CpG island methylator phenotype is an independent predictor of survival benefit from 5-fluorouracil in stage III colorectal cancer.

[1]  B. Iacopetta,et al.  Characterisation of colorectal cancers showing hypermethylation at multiple CpG islands , 2002, Gut.

[2]  King-Jen Chang,et al.  High‐frequency microsatellite instability predicts better chemosensitivity to high‐dose 5‐fluorouracil plus leucovorin chemotherapy for stage IV sporadic colorectal cancer after palliative bowel resection , 2002, International journal of cancer.

[3]  R. Ward,et al.  CpG island methylation in sporadic colorectal cancers and its relationship to microsatellite instability. , 2002, Gastroenterology.

[4]  A. Neugut,et al.  Survival Associated with 5-FluorouracilBased Adjuvant Chemotherapy among Elderly Patients with Node-Positive Colon Cancer , 2002, Annals of Internal Medicine.

[5]  T. Wiggers,et al.  Adjuvant 5FU plus levamisole in colonic or rectal cancer: improved survival in stage II and III , 2001, British Journal of Cancer.

[6]  R. Ward,et al.  Sporadic colorectal cancers with microsatellite instability and their possible origin in hyperplastic polyps and serrated adenomas. , 2001, Journal of the National Cancer Institute.

[7]  B. Iacopetta,et al.  Methylation of the hMLH1, p16, and MDR1 genes in colorectal carcinoma: associations with clinicopathological features. , 2001, Cancer letters.

[8]  B. Iacopetta,et al.  P53 alteration and microsatellite instability have predictive value for survival benefit from chemotherapy in stage III colorectal carcinoma. , 2001, Clinical cancer research : an official journal of the American Association for Cancer Research.

[9]  J. Jass Serrated route to colorectal cancer: back street or super highway? , 2001, The Journal of pathology.

[10]  David Joseph,et al.  Association of tumour site and sex with survival benefit from adjuvant chemotherapy in colorectal cancer , 2000, The Lancet.

[11]  S. Groshen,et al.  Colorectal tumors responding to 5-fluorouracil have low gene expression levels of dihydropyrimidine dehydrogenase, thymidylate synthase, and thymidine phosphorylase. , 2000, Clinical cancer research : an official journal of the American Association for Cancer Research.

[12]  B. Iacopetta,et al.  Routine analysis of p53 mutation in clinical breast tumor specimens using fluorescence-based polymerase chain reaction and single strand conformation polymorphism. , 2000, Diagnostic molecular pathology : the American journal of surgical pathology, part B.

[13]  B. Iacopetta,et al.  Routine detection of the replication error phenotype in clinical tumor specimens using fluorescence-SSCP. , 2000, BioTechniques.

[14]  N. Ahuja,et al.  Distinct genetic profiles in colorectal tumors with or without the CpG island methylator phenotype. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[15]  King-Jen Chang,et al.  Hypermethylation of the p16 Gene in Sporadic T3N0M0 Stage Colorectal Cancers: Association with DNA Replication Error and Shorter Survival , 1999, Oncology.

[16]  J. Herman,et al.  CpG island methylator phenotype in colorectal cancer. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[17]  R. Miike,et al.  Aberrant methylation of p16INK4a in anatomic and gender-specific subtypes of sporadic colorectal cancer. , 1999, Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology.

[18]  Peter A. Jones,et al.  Cancer-epigenetics comes of age , 1999, Nature Genetics.

[19]  R. Kronmal,et al.  Assessing the sensitivity of regression results to unmeasured confounders in observational studies. , 1998, Biometrics.

[20]  J. Herman,et al.  Incidence and functional consequences of hMLH1 promoter hypermethylation in colorectal carcinoma. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[21]  S. Groshen,et al.  p53 point mutations and thymidylate synthase messenger RNA levels in disseminated colorectal cancer: an analysis of response and survival. , 1998, Clinical cancer research : an official journal of the American Association for Cancer Research.

[22]  P. Bunn,et al.  Ki-ras mutation and p53 overexpression predict the clinical behavior of colorectal cancer: a Southwest Oncology Group study. , 1998, Cancer research.

[23]  S. Groshen,et al.  Quantitation of intratumoral thymidylate synthase expression predicts for disseminated colorectal cancer response and resistance to protracted-infusion fluorouracil and weekly leucovorin. , 1997, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[24]  J. Herman,et al.  Association between CpG island methylation and microsatellite instability in colorectal cancer. , 1997, Cancer research.

[25]  M. Loda,et al.  Methylation of the hMLH1 promoter correlates with lack of expression of hMLH1 in sporadic colon tumors and mismatch repair-defective human tumor cell lines. , 1997, Cancer research.

[26]  J. Herman,et al.  Methylation-specific PCR: a novel PCR assay for methylation status of CpG islands. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[27]  C. Tangen,et al.  Fluorouracil plus Levamisole as Effective Adjuvant Therapy after Resection of Stage III Colon Carcinoma: A Final Report , 1995, Annals of Internal Medicine.

[28]  J. Mason,et al.  Folate and carcinogenesis: an integrated scheme. , 2000, The Journal of nutrition.

[29]  J. Herman,et al.  Hypermethylation-associated inactivation of p14(ARF) is independent of p16(INK4a) methylation and p53 mutational status. , 2000, Cancer research.

[30]  R. Miike,et al.  Aberrant Methylation of p 16 INK 4 a in Anatomic and Gender-specific Subtypes of Sporadic Colorectal Cancer 1 , 1999 .