Molecular alterations in colitis-associated colorectal neoplasia: Study from a low prevalence area using magnifying chromo colonoscopy

Bhadravathi Marigowda Shivakumar, Balasubramanian Lakshman Kumar, Ganesh Bhat, Deepak Suvarna, Lakshmi Rao, C. Ganesh Pai, Kapaettu Satyamoorthy

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Background and aim: Longstanding ulcerative colitis (UC) predisposes to colorectal cancer (CRC). To understand the molecular pathogenesis of colitis-associated colorectal neoplasia (UC-CRN), we studied the frequency of microsatellite instability (MSI) and mutations in . p53, . BRAF and . KRAS genes in the tissues of patients with long standing UC with or without neoplasia and compared them with colitis patients without risk of neoplasia, and those with sporadic colorectal neoplasia (S-CRN) in an area with lower prevalence for either disease. Methods: Biopsies were obtained during magnifying chromo colonoscopy or routine colonoscopy in consecutive UC patients with high risk (UC-HR) and low risk (UC-LR) of neoplasia, and those with S-CRN. MSI (NCI-Bethesda panel) and mutations in . p53, . KRAS and . BRAF genes were analysed. Results: Twenty-eight patients with UC-HR, 30 with UC-LR and 30 with S-CRN were included. Six (21.4%) of UC-HR had neoplasia (Progressors). MSI was not detected in the UC-CRN group as compared to 5 (16.7%) in the S-CRN group. . p53 mutations occurred in 1 (3.3%) of UC-LR, increasing to 6 (27.3%, . P<. 0.05) and 3 (50%, . P<. 0.05) in the UC-HR subgroups without and with neoplasia respectively, as against 10 (33.3%) in sporadic neoplasia group. . KRAS mutations were found only in the presence of neoplasia. None showed the . BRAF mutation. Conclusions: In a population with a lower prevalence for UC and CRC, the molecular pathogenesis of colitis-associated colorectal neoplasia is comparable to that reported from areas with a higher prevalence of these diseases, MSI being an exception.

Original languageEnglish
Pages (from-to)647-654
Number of pages8
JournalJournal of Crohn's and Colitis
Volume6
Issue number6
DOIs
Publication statusPublished - 07-2012

Fingerprint

Colitis
Colonoscopy
Ulcerative Colitis
Neoplasms
Microsatellite Instability
Mutation
Colorectal Neoplasms
Genes

All Science Journal Classification (ASJC) codes

  • Gastroenterology

Cite this

Shivakumar, Bhadravathi Marigowda ; Kumar, Balasubramanian Lakshman ; Bhat, Ganesh ; Suvarna, Deepak ; Rao, Lakshmi ; Pai, C. Ganesh ; Satyamoorthy, Kapaettu. / Molecular alterations in colitis-associated colorectal neoplasia : Study from a low prevalence area using magnifying chromo colonoscopy. In: Journal of Crohn's and Colitis. 2012 ; Vol. 6, No. 6. pp. 647-654.
@article{046ec0796b8f4b86ae9af2951a81cbd5,
title = "Molecular alterations in colitis-associated colorectal neoplasia: Study from a low prevalence area using magnifying chromo colonoscopy",
abstract = "Background and aim: Longstanding ulcerative colitis (UC) predisposes to colorectal cancer (CRC). To understand the molecular pathogenesis of colitis-associated colorectal neoplasia (UC-CRN), we studied the frequency of microsatellite instability (MSI) and mutations in . p53, . BRAF and . KRAS genes in the tissues of patients with long standing UC with or without neoplasia and compared them with colitis patients without risk of neoplasia, and those with sporadic colorectal neoplasia (S-CRN) in an area with lower prevalence for either disease. Methods: Biopsies were obtained during magnifying chromo colonoscopy or routine colonoscopy in consecutive UC patients with high risk (UC-HR) and low risk (UC-LR) of neoplasia, and those with S-CRN. MSI (NCI-Bethesda panel) and mutations in . p53, . KRAS and . BRAF genes were analysed. Results: Twenty-eight patients with UC-HR, 30 with UC-LR and 30 with S-CRN were included. Six (21.4{\%}) of UC-HR had neoplasia (Progressors). MSI was not detected in the UC-CRN group as compared to 5 (16.7{\%}) in the S-CRN group. . p53 mutations occurred in 1 (3.3{\%}) of UC-LR, increasing to 6 (27.3{\%}, . P<. 0.05) and 3 (50{\%}, . P<. 0.05) in the UC-HR subgroups without and with neoplasia respectively, as against 10 (33.3{\%}) in sporadic neoplasia group. . KRAS mutations were found only in the presence of neoplasia. None showed the . BRAF mutation. Conclusions: In a population with a lower prevalence for UC and CRC, the molecular pathogenesis of colitis-associated colorectal neoplasia is comparable to that reported from areas with a higher prevalence of these diseases, MSI being an exception.",
author = "Shivakumar, {Bhadravathi Marigowda} and Kumar, {Balasubramanian Lakshman} and Ganesh Bhat and Deepak Suvarna and Lakshmi Rao and Pai, {C. Ganesh} and Kapaettu Satyamoorthy",
year = "2012",
month = "7",
doi = "10.1016/j.crohns.2011.11.013",
language = "English",
volume = "6",
pages = "647--654",
journal = "Journal of Crohn's and Colitis",
issn = "1873-9946",
publisher = "Elsevier",
number = "6",

}

Molecular alterations in colitis-associated colorectal neoplasia : Study from a low prevalence area using magnifying chromo colonoscopy. / Shivakumar, Bhadravathi Marigowda; Kumar, Balasubramanian Lakshman; Bhat, Ganesh; Suvarna, Deepak; Rao, Lakshmi; Pai, C. Ganesh; Satyamoorthy, Kapaettu.

In: Journal of Crohn's and Colitis, Vol. 6, No. 6, 07.2012, p. 647-654.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Molecular alterations in colitis-associated colorectal neoplasia

T2 - Study from a low prevalence area using magnifying chromo colonoscopy

AU - Shivakumar, Bhadravathi Marigowda

AU - Kumar, Balasubramanian Lakshman

AU - Bhat, Ganesh

AU - Suvarna, Deepak

AU - Rao, Lakshmi

AU - Pai, C. Ganesh

AU - Satyamoorthy, Kapaettu

PY - 2012/7

Y1 - 2012/7

N2 - Background and aim: Longstanding ulcerative colitis (UC) predisposes to colorectal cancer (CRC). To understand the molecular pathogenesis of colitis-associated colorectal neoplasia (UC-CRN), we studied the frequency of microsatellite instability (MSI) and mutations in . p53, . BRAF and . KRAS genes in the tissues of patients with long standing UC with or without neoplasia and compared them with colitis patients without risk of neoplasia, and those with sporadic colorectal neoplasia (S-CRN) in an area with lower prevalence for either disease. Methods: Biopsies were obtained during magnifying chromo colonoscopy or routine colonoscopy in consecutive UC patients with high risk (UC-HR) and low risk (UC-LR) of neoplasia, and those with S-CRN. MSI (NCI-Bethesda panel) and mutations in . p53, . KRAS and . BRAF genes were analysed. Results: Twenty-eight patients with UC-HR, 30 with UC-LR and 30 with S-CRN were included. Six (21.4%) of UC-HR had neoplasia (Progressors). MSI was not detected in the UC-CRN group as compared to 5 (16.7%) in the S-CRN group. . p53 mutations occurred in 1 (3.3%) of UC-LR, increasing to 6 (27.3%, . P<. 0.05) and 3 (50%, . P<. 0.05) in the UC-HR subgroups without and with neoplasia respectively, as against 10 (33.3%) in sporadic neoplasia group. . KRAS mutations were found only in the presence of neoplasia. None showed the . BRAF mutation. Conclusions: In a population with a lower prevalence for UC and CRC, the molecular pathogenesis of colitis-associated colorectal neoplasia is comparable to that reported from areas with a higher prevalence of these diseases, MSI being an exception.

AB - Background and aim: Longstanding ulcerative colitis (UC) predisposes to colorectal cancer (CRC). To understand the molecular pathogenesis of colitis-associated colorectal neoplasia (UC-CRN), we studied the frequency of microsatellite instability (MSI) and mutations in . p53, . BRAF and . KRAS genes in the tissues of patients with long standing UC with or without neoplasia and compared them with colitis patients without risk of neoplasia, and those with sporadic colorectal neoplasia (S-CRN) in an area with lower prevalence for either disease. Methods: Biopsies were obtained during magnifying chromo colonoscopy or routine colonoscopy in consecutive UC patients with high risk (UC-HR) and low risk (UC-LR) of neoplasia, and those with S-CRN. MSI (NCI-Bethesda panel) and mutations in . p53, . KRAS and . BRAF genes were analysed. Results: Twenty-eight patients with UC-HR, 30 with UC-LR and 30 with S-CRN were included. Six (21.4%) of UC-HR had neoplasia (Progressors). MSI was not detected in the UC-CRN group as compared to 5 (16.7%) in the S-CRN group. . p53 mutations occurred in 1 (3.3%) of UC-LR, increasing to 6 (27.3%, . P<. 0.05) and 3 (50%, . P<. 0.05) in the UC-HR subgroups without and with neoplasia respectively, as against 10 (33.3%) in sporadic neoplasia group. . KRAS mutations were found only in the presence of neoplasia. None showed the . BRAF mutation. Conclusions: In a population with a lower prevalence for UC and CRC, the molecular pathogenesis of colitis-associated colorectal neoplasia is comparable to that reported from areas with a higher prevalence of these diseases, MSI being an exception.

UR - http://www.scopus.com/inward/record.url?scp=84862190172&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84862190172&partnerID=8YFLogxK

U2 - 10.1016/j.crohns.2011.11.013

DO - 10.1016/j.crohns.2011.11.013

M3 - Article

C2 - 22398042

AN - SCOPUS:84862190172

VL - 6

SP - 647

EP - 654

JO - Journal of Crohn's and Colitis

JF - Journal of Crohn's and Colitis

SN - 1873-9946

IS - 6

ER -