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01.12.2016 | Research article | Ausgabe 1/2016 Open Access

BMC Cancer 1/2016

Comparative analysis of copy number variations in ulcerative colitis associated and sporadic colorectal neoplasia

BMC Cancer > Ausgabe 1/2016
B. M. Shivakumar, Sanjiban Chakrabarty, Harish Rotti, Venu Seenappa, Lakshmi Rao, Vasudevan Geetha, B. V. Tantry, Hema Kini, Rajesh Dharamsi, C. Ganesh Pai, Kapaettu Satyamoorthy
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​s12885-016-2303-4) contains supplementary material, which is available to authorized users.

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

Conception and design: BMS, CGP and KS. Development of methodology: BMS, CGP and KS. Acquisition of data (provided animals acquired and managed patients, provided facilities, etc.): BMS, HR, SC, LR, VG, BVT, HK, R D, CGP and KS. Analysis and interpretation of data (e.g., statistical analysis, biostatistics, computational analysis): BMS, HR and SC. Writing, review, and/or revision of the manuscript: BMS, HR, SC, LR, VG, BVT, HK, R D, CGP and KS. Administrative, technical, or material support (i.e., reporting or organizing data, constructing databases): BMS, HR, VS, LR, CGP and KS. Study supervision: CGP, LR and KS. Contributed clinical information and patients: BMS, LR, VG, BVT, HK, RD and CGP. All authors read and approved the final manuscript.



The incidence of and mortality from colorectal cancers (CRC) can be reduced by early detection. Currently there is a lack of established markers to detect early neoplastic changes. We aimed to identify the copy number variations (CNVs) and the associated genes which could be potential markers for the detection of neoplasia in both ulcerative colitis-associated neoplasia (UC-CRN) and sporadic colorectal neoplasia (S-CRN).


We employed array comparative genome hybridization (aCGH) to identify CNVs in tissue samples of UC nonprogressor, progressor and sporadic CRC. Select genes within these CNV regions as a panel of markers were validated using quantitative real time PCR (qRT-PCR) method along with the microsatellite instability (MSI) in an independent cohort of samples. Immunohistochemistry (IHC) analysis was also performed.


Integrated analysis showed 10 overlapping CNV regions between UC-Progressor and S-CRN, with the 8q and 12p regions showing greater overlap. The qRT-PCR based panel of MYC, MYCN, CCND1, CCND2, EGFR and FNDC3A was successful in detecting neoplasia with an overall accuracy of 54 % in S-CRN compared to that of 29 % in UC neoplastic samples. IHC study showed that p53 and CCND1 were significantly overexpressed with an increasing frequency from pre-neoplastic to neoplastic stages. EGFR and AMACR were expressed only in the neoplastic conditions.


CNVs that are common and unique to both UC-associated and sporadic colorectal neoplasm could be the key players driving carcinogenesis. Comparative analysis of CNVs provides testable driver aberrations but needs further evaluation in larger cohorts of samples. These markers may help in developing more effective neoplasia-detection strategies during screening and surveillance programs.
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