Pathways of Colorectal Carcinogenesis and Their Clinical Implications

Revista Colombiana de Cancerología

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Field Value
 
Title Pathways of Colorectal Carcinogenesis and Their Clinical Implications
Vías de carcinogénesis colorrectal y sus implicaciones clínicas
 
Creator Sanabria, María C.
Umaña, Adriana
L. Serrano, Martha
Sánchez, Myriam
Mesa, Jorge
Hernández, Gustavo A.
 
Subject Aberrant crypt foci
colorectal neoplasms
colonic polyps
chromosomal instability
microsatellite instability
Focos de criptas aberrantes
neoplasias colorrectales
pólipos del colon
inestabilidad cromosómica
inestabilidad de microsatélites
 
Description Colorectal cancer (CRC) is ranked fourth among causes of cancer mortality in Colombia and in the world, for both genders; it is therefore regarded as a public health issue. CRC ́s phenotype and genotype are highly heterogeneous, a fact related to the various carcinogenic pathways described, and which is also implicated in the different progression mechanisms and the aggressiveness of the disease. The classic pathways, suppressive and mutable, are characterized by a series of genetic alterations related to phenotype changes in the morphologic progression of the adenoma-carcinoma sequence. The alternate pathways, originated by BRAF and KRAS gene mutations, are linked to the serrated polyp progression to carcinoma. Knowledge of these pathways is very important in achieving a fuller understanding of the disease and for broadening the study of mechanisms for its control; these include: early diagnosis, treatment and follow-up.
El cáncer colorrectal (CCR) es la cuarta causa de mortalidad por cáncer en Colombia y en el mundo, en ambos sexos; por esta razón, es considerado un problema de salud pública. El CCR es altamente heterogéneo en su fenotipo y genotipo, lo que está en relación con las diferentes vías de carcinogénesis descritas que implican diferentes mecanismos de progresión y agresividad de la enfermedad. Las vías clásicas, supresora y mutadora, se caracterizan por una serie de alteraciones genéticas relacionadas con los cambios fenotípicos de la progresión morfológica en la secuencia adenoma-carcinoma. Las vías alternas, originadas por mutaciones en los genes, BRAF y KRAS, se relacionan con la progresión de pólipo aserrado a carcinoma. Conocer estas vías es muy importante para comprender la enfermedad de manera integral y profundizar en el estudio de sus mecanismos de control, que incluyen: diagnóstico temprano, tratamiento y seguimiento.
 
Publisher Instituto Nacional de Cancerología
 
Date 2020-09-01
 
Type info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
 
Format application/pdf
 
Identifier https://www.revistacancercol.org/index.php/cancer/article/view/402
 
Source Revista Colombiana de Cancerología; Vol. 16 No. 3 (2012); 170-181
Revista Colombiana de Cancerología; Vol. 16 Núm. 3 (2012); 170-181
Revista Colombiana de Cancerología; v. 16 n. 3 (2012); 170-181
2346-0199
0123-9015
 
Language spa
 
Relation https://www.revistacancercol.org/index.php/cancer/article/view/402/262
/*ref*/Ferlay J, Shin HR, Bray F, et al. GLOBOCAN 2008, Cancer incidence and mortality worldwide IARC CancerBase No 10 [internet]. 2008 [citado: 16 de agosto de 2012]. Disponible en: http://globocan.iarc.fr
/*ref*/Piñeros M, Pardo C, Gamboa O. Atlas de mortalidad por cáncer en Colombia. Bogotá: Imprenta Nacional; 2010.
/*ref*/Van de Wetering M, Sancho E, Verweij C, et al. The betacatenin/TCF-4 complex imposes a crypt progenitor phenotype on colorectal cancer cells. Cell. 2002;111:241-50. https://doi.org/10.1016/S0092-8674(02)01014-0
/*ref*/Graham TA, Humphries A, Sanders T, et al. Use of methylation patterns to determine expansion of stem cell clones in human colon tissue. Gastroenterology. 2011;140:1241-50. https://doi.org/10.1053/j.gastro.2010.12.036
/*ref*/Fevr T, Robine S, Louvard D, et al. Wnt/betacatenin is essential for intestinal homeostasis and maintenance of intestinal stem cells. Mol Cell Biol. 2007;27:7551-9. https://doi.org/10.1128/MCB.01034-07
/*ref*/Kosinski C, Li VS, Chan AS, et al. Gene expression patterns of human colon tops and basal crypts and BMP antagonists as intestinal stem cell niche factors. Proc Natl Acad Sci U S A. 2007;104;15418-23. https://doi.org/10.1073/pnas.0707210104
/*ref*/Smith KJ, Johnson KA, Bryan TM, et al. The APC gene product in normal and tumor cells. Proc Natl Acad Sci U S A. 1993;90:2846-50. https://doi.org/10.1073/pnas.90.7.2846
/*ref*/Sinicrope FA, Ruan SB, Cleary KR, et al. Bcl-2 and p53 oncoprotein expression during colorectal tumorigenesis. Cancer Res. 1995;55:237-41.
/*ref*/Roncucci L, Pedroni M, Vaccina F, et al. Aberrant crypt foci in colorectal carcinogenesis. Cell and crypt dynamics. Cell proliferation. 2001;33:1-18. https://doi.org/10.1046/j.1365-2184.2000.00159.x
/*ref*/Colina F, Ibarrola C. Protocolo e información sistematizada para los estudios histopatológicos relacionados con el carcinoma Colorrectal. Rev Esp Patol. 2004;37:73-90.
/*ref*/Konishi F, Morson BC. Pathology of colorectal adenomas: a colonoscopic survey. J Clin Pathol. 1982;35:830-41. https://doi.org/10.1136/jcp.35.8.830
/*ref*/Higuchi T, Sugihara K, Jass JR. Demographic and pathological characteristics of serrated polyps of colorectum. Histopathology. 2005;47:32-40. https://doi.org/10.1111/j.1365-2559.2005.02180.x
/*ref*/Snover D, Ahnen D, Burt R. Serrated polyps of the colon and rectum and serrated ('hyperplastic') polyposis. En: Bozman FT, Carneiro F, Hruban RH (Eds). WHO Classification of Tumours. Pathology and Genetics. Tumours of the Digestive System. 4th ed. Berlin: Springer-Verlag; 2010.
/*ref*/Torlakovic EE, Gómez JD, Driman DK, et al. Sessile serrated adenoma (SSA) vs. traditional serrated adenoma (TSA). Am J Surg Pathol. 2008;32:21-9. https://doi.org/10.1097/PAS.0b013e318157f002
/*ref*/Iacopetta B. Mini review-Are there two sides to colorectal cancer? Int J Cancer. 2002;101:403-8. https://doi.org/10.1002/ijc.10635
/*ref*/Li FY, Lai MD. Colorectal cancer, one entity or three. J Zhejiang Univ Sci B. 2009;10:219-29. https://doi.org/10.1631/jzus.B0820273
/*ref*/Azzoni C, Bottarelli L, Campanini N, et al. Distinct molecular patterns based on proximal and distal sporadic colorectal cancer: arguments for different mechanisms in the tumorigenesis. Int J Colorectal Dis. 2007;22:115-26. https://doi.org/10.1007/s00384-006-0093-x
/*ref*/Delattre O, Olschwang S, Law DJ, et al. Multiple genetic alterations in distal and proximal colorectal cancer. Lancet. 1989;2:353-6. https://doi.org/10.1016/S0140-6736(89)90537-0
/*ref*/Fujita K, Yamamoto H, Matsumoto T, et al. Sessile serrated adenoma with early neoplastic progression: a clinicopathologic and molecular study. Am J Surg Pathol. 2011;35:295-304. https://doi.org/10.1097/PAS.0b013e318205df36
/*ref*/Hawkins N, Norrie M, Cheong K, et al. CpG island methylation in sporadic colorectal cancers and its relationship to microsatellite instability. Gastroenterology. 2002;122:1376-87. https://doi.org/10.1053/gast.2002.32997
/*ref*/Liu LU, Holt PR, Krivosheyev V, et al. Human right and left colon differ in epithelial cell apoptosis and in expression of Bak, a pro-apoptotic Bcl-2 homologue. Gut. 1999;45:45-50. https://doi.org/10.1136/gut.45.1.45
/*ref*/Reichmann A, Levin B, Martin P. Human large-bowel cancer: correlation of clinical and histopathological features with banded chromosomes. Int J Cancer. 1982;29:625-9. https://doi.org/10.1002/ijc.2910290605
/*ref*/Søreide K, Nedrebø BS, Knapp JC, et al. Evolving molecular classification by genomic and proteomic biomarkers in colorectal cancer: potential implications for the surgical oncologist. Surgical Oncology. 2009;18:31-50. https://doi.org/10.1016/j.suronc.2008.06.006
/*ref*/Van Puijenbroek M. Molecular pathology of colorectal cancer predisposing síndromes. Leiden, Holanda: Leiden University; 2008.
/*ref*/Gunter MJ, Leitzmann MF. Obesity and colorectal cancer: epidemiology, mechanisms and candidate genes. J Nutr Biochem. 2006;17:145-56. https://doi.org/10.1016/j.jnutbio.2005.06.011
/*ref*/Hauret KG, Bostick RM, Matthews CE, et al. Physical activity and reduced risk of incident sporadic colorectal adenomas: observational support for mechanisms involving energy balance and inflammation modulation. Am J Epidemiol. 2004;159:983-92. https://doi.org/10.1093/aje/kwh130
/*ref*/Curtin K, Wolff RK, Herrick JS, et al. Exploring multilocus associations of inflammation genes and colorectal cancer risk using hapConstructor. BMC Med Genet. 2010 ;11:170. https://doi.org/10.1186/1471-2350-11-170
/*ref*/Houlston RS, Cheadle J, Dobbins SE, et al. Meta-analysis of three genome-wide association studies identifies susceptibility loci for colorectal cancer at 1q41, 3q26.2, 12q13.13 and 20q13.33. Nat Genet. 2010;42:973-7. https://doi.org/10.1038/ng.670
/*ref*/Houlston RS, Tomlinson IPM. Polymorphisms and colorectal tumor risk. Gastroenterology. 2001;121:282-301. https://doi.org/10.1053/gast.2001.26265
/*ref*/Kury S, Buecher B, Robiou-du-Pont S, et al. Low-penetrance alleles predisposing to sporadic colorectal cancers: a French case-controlled genetic association study. BMC Cancer. 2008;8:326. https://doi.org/10.1186/1471-2407-8-326
/*ref*/Pomerantz MM, Ahmadiyeh N, Jia L, et al. The 8q24 cancer risk variant rs6983267 shows long-range interaction with MYC in colorectal cancer. Nat Genet. 2009;41:882-4. https://doi.org/10.1038/ng.403
/*ref*/von Holst S, Picelli S, Edler D, et al. Association studies on 11 published colorectal cancer risk loci. Br J Cancer. 2010;103:575-80. https://doi.org/10.1038/sj.bjc.6605774
/*ref*/Webb EL, Rudd MF, Sellick GS, et al. Search for low penetrance alleles for colorectal cancer through a scan
/*ref*/of 1467 non-synonymous SNPs in 2575 cases and 2707 controls with validation by kin-cohort analysis of 14 704 first-degree relatives. Hum Mol Genet. 2006;15:3263-71. https://doi.org/10.1093/hmg/ddl401
/*ref*/Galiano MT. Cáncer colorrectal (CCR). Rev Colomb Gastroenterol. 2005;20:43-53.
/*ref*/Eide TJ. Prevalence and morphological features of adenomas of the large intestine in individuals with and without colorectal carcinoma. Histopathology. 1986;10:111-8. https://doi.org/10.1111/j.1365-2559.1986.tb02467.x
/*ref*/Vogelstein B, Fearon ER, Hamilton SR, et al. Genetic alterations during colorectal-tumor development. N Eng J Med. 1988;319:525-32. https://doi.org/10.1056/NEJM198809013190901
/*ref*/Liu B, Nicolaides NC, Markowitz S, et al. Mismatch repair gene defects in sporadic colorectal cancers with microsatellite instability. Nat Genet. 1995;9:48-55. https://doi.org/10.1038/ng0195-48
/*ref*/Moran A, Ortega P, de Juan C, et al. Differential colorectal carcinogenesis: Molecular basis and clinical relevance. World J Gastrointest Oncol. 2010;2:151-8. https://doi.org/10.4251/wjgo.v2.i3.151
/*ref*/Kim IJ, Kang HC, Jang SG, et al. Oligonucleotide microarray analysis of distinct gene expression patterns in colorectal cancer tissues harboring BRAF and K-ras mutations. Carcinogenesis. 2006;27:392-404. https://doi.org/10.1093/carcin/bgi237
/*ref*/Scholer-Dahirel A, Schlabach MR, Loo A, et al. Maintenance of adenomatous polyposis coli (APC)- mutant colorectal cancer is dependent on Wnt/ betacatenin signaling. Proc Natl Acad Sci U S A. 2011;108:17135-40. https://doi.org/10.1073/pnas.1104182108
/*ref*/Yuan P, Sun MH, Zhang JS, et al. APC and K-ras gene mutation in aberrant crypt foci of human colon. World J Gastroenterol. 2001;7:352-6. https://doi.org/10.3748/wjg.v7.i3.352
/*ref*/Haigis KM, Kendall KR, Wang Y, et al. Differential effects of oncogenic K-Ras and N-Ras on proliferation, differentiation and tumor progression in the colon. Nat Genet. 2008;40:600-8. https://doi.org/10.1038/ng.115
/*ref*/Fearon ER, Cho KR, Nigro JM, et al. Identification of a chromosome 18q gene that is altered in colorectal cancers. Science. 1990;247:49-56. https://doi.org/10.1126/science.2294591
/*ref*/Gallione C, Aylsworth AS, Beis J, et al. Overlapping spectra of SMAD4 mutations in juvenile polyposis (JP) and JP-HHT syndrome. Am J Med Genet A. 2010;152A:333-9. https://doi.org/10.1002/ajmg.a.33206
/*ref*/Herbst A, Bommer GT, Kriegl L, et al. ITF-2 is disrupted via allelic loss of chromosome 18q21, and ITF-2B expression is lost at the adenoma-carcinoma transition. Gastroenterology. 2009;137:639-48. https://doi.org/10.1053/j.gastro.2009.04.049
/*ref*/Hibi K, Mizukami H, Shirahata A, et al. Aberrant methylation of the netrin-1 receptor genes UNC5C and DCC detected in advanced colorectal cancer. World J Surg. 2009;33:1053-7. https://doi.org/10.1007/s00268-008-9909-x
/*ref*/Langeveld D, Van Hattem WA, de Leng WW, et al. SMAD4 immunohistochemistry reflects genetic status in juvenile polyposis syndrome. Clin Cancer Res. 2010;16:4126-34. https://doi.org/10.1158/1078-0432.CCR-10-0168
/*ref*/Kamada R, Nomura T, Anderson CW, et al. Cancerassociated p53 tetramerization domain mutants: quantitative analysis reveals a low threshold for tumor suppressor inactivation. J Biol Chem. 2011;286:252-8. https://doi.org/10.1074/jbc.M110.174698
/*ref*/Kouidou S, Malousi A, Maglaveras N. Li-Fraumeni and Li- Fraumeni-like syndrome mutations in p53 are associated with exonic methylation and splicing regulatory elements. Mol Carcinog. 2009;48:895-902. https://doi.org/10.1002/mc.20537
/*ref*/Cooke T, Kirkham N, Stainthorp DH, et al. Detection of early neoplastic changes in experimentally induced colorectal cancer using scanning electron microscopy and cell kinetic studies. Gut. 1984;25:748-55. https://doi.org/10.1136/gut.25.7.748
/*ref*/Hu Y, Le Leu RK, Young GP. Detection of K-ras mutations in azoxymethane-induced aberrant crypt foci in mice using LNA-mediated real-time PCR clamping and mutantspecific probes. Mutat Res. 2009;677:27-32. https://doi.org/10.1016/j.mrgentox.2009.05.003
/*ref*/Ochiai M, Ushigome M, Fujiwara K, et al. Characterization of dysplastic aberrant crypt foci in the rat colon induced by 2-amino-1-methyl-6- phenylimidazo[4,5-b] pyridine. Am J Pathol. 2003;163:1607-14. https://doi.org/10.1016/S0002-9440(10)63517-1
/*ref*/Kim IJ, Kang HC, Park JH, et al. Development and applications of a beta-catenin oligonucleotide microarray: beta- catenin mutations are dominantly found in the proximal colon cancers with microsatellite instability. Clin Cancer Res. 2003;9:2920-5.
/*ref*/Souza RF, Wang S, Thakar M, et al. Expression of the wildtype insulin-like growth factor II receptor gene suppresses growth and causes death in colorectal carcinoma cells. Oncogene. 1999;18:4063-8. https://doi.org/10.1038/sj.onc.1202768
/*ref*/Yashiro M, Hirakawa K, Boland CR. Mutations in TGFbeta-RII and BAX mediate tumor progression in the later stages of colorectal cancer with microsatellite instability. BMC Cancer. 2010;10:303. https://doi.org/10.1186/1471-2407-10-303
/*ref*/Narayan S, Roy D. Role of APC and DNA mismatch repair genes in the development of colorectal cancers. Mol Cancer. 2003;2:41. https://doi.org/10.1186/1476-4598-2-41
/*ref*/Samowitz WS, Holden JA, Curtin K, et al. Inverse relationship between microsatellite instability and K-ras and p53 gene alterations in colon cancer. Am J Pathol. 2001;158:1517-24. https://doi.org/10.1016/S0002-9440(10)64102-8
/*ref*/Olschwang S, Hamelin R, Laurent-Puig P, et al. Alternative genetic pathways in colorectal carcinogenesis. Proceedings of the National Academy of Sciences of the United States of America. 1997;94:12122. https://doi.org/10.1073/pnas.94.22.12122
/*ref*/Kim KM, Lee EJ, Kim YH, et al. KRAS mutations in traditional serrated adenomas from Korea herald an aggressive phenotype. Am J Surg Pathol. 2010;34:667-75. https://doi.org/10.1097/PAS.0b013e3181d40cb2
/*ref*/Azimuddin K, Stasik JJ, Khubchandani IT, et al. Hy- perplastic polyps: "more than meets the eye"? Report of sixteen cases. Dis Colon Rectum. 2000;43:1309-13. https://doi.org/10.1007/BF02237443
/*ref*/Longacre TA, Fenoglio-Preiser CM. Mixed hyperplastic adenomatous polyps/serrated adenomas. A distinct form of colorectal neoplasia. Am J Surg Pathol. 1990;14:524-37. https://doi.org/10.1097/00000478-199006000-00003
/*ref*/Hawkins NJ, Ward RL. Sporadic colorectal cancers with microsatellite instability and their possible origin in hyperplastic polyps and serrated adenomas. J Natl Cancer Inst. 2001;93:1307-13. https://doi.org/10.1093/jnci/93.17.1307
/*ref*/Jeevaratnam P, Cottier DS, Browett PJ, et al. Familial giant hyperplastic polyposis predisposing to colorectal cancer: a new hereditary bowel cancer syndrome. J Pathol. 1996;179:20-5. https://doi.org/10.1002/(SICI)1096-9896(199605)179:1<20::AID-PATH538>3.0.CO;2-C
/*ref*/O'Brien MJ, Yang S, Mack C, et al. Comparison of microsatellite instability, CpG island methylation phenotype, BRAF and KRAS status in serrated polyps and traditional adenomas indicates separate pathways to distinct colorectal carcinoma end points. Am J Surg Pathol. 2006;30:1491-501. https://doi.org/10.1097/01.pas.0000213313.36306.85
/*ref*/Kalady MF, Jarrar A, Leach B, et al. Defining phenotypes and cancer risk in hyperplastic polyposis syndrome. Dis Colon Rectum. 2011;54:164-70. https://doi.org/10.1007/DCR.0b013e3181fd4c15
/*ref*/Lu FI, Van Niekerk de W, Owen D, et al. Longitudinal outcome study of sessile serrated adenomas of the colorectum: an increased risk for subsequent right-sided colorectal carcinoma. Am J Surg Pathol. 2010;34:927-34. https://doi.org/10.1097/PAS.0b013e3181e4f256
/*ref*/Musulén E, López-Martos R, Sanz C, et al. Clinicopathological and morphological characteristics of colorectal carcinoma in hyperplastic polyposis syndrome. Rev Esp Patol. 2011;44:75-82. https://doi.org/10.1016/j.patol.2011.02.014
/*ref*/Sarli L, Bottarelli L, Bader G, et al. Association between recurrence of sporadic colorectal cancer, high level of microsatellite instability, and loss of heterozygosity at chromosome 18q. Dis Colon Rectum. 2004;47:1467-82. https://doi.org/10.1007/s10350-004-0628-6
/*ref*/Gryfe R, Kim H, Hsieh ET, et al. Tumor microsatellite instability and clinical outcome in young patients with colorectal cancer. N Engl J Med. 2000;342:69-77. https://doi.org/10.1056/NEJM200001133420201
/*ref*/Samowitz WS, Curtin K, Ma KN, et al. Microsatellite instability in sporadic colon cancer is associated with an improved prognosis at the population level. Cancer Epidemiol Biomarkers Prev. 2001;10:917-23.
/*ref*/Liu XQ, Rajput A, Geng L, et al. Restoration of transforming growth factor-beta receptor II expression in colon cancer cells with microsatellite instability increases metastatic potential in vivo. J Biol Chem. 2011;286:16082-90. https://doi.org/10.1074/jbc.M111.221697
/*ref*/Shima K, Morikawa T, Yamauchi M, et al. TGFBR2 and BAX mononucleotide tract mutations, microsatellite instability, and prognosis in 1072 colorectal cancers. PLoS One. 2011;6:e25062. https://doi.org/10.1371/journal.pone.0025062
/*ref*/Elsaleh H, Iacopetta B. Microsatellite instability is a predictive marker for survival benefit from adjuvant chemotherapy in a population-based series of stage III colorectal carcinoma. Clin Colorectal Cancer. 2001;1:104-9. https://doi.org/10.3816/CCC.2001.n.010
/*ref*/Popat S, Hubner R, Houlston RS. Systematic review of microsatellite instability and colorectal cancer prognosis. J Clin Oncol. 2005;23:609-18. https://doi.org/10.1200/JCO.2005.01.086
/*ref*/Benatti P, Gafa R, Barana D, et al. Microsatellite instability and colorectal cancer prognosis. Clin Cancer Res. 2005;11:8332-40. https://doi.org/10.1158/1078-0432.CCR-05-1030
/*ref*/Ribic CM, Sargent DJ, Moore MJ, et al. Tumor microsatellite-instability status as a predictor of benefit from fluorouracil-based adjuvant chemotherapy for colon cancer. N Engl J Med. 2003;349:247-57. https://doi.org/10.1056/NEJMoa022289
/*ref*/Shaukat A, Arain M, Thaygarajan B, et al. Is BRAF mutation associated with interval colorectal cancers? Dig Dis Sci. 2010;55:2352-6. https://doi.org/10.1007/s10620-010-1182-9
/*ref*/Aust DE, Baretton GB. Serrated polyps of the colon and rectum (hyperplastic polyps, sessile serrated adenomas, traditional serrated adenomas, and mixed polyps)-proposal for diagnostic criteria. Virchows Arch. 2010;457:291-7. https://doi.org/10.1007/s00428-010-0945-1
/*ref*/Huang CS, Farraye FA, Yang S, et al. The clinical significance of serrated polyps. Am J Gastroenterol. 2010;106:229-40; quiz 41. https://doi.org/10.1038/ajg.2010.429
/*ref*/Lazarus R, Junttila OE, Karttunen TJ, et al. The risk of metachronous neoplasia in patients with serrated adenoma. Am J Clin Pathol. 2005;123:349-59. https://doi.org/10.1309/VBAGV3BR96N2EQTR
/*ref*/Young J, Jenkins M, Parry S, et al. Serrated pathway colorectal cancer in the population: genetic consideration. Gut. 2007;56:1453-9. https://doi.org/10.1136/gut.2007.126870
/*ref*/Lascorz J, Forsti A, Chen B, et al. Genome-wide association study for colorectal cancer identifies risk polymorphisms in German familial cases and implicates MAPK signalling pathways in disease susceptibility. Carcinogenesis. 2010;31:1612-9. https://doi.org/10.1093/carcin/bgq146
/*ref*/Pittman AM, Naranjo S, Jalava SE, et al. Allelic variation at the 8q23.3 colorectal cancer risk locus functions as a cis-acting regulator of EIF3H. PLoS Genet. 2010;6 pii: e10 01126. https://doi.org/10.1371/journal.pgen.1001126
/*ref*/Tenesa A, Farrington SM, Prendergast JG, et al. Genomewide association scan identifies a colorectal cancer susceptibility locus on 11q23 and replicates risk loci at 8q24 and 18q21. Nat Genet. 2008;40:631-7. https://doi.org/10.1038/ng.133
/*ref*/Tomlinson I, Webb E, Carvajal-Carmona L, et al. A genome-wide association scan of tag SNPs identifies a susceptibility variant for colorectal cancer at 8q24.21. Nat Genet. 2007;39:984-8. https://doi.org/10.1038/ng2085
/*ref*/Tomlinson IP, Webb E, Carvajal-Carmona L, et al. A genome-wide association study identifies colorectal cancer susceptibility loci on chromosomes 10p14 and 8q23.3. Nat Genet. 2008;40:623-30. https://doi.org/10.1038/ng.111
/*ref*/Tuupanen S, Turunen M, Lehtonen R, et al. The common colorectal cancer predisposition SNP rs6983267 at chromosome 8q24 confers potential to enhanced Wnt signaling. Nat Genet. 2009;41:885-90. https://doi.org/10.1038/ng.406
/*ref*/Zanke BW, Greenwood CM, Rangrej J, et al. Genomewide association scan identifies a colorectal cancer susceptibility locus on chromosome 8q24. Nat Genet. 2007;39:989-94. https://doi.org/10.1038/ng2089
/*ref*/Bertucci F, Salas S, Eysteries S, et al. Gene expression profiling of colon cancer by DNA microarrays and correlation with histoclinical parameters. Oncogene. 2004;23:1377-91. https://doi.org/10.1038/sj.onc.1207262
/*ref*/Carrer A, Zacchigna S, Balani A, et al. Expression profiling of angiogenic genes for the characterisation of colorectal carcinoma. Eur J Cancer. 2008;44:1761-9. https://doi.org/10.1016/j.ejca.2008.05.014
/*ref*/Galamb O, Sipos F, Solymosi N, et al. Diagnostic mRNA expression patterns of inflamed, benign, and malignant colorectal biopsy specimen and their correlation with peripheral blood results. Cancer Epidemiol Biomarkers Prev. 2008;17:2835-45. https://doi.org/10.1158/1055-9965.EPI-08-0231
/*ref*/Glebov OK, Rodríguez LM, Soballe P, et al. Gene expression patterns distinguish colonoscopically isolated human aberrant crypt foci from normal colonic mucosa. Cancer Epidemiology Biomarkers & Prevention. 2006;15:2253-62. https://doi.org/10.1158/1055-9965.EPI-05-0694
/*ref*/Han M, Liew CT, Zhang HW, et al. Novel blood-based, five-gene biomarker set for the detection of colorectal cancer. Clin Cancer Res. 2008;14:455-60. https://doi.org/10.1158/1078-0432.CCR-07-1801
/*ref*/Mazzanti R, Solazzo M, Fantappie O, et al. Differential expression proteomics of human colon cancer. Am J Physiol Gastrointest Liver Physiol. 2006;290:G1329-38. https://doi.org/10.1152/ajpgi.00563.2005
/*ref*/Ibrahim AE, Arends MJ, Silva AL, et al. Sequential DNA methylation changes are associated with DNMT3B overexpression in colorectal neoplastic progression. Gut. 2011;60:499-508. https://doi.org/10.1136/gut.2010.223602
/*ref*/Vaughn CP, Wilson AR, Samowitz WS. Quantitative evaluation of CpG island methylation in hyperplastic polyps. Mod Pathol. 2010;23:151-6. https://doi.org/10.1038/modpathol.2009.150
 

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