Genetic and epigenetic alterations in primary colorectal cancers and related lymph node and liver metastases

Cancer

Volumn 119, Issue 2, 2013, Pages 266-276

  Miranda, Elena ^a   Bianchi, Paolo ^a   Destro, Annarita ^a   Morenghi, Emanuela ^a   Malesci, Alberto ^a   Santoro, Armando ^a   Laghi, Luigi ^a   Roncalli, Massimo ^a,b  

^a HUMANITAS CLINICAL AND RESEARCH CENTER   (Italy)

^b UNIVERSITY OF MILAN   (Italy)

Author keywords

genetic and epigenetic alterations; liver metastases; lymph node metastases; molecular heterogeneity; primary colorectal cancer

Indexed keywords

B RAF KINASE; CYCLIN DEPENDENT KINASE INHIBITOR 2A; K RAS PROTEIN; PROTEIN P53; RAS ASSOCIATION DOMAIN FAMILY PROTEIN 1A; UVOMORULIN;

ARTICLE; BRAF GENE; CANCER STAGING; CODON; COLORECTAL CANCER; CONTROLLED STUDY; DISEASE COURSE; E CAD GENE; EPIGENETICS; GENE FREQUENCY; GENE MUTATION; GENETIC HETEROGENEITY; HUMAN; HUMAN CELL; HUMAN TISSUE; LIVER METASTASIS; LYMPH NODE METASTASIS; MAJOR CLINICAL STUDY; METHYLATION; ONCOGENE; ONCOGENE K RAS; P16INK4A GENE; P53 GENE; PRIORITY JOURNAL; PROTEIN EXPRESSION; RASSF1A GENE;

CADHERINS; COLORECTAL NEOPLASMS; CYCLIN-DEPENDENT KINASE INHIBITOR P16; DNA METHYLATION; DNA MUTATIONAL ANALYSIS; EPIGENESIS, GENETIC; HUMANS; LIVER NEOPLASMS; LYMPHATIC METASTASIS; MUTATION; NEOPLASM STAGING; ONCOGENE PROTEINS V-RAF; PROMOTER REGIONS, GENETIC; PROTO-ONCOGENE PROTEINS; PROTO-ONCOGENE PROTEINS B-RAF; RAS PROTEINS; TUMOR SUPPRESSOR PROTEIN P53; TUMOR SUPPRESSOR PROTEINS;

EID: 84872055165     PISSN: 0008543X     EISSN: 10970142     Source Type: Journal    
DOI: 10.1002/cncr.27722     Document Type: Article

References (22)

1. Gryfe R, Swallow C, Bapat B, Redston M, Gallinger S, Couture J,. Molecular biology of colorectal cancer. Curr Probl Cancer. 1997; 21: 233-300.
2. Heijstek MW, Kranenburg O, Borel Rinkes IH,. Mouse models of colorectal cancer and liver metastases. Dig Surg. 2005; 22: 16-25.
3. Meyerhardt JA, Mayer RJ,. Systemic therapy for colorectal cancer. N Engl J Med. 2005; 352: 476-487.
4. Van Cutsem E, Peeters M, Siena S, et al. Open-label phase III trial of panitumumab plus best supportive care compared with best supportive care alone in patients with chemotherapy-refractory metastatic colorectal cancer. J Clin Oncol. 2007; 25: 1658-1664.
5. Amado RG, Wolf M, Peeters M, et al. Wild-type KRAS is required for panitumumab efficacy in patients with metastatic colorectal cancer. J Clin Oncol. 2008; 26: 1626-1634.
6. Messick CA, Sanchez J, Dejulius KL, Church JM, Kalady MF,. Genetic and molecular diversity of colon cancer hepatic metastases. Surgery. 2009; 146: 227-231.
7. Nguyen DX,. Tracing the origins of metastasis. J Pathol. 2011; 223: 195-204.
8. Fidler IJ, Talmadge JE,. The evolution of biologic diversity in metastases. Transplant Proc. 1984; 16: 370-372.
9. Miranda E, Destro A, Malesci A, et al. Genetic and epigenetic changes in primary metastatic and nonmetastatic colorectal cancer. Br J Cancer. 2006; 95: 1101-1107.
10. Roncalli M, Bianchi P, Bruni B, et al. Methylation framework of cell cycle gene inhibitors in cirrhosis and associated hepatocellular carcinoma. Hepatology. 2002; 36: 427-432.
11. Lievre A, Bachet JB, Le Corre D, et al. KRAS mutation status is predictive of response to cetuximab therapy in colorectal cancer. Cancer Res. 2006; 66: 3992-3995.
12. Baas JM, Krens LL, Guchelaar HJ, Morreau H, Gelderblom H,. Concordance of predictive markers for EGFR inhibitors in primary tumors and metastases in colorectal cancer: a review. Oncologist. 2011; 16: 1239-1249.
13. Di Gioia S, Bianchi P, Destro A, et al. Quantitative evaluation of RASSF1A methylation in the non-lesional, regenerative and neoplastic liver [serial online]. BMC Cancer. 2006; 6: 89.
14. Jie G, Zhixiang S, Lei S, Hesheng L, Xiaojun T,. Relationship between expression and methylation status of p16INK4a and the proliferative activity of different areas' tumour cells in human colorectal cancer. Int J Clin Pract. 2007; 61: 1523-1529.
15. Jung A, Schrauder M, Oswald U, et al. The invasion front of human colorectal adenocarcinomas shows co-localization of nuclear beta-catenin, cyclin D1, and p16INK4A and is a region of low proliferation. Am J Pathol. 2001; 159: 1613-1617.
16. Merlo LM, Pepper JW, Reid BJ, Maley CC,. Cancer as an evolutionary and ecological process. Nat Rev Cancer. 2006; 6: 924-935.
17. Molinari F, Martin V, Saletti P, et al. Differing deregulation of EGFR and downstream proteins in primary colorectal cancer and related metastatic sites may be clinically relevant. Br J Cancer. 2009; 100: 1087-1094.
18. Santini D, Loupakis F, Vincenzi B, et al. High concordance of KRAS status between primary colorectal tumors and related metastatic sites: implications for clinical practice. Oncologist. 2008; 13: 1270-1275.
19. Vermaat JS, Nijman IJ, Koudijs MJ, et al. Primary colorectal cancers and their subsequent hepatic metastases are genetically different: implications for selection of patients for targeted treatment. Clin Cancer Res. 2012; 18: 688-699.
20. Baldus SE, Schaefer KL, Engers R, Hartleb D, Stoecklein NH, Gabbert HE,. Prevalence and heterogeneity of KRAS, BRAF, and PIK3CA mutations in primary colorectal adenocarcinomas and their corresponding metastases. Clin Cancer Res. 2010; 16: 790-799.
21. Losi L, Baisse B, Bouzourene H, Benhattar J,. Evolution of intratumoral genetic heterogeneity during colorectal cancer progression. Carcinogenesis. 2005; 26: 916-922.
22. Maughan TS, Adams RA, Smith CG, et al. Addition of cetuximab to oxaliplatin-based first-line combination chemotherapy for treatment of advanced colorectal cancer: Results of the randomised phase 3 MRC COIN trial. Lancet. 2011; 377: 2103-2114.