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Open Access Research article

Genomic profiling of rectal adenoma and carcinoma by array-based comparative genomic hybridization

Zhi-Zhou Shi1, Yue-Ming Zhang2, Li Shang1, Jia-Jie Hao1, Tong-Tong Zhang1, Bo-Shi Wang1, Jian-Wei Liang3, Xi Chen1, Ying Zhang1, Gui-Qi Wang2, Ming-Rong Wang1* and Yu Zhang1*

Author affiliations

1 State Key Laboratory of Molecular Oncology, Cancer Institute /Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China

2 Department of Endoscopy, Cancer Institute (Hospital), Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China

3 Department of Abdominal Surgery, Cancer Institute/Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China

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Citation and License

BMC Medical Genomics 2012, 5:52  doi:10.1186/1755-8794-5-52

Published: 16 November 2012

Abstract

Background

Rectal cancer is one of the most common cancers in the world. Early detection and early therapy are important for the control of death caused by rectal cancer. The present study aims to investigate the genomic alterations in rectal adenoma and carcinoma.

Methods

We detected the genomic changes of 8 rectal adenomas and 8 carcinomas using array CGH. Then 14 genes were selected for analyzing the expression between rectal tumor and paracancerous normal tissues as well as from adenoma to carcinoma by real-time PCR. The expression of GPNMB and DIS3 were further investigated in rectal adenoma and carcinoma tissues by immunohistochemistry.

Results

We indentified ten gains and 22 losses in rectal adenoma, and found 25 gains and 14 losses in carcinoma. Gains of 7p21.3-p15.3, 7q22.3-q32.1, 13q13.1-q14.11, 13q21.1-q32.1, 13q32.2-q34, 20p11.21 and 20q11.23-q12 and losses of 17p13.1-p11.2, 18p11.32-p11.21 and 18q11.1-q11.2 were shared by both rectal adenoma and carcinoma. Gains of 1q, 6p21.33-p21.31 and losses of 10p14-p11.21, 14q12-q21.1, 14q22.1-q24.3, 14q31.3-q32.1, 14q32.2-q32.32, 15q15.1-q21.1, 15q22.31 and 15q25.1-q25.2 were only detected in carcinoma but not in adenoma. Copy number and mRNA expression of EFNA1 increased from rectal adenoma to carcinoma. C13orf27 and PMEPA1 with increased copy number in both adenoma and carcinoma were over expressed in rectal cancer tissues. Protein and mRNA expression of GPNMB was significantly higher in cancer tissues than rectal adenoma tissues.

Conclusion

Our data may help to identify the driving genes involved in the adenoma-carcinoma progression.