different 5-FU treatment regimens can result in different patterns of resistance including alterations in activation pathway enzymes, such as UMPK.
  • Pizzorno G, Handschumacher RE. Effect of clinically modeled regimens on the growth response and development of resistance in human colon carcinoma cell lines. Biochem. Phatmacol 49, 599–605 (1995).
  • Etienne MC, Cheradame S, Fischel JL et al. Response to fluorouracil therapy in cancer patients: the role of tumoral dihydropyrimidine dehydrogenase activity.j Clin. Oncol 13, 1663–1670 (1995).
  • Diasio RB, Lu Z. Dihydropyrimidine dehydrogenase activity and fluorouracil chemotherapy. j Clin. Oncol 12, 2239–2242 (1994).
  • Metzger R, Danenberg K, Leichman CG et al High basal level gene expression of thymidine phosphorylase (platelet derived endothelial growth factor) in colorectal tumors is associated with non-response to 5-fluorouracil. Clin. Cancer Res. 4, 2371–2376 (1998).
  • Salonga 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. Gun. Cancer Res. 6, 1322–1327 (2000). Demonstrated that the level of expression of all three genes predicted response and they were independent of each other. Patients with low expression of all three genes had an increased survival.
  • Conti JA, Kemeny NE, Saltz LB et al Irinotecan is an active agent in untreated patients with metastatic colorectal cancer. J. Clin. Oncol 14, 709–715 (1996).
  • Van Cutsem E, Cunningham D, Ten Bokkel Huinink WW et al Clinical activity and benefit of irinotecan (CPT-11) in patients with colorectal cancer truly resistant to 5-fluorouracil (5-FU). Eur Cancer35, 54–59 (1999).
  • •In patients with colorectal cancer and documented progression of disease while on 5-FU, hinotecan achieved a response rate of 13.7%.
  • Saltz L, Danenberg K, Paty P et al High thymidylate synthase (TS) expression does not preclude activity of CPT-11 in colorectal cancer (CRC). Proc. Am. Soc. Clin. Oncol 17, 281 (1998).
  • Li M-X, Banerjee D, Zhao S-C et al development of a retroviral construct containing a human mutated dhfr cDNA for hematopoietic stem cell transduction. Blood33, 3403–3408 (1994).
  • Banerjee D, Zhao S-C, Mineishi S, Bertino JR. Post-transplant methotrexate administration leads to improved curability of mice bearing a mammary tumor transplanted with marrow transduced with a mutant human dihydrofolate reductase cDNA. Hum. Gene Ther. 8, 903–909 (1997).
  • Flasshove M, Banerjee D, Mineishi S, Li M-X, Bertino JR, Moore MAS. Ex vivo expansion and selection of human CD34+ peripheral blood progenitor cells after introduction of a mutated dihydrofolate reductase cDNA via retroviral gene transfer. Blood 85, 566–574 (1995).

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