Accomplishments in 2008 in biologic markers for gastrointestinal cancers-focus on colorectal cancer.

OverviewPredictive/Prognostic FactorsKRAS StatusLigands of EGFRPhosphoinositide 3-kinases (PI3Ks)Phosphatase and Tensin Homolog (PTEN)Microsatellite Instability (MSI)Inflammatory Bowel Disease (IBD) and Colon CancerFlat and Polypoid DysplasiaOther Non-Morphology-Based Predictive Markers of Cancer in IBDPotential Applications in Clinical PracticeTargeting TherapyFuture Directions.

[1]  R. Pearson,et al.  Cetuximab and Chemotherapy as Initial Treatment for Metastatic Colorectal Cancer , 2010 .

[2]  J. Vandesompele,et al.  Amphiregulin and epiregulin mRNA expression in primary tumors predicts outcome in metastatic colorectal cancer treated with cetuximab. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[3]  D. Lambrechts,et al.  The role of KRAS, BRAF, NRAS, and PIK3CA mutations as markers of resistance to cetuximab in chemorefractory metastatic colorectal cancer. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[4]  Francesca Molinari,et al.  PIK3CA mutations in colorectal cancer are associated with clinical resistance to EGFR-targeted monoclonal antibodies. , 2009, Cancer research.

[5]  C. Bokemeyer,et al.  Fluorouracil, leucovorin, and oxaliplatin with and without cetuximab in the first-line treatment of metastatic colorectal cancer. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[6]  Wanlong Ma,et al.  K-ras mutations and cetuximab in colorectal cancer. , 2009, The New England journal of medicine.

[7]  Giampietro Gasparini,et al.  K-ras mutations and cetuximab in colorectal cancer. , 2009, The New England journal of medicine.

[8]  L. Mazzucchelli,et al.  Wild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer. , 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[9]  Dongsheng Tu,et al.  K-ras mutations and benefit from cetuximab in advanced colorectal cancer. , 2008, The New England journal of medicine.

[10]  E. Van Cutsem,et al.  Clinical Usefulness of EGFR Gene Copy Number as a Predictive Marker in Colorectal Cancer Patients Treated with Cetuximab: A Fluorescent In situ Hybridization Study , 2008, Clinical Cancer Research.

[11]  A. Bardelli,et al.  Role of KRAS mutation in predicting response, progression-free survival, and overall survival in irinotecan-refractory patients treated with cetuximab plus irinotecan for a metastatic colorectal cancer: Analysis of 281 individual data from published series , 2008 .

[12]  R. Labianca,et al.  Confirmation of deficient mismatch repair (dMMR) as a predictive marker for lack of benefit from 5-FU based chemotherapy in stage II and III colon cancer (CC): A pooled molecular reanalysis of randomized chemotherapy trials , 2008 .

[13]  Daniel J. Freeman,et al.  Wild-type KRAS is required for panitumumab efficacy in patients with metastatic colorectal cancer. , 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[14]  E. Van Cutsem,et al.  KRAS wild-type state predicts survival and is associated to early radiological response in metastatic colorectal cancer treated with cetuximab. , 2008, Annals of oncology : official journal of the European Society for Medical Oncology.

[15]  A. Lièvre,et al.  KRAS mutations as an independent prognostic factor in patients with advanced colorectal cancer treated with cetuximab. , 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[16]  N. Harpaz,et al.  Histologic inflammation is a risk factor for progression to colorectal neoplasia in ulcerative colitis: a cohort study. , 2007, Gastroenterology.

[17]  P. Jänne,et al.  EGFR, HER2 and Kras as predictive factors for cetuximab sensitivity in colorectal cancer , 2007 .

[18]  Manuel Hidalgo,et al.  Expression of epiregulin and amphiregulin and K-ras mutation status predict disease control in metastatic colorectal cancer patients treated with cetuximab. , 2007, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[19]  T. Frebourg,et al.  Clinical relevance of KRAS mutation detection in metastatic colorectal cancer treated by Cetuximab plus chemotherapy , 2007, British Journal of Cancer.

[20]  Silvia Benvenuti,et al.  Oncogenic activation of the RAS/RAF signaling pathway impairs the response of metastatic colorectal cancers to anti-epidermal growth factor receptor antibody therapies. , 2007, Cancer research.

[21]  T. Thomas,et al.  Meta‐analysis: cancer risk of low‐grade dysplasia in chronic ulcerative colitis , 2007, Alimentary pharmacology & therapeutics.

[22]  S. Itzkowitz.  Molecular biology of dysplasia and cancer in inflammatory bowel disease. , 2006, Gastroenterology clinics of North America.

[23]  R. Odze.  Pathology of dysplasia and cancer in inflammatory bowel disease. , 2006, Gastroenterology clinics of North America.

[24]  A. Lièvre,et al.  KRAS mutation status is predictive of response to cetuximab therapy in colorectal cancer. , 2006, Cancer research.

[25]  L. Melton,et al.  Risk of intestinal cancer in inflammatory bowel disease: a population-based study from olmsted county, Minnesota. , 2006, Gastroenterology.

[26]  A. Forbes,et al.  Thirty-year analysis of a colonoscopic surveillance program for neoplasia in ulcerative colitis. , 2006, Gastroenterology.

[27]  J. Terdiman,et al.  Effect of 5-Aminosalicylate Use on Colorectal Cancer and Dysplasia Risk: A Systematic Review and Metaanalysis of Observational Studies , 2005, The American Journal of Gastroenterology.

[28]  Silvia Benvenuti,et al.  Gene copy number for epidermal growth factor receptor (EGFR) and clinical response to antiEGFR treatment in colorectal cancer: a cohort study. , 2005, The Lancet. Oncology.

[29]  A. Forbes,et al.  Most dysplasia in ulcerative colitis is visible at colonoscopy. , 2004, Gastrointestinal endoscopy.

[30]  R. Odze,et al.  Long-term follow-up after polypectomy treatment for adenoma-like dysplastic lesions in ulcerative colitis. , 2004, Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association.

[31]  Noam Harpaz,et al.  Diagnosis and management of dysplasia in patients with inflammatory bowel diseases. , 2004, Gastroenterology.

[32]  Alastair Forbes,et al.  Severity of inflammation is a risk factor for colorectal neoplasia in ulcerative colitis. , 2004, Gastroenterology.

[33]  D. Forman,et al.  Ten year follow up of ulcerative colitis patients with and without low grade dysplasia , 2003, Gut.

[34]  T. Ullman.  Dysplasia and Colorectal Cancer in Crohn's Disease , 2003, Journal of clinical gastroenterology.

[35]  K. Abrams,et al.  The risk of colorectal cancer in ulcerative colitis: a meta-analysis , 2001, Gut.

[36]  S. Mackell,et al.  Immunohistochemical assessment of Ki67 and p53 expression assists the diagnosis and grading of ulcerative colitis‐related dysplasia , 2000, Histopathology.

[37]  N. Harpaz,et al.  Colonoscopic polypectomy in chronic colitis: conservative management after endoscopic resection of dysplastic polyps. , 1999, Gastroenterology.

[38]  M. Kulaylat,et al.  Carcinoma arising in anorectal fistulas of crohn's disease , 1999, Diseases of the colon and rectum.

[39]  F. Waldman,et al.  Genomic instability is an early event during the progression pathway of ulcerative-colitis-related neoplasia. , 1999, The American journal of pathology.

[40]  R. Odze.  Adenomas and adenoma-like DALMs in chronic ulcerative colitis: a clinical, pathological, and molecular review , 1999, American Journal of Gastroenterology.

[41]  C. Williams,et al.  Factors affecting the outcome of endoscopic surveillance for cancer in ulcerative colitis. , 1994, Gastroenterology.

[42]  C. Rubio,et al.  DNA aneuploidy and histologic dysplasia in long-standing ulcerative colitis , 1994, Diseases of the colon and rectum.

[43]  D. Shibata,et al.  Genomic instability in repeated sequences is an early somatic event in colorectal tumorigenesis that persists after transformation , 1994, Nature Genetics.

[44]  M. Kamm,et al.  Lower gastrointestinal malignancy in Crohn's disease. , 1994, Gut.

[45]  C. Bernstein,et al.  Are we telling patients the truth about surveillance colonoscopy in ulcerative colitis? , 1994, The Lancet.

[46]  M. Kimmey,et al.  DNA aneuploidy in colonic biopsies predicts future development of dysplasia in ulcerative colitis. , 1992, Gastroenterology.

[47]  P. Rabinovitch,et al.  Neoplastic progression in ulcerative colitis: histology, DNA content, and loss of a p53 allele. , 1992, Gastroenterology.

[48]  J. Jass,et al.  Dysplasia and deoxyribonucleic acid aneuploidy in the assessment of precancerous changes in chronic ulcerative colitis. Observer variation and correlations. , 1988, Gastroenterology.

[49]  H. Roels,et al.  The DNA content in cancer and dysplasia in chronic ulcerative colitis , 1987, Histopathology.

[50]  R. Löfberg,et al.  Flow cytometric DNA analysis in longstanding ulcerative colitis: a method of prediction of dysplasia and carcinoma development? , 1987, Gut.

[51]  P. Quirke,et al.  DNA aneuploidy in ulcerative colitis. , 1986, Gut.

[52]  P. Slezak,et al.  Early detection of malignancy in ulcerative colitis a flow‐cytometric dna study , 1984, Cancer.

[53]  D. Ransohoff,et al.  Dysplasia in inflammatory bowel disease: standardized classification with provisional clinical applications. , 1983, Human pathology.