Status of microsatellite instability in different histomorphological patterns of colorectal carcinoma among a group of Bangladeshi people
Keywords:Colorectal carcinoma, Histomorphology, Microsatellite instability
Background: This cross- sectional observational study was carried out with an aim to look for microsatellite instability (MSI) status in colorectal carcinoma and their association with different histomorphological patterns and biological behavior of colorectal carcinoma.
Methods: This cross-sectional observational study was done in the Department of Pathology, Bangabandhu Sheikh Mujib Medical University Hospital (BSMMU), Dhaka, Bangladesh during September 2014 to October 2015. A total of 39 surgically resected sample of colorectal carcinoma were included. Consent from each patient was taken. The samples were histopathologically evaluated according to the standard protocol. The statistical analyses were done using Statistical packages for social sciences (SPSS 15) for Windows.
Results: A total of 39 cases of colorectal carcinoma were included in this study. Majority of the patients (55.5%) was in 6th decade in MSI and 29.1% were MSI absent group. The mean age was found 47.67±10.97 years in present group and 47.84±14.26 years in absent group. The difference was not statistically significant (p>0.05). TNM stage with MSI was observed. The mean CEA level was 100.74±103.66 and 60.43±91.72. The mean Hb was 9.72±1.99 % and 9.92±2.17, the range was 7.2-12.2 and 4.6-13.4 among the groups. The mean difference was not statistically significant (p>0.05). Ulcerated was 3 (33.3%) and 19 (64.5%). Stage 3 tumor was 4 (44.4%) and 16 (51.6%). Grade 2 tumor was 5 (55.6%) and 17 (58.0%).
Conclusions: For the first time in Bangladesh, this study was undertaken to evaluate the microsatellite instability (MSI) status in colorectal cancer tissue and their association with different histomorphological patterns of colorectal carcinoma.
Afroza A, Hasan S, Rukunuzzaman M, Hussain SA, and Amin R. Carcinoma Rectum in an 11 Years old Boy. Mymensingh Medical college Journal. 2007;16:70-2.
Aljebreen AM. Clinico-Pathological Patterns of Colorectal Cancer in Saudi Arabia: Younger with an Advanced Stage Presentation. The Saudi Journal of Gastroenterology. 2007;33:84-7.
American Cancer Society, Cancer Facts & Figures 2011, Atlanta, GA. American Cancer Society. 2010. Available at: https://www.cancer.org/research/cancer-facts-statistics/all-cancer-facts-figures/cancer-facts-figures-2011.html.
Baker S, Preisinger A, Jessup J, Paraskeva C, Markowitz S, Willson J, Hamilton S. and Vogelstein B. 'p53 gene mutations occur in combination with 17p allelic deletions as late events in colorectal tumorigenesis. Cancer Res. 1990;50:7717-22.
Baker SJ, Fearon ER, Nigro JM, Hamilton SR, Preisinger AC, Jessup JM et al. Chromosome 17 deletions and p53 gene mutations in colorectal carcinomas. Science. 1989;244:217-21.
Baker SJ, Markowitz S, Fearon ER, Willson JK, Vogelstein B. Suppression of human colorectal carcinoma cell growth by wild-type p53. Science. 1990;249:912-5.
Barault L, Charon-Barra C, Jooste V, de la Vega M, Martin L, Roignot P et al. Hypermethylator phenotype in sporadic colon cancer: study on a population-based series of 582 cases. Cancer Res. 2008;68:8541-6.
Barber T, McManus K, Yuen K, Reis M, Parmigiani G, Shen D et al. Chromatid cohesion defects may underlie chromosome instability in human colorectal cancers. Proc Natl Acad Sci U S A. 2008;105:3443-8.
Bussey H. Familial polyposis coli: family studies, histopathology, differential diagnosis and results of treatment. Baltimore: Johns Hopkins University Press. 1975.
Dhall D, Mertens R, Bresee C, Parakh R, Wang HL, Li M et al. Ki-67 proliferative index predicts progression-free survival of patients with well-differentiated ileal neuroendocrine tumors. Human Pathology. 2012;489-95.
Ekem TE, Bahadir B, Gun BD, Bektas S, Kertis G, Yurdakan G et al. Colorectal carcinomas: Clinicopathologic investigation, correlation with expression of estrogen and progesterone receptors. Turkish Journal of Cancer. 2008;38:118-22.
Gurzu S, Jung J, Mezei T, Pavai Z. The correlation between the immunostains for p53 and Ki67 with bcl-2 expression and classical prognostic factors in colorectal carcinomas. Romanian Journal of Morphology and Embryology. 2007;48:95-9.
Jensen T, Cottrell S, Bicknell D, Kaklamanis L, Bodmer WF. Molecular analysis of KRAS mutations in familial adenomatous polyposis and sporadic colon carcinomas. Lancet. 2009;225:526-36.
Jorovinen HJ, Aarnio M, Mustonen H, Aktan-Collan K, Aaltonen LA et al. Controlled 15-year trial on screening for colorectal cancer in families with hereditary nonpolyposis colorectal cancer. Gastroenterology. 2000;118:829-34.
Lambertic S, Mishra R, Goldman H, Kolodner R. Methylation of the hMLH1 promoter correlates with lack of expression of hMLH1 in sporadic colon tumors and mismatch repair-defective human tumor cell lines. Cancer Res. 1999;37:422-36.
Ozaslan M, Aytekin T. Loss of heterogygosity in colorectal cancer’, African Journal of Biotechnology. 2009;8:7308-12.
Paul R. Clinical, morphological and laboratory investigation findings differences between the right and left sided colorectal cancer and loss of heterozygosity status analysis in colorectal cancer cells in a group of Bangladeshi patients. 2011.
Raza A, K, M, M. Clinopathologic pattern and DNA methylation status of colorectal carcinoma in a group of Bangladeshi population. Bangabandhu Sheikh Mujib Medical University, Dhaka. 2010.
Rosai J, Sobin L. Tumors of the Mammary Gland. Washington DC: Armed Forces Institute of Pathology. 1993.
Turner JR. The Gastrointestinal Tract’ in Robbins and Cotran Pathologic Basis of Disease, 8th edition. Kumar V, Abbas AK, Fausto N, Aster J.C (editors). W B Saunders company, Philadelphia, Pennsylvania, 2010;822-5.
Valerdiz H, Bicknell D, Kaklamanis L, and Bodmer WF. Molecular analysis of APC mutations in familial adenomatous polyposis and sporadic colon carcinomas. Lancet. 1992;235:635-47.