Study of chromosomal changes in Ki-1 positive non-Hodgkin's lymphoma

碩士 === 國立陽明大學 === 遺傳學研究所 === 87 === Ki-1 positive non-Hodgkin掇 lymphoma (Ki-1 NHL) was recognized as a distinct clinicopathologic and morphologic entity. It is a highly aggressive lymphoma with frequent skin involvement. Although Ki-1 NHL has been well studied in Western countries but sti...

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Bibliographic Details
Main Authors: Yiin-Jeng Jong, 鍾尹禎
Other Authors: Sheng Wang-Wuu
Format: Others
Language:zh-TW
Published: 1999
Online Access:http://ndltd.ncl.edu.tw/handle/13046438241920898738
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Summary:碩士 === 國立陽明大學 === 遺傳學研究所 === 87 === Ki-1 positive non-Hodgkin掇 lymphoma (Ki-1 NHL) was recognized as a distinct clinicopathologic and morphologic entity. It is a highly aggressive lymphoma with frequent skin involvement. Although Ki-1 NHL has been well studied in Western countries but still poorly described in Asia. Com-parative Genomic Hybridization (CGH) is a newly described molecular cy-togenetic technique that globally assays for chromosomal gains and losses in a genomic complement. In a typical CGH experiment, genomic DNA from tumor and normal tissues are separately labeled with different fluorochromes. These differentially labeled DNA probes are hybridized simultaneously to metaphase chromosome spreads prepared from normal individuals. Regions of gain or loss of DNA sequences, such as deletion, duplications, and amplifications, are observed as changes in the ratio of the two fluorescence intensity profiles along the target chromosomes. To screen the unbalanced chromosomal changes, we performed the CGH on Ki-1 NHL. A total of 24 tumor surgical samples were collected and analyzed by CGH. Chromosomal aberrations found in the advanced tumors were more complex than those found in earlier stages. In these cases, the most common gains were detected at 1q21, 1p36, 9q34, 3q29, 6p, 7p22, 7q21q35, 12p, 16p and X, whereas the most frequent losses involved 6q16q21, 13q21q22, 4q28q35, 5p14 and 8p. CGH findings on four Ki-1 NHL cell lines are consistent with those observed using conventional cytogenetic analysis. These data suggested the existence of oncogenes and tumor suppressor genes in these "hot spots" that probably involved in tumor initiation and progression. Especially, overrepresentation of 1p36 (where Ki-1 gene is located) might reflect the amplification of Ki-1 gene and correlate with tumorigenesis of Ki-1 NHL.