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[Cancer Research 59, 5662-5665, November 1, 1999]
© 1999 American Association for Cancer Research

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[Cancer Research 59, 5662-5665, November 15, 1999]
© 1999 American Association for Cancer Research


Advances in Brief

The Association of Chromosome 8p Deletion and Tumor Metastasis in Human Hepatocellular Carcinoma1

Lun-Xiu Qin, Zhao-You Tang, Jonathan S. T. Sham, Zeng-Chen Ma, Sheng-Long Ye, Xin-Da Zhou, Zhi-Quan Wu, Jeffrey M. Trent and Xin-Yuan Guan2

Liver Cancer Institute, Zhongshan Hospital, Shanghai Medical University, Shanghai, Peoples Republic of China [L-X. Q., Z-Y. T., Z-C. M., S-L. Y., X-D. Z., Z-Q. W.]; Department of Clinical Oncology, Queen Mary Hospital, University of Hong Kong, Hong Kong [J. S. T. S., X-Y. G.]; and Cancer Genetics Branch, National Human Genome Research Institute, NIH, Bethesda, Maryland [J. M. T.]

To understand the genetic mechanisms underlying the progression of hepatocellular carcinoma (HCC) metastasis, differences of genomic alterations between 10 pairs of primary HCC tumors and their matched metastatic lesions were analyzed by comparative genomic hybridization. Several chromosomal alterations including loss of 8p, 4q, 17p, and 19p, gain of 5p and high-level amplification of 1q12-q22 were detected in two or more cases. The most significant finding is the loss of 8p which was detected in 8 metastatic tumors but only in 3 corresponding primary tumors (P = 0.03). This result suggests that the deletion of chromosome 8p might contribute to the development of HCC metastasis. Another interesting result is the detection of a minimum high-level amplification region at 1q12-q22 in HCC. This result provides a candidate amplification region in HCC for further study to identify amplified oncogenes related to the development or progression of HCC. Finally, this study provides a practicable model to detect specific genetic alterations related to the tumor metastasis through comparing the primary tumor and its corresponding metastatic lesion using comparative genomic hybridization technique.




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Copyright © 1999 by the American Association for Cancer Research.