Chromosomal aberrations of malignant pleural effusions of lung adenocarcinoma: different cytogenetic changes are correlated with genders and smoking habits.
Chromosomal aberrations of malignant cells from pleural effusions of 31 cases of lung adenocarcinoma were analyzed. Pooled CGH results showed frequent amplifications on chromosome arms 1p (22.6%), 1q (35.5%), 2q (25.8%), 3q (38.7%), 4q (41.9%), 5p (41.9%), 5q (51.6%), 6p (19.4%), 6q (25.8%), 7p (41.9%), 7q (35.5%), 8q (32.3%), 12q (38.7%), 13q (22.6%), 14q (35.5%), 17q (19.4%), Xp (22.6%), and Xq (38.7%). Frequent deletions were found on 1p (19.4%), 3p (16.1%), 4q (16.1%), 8p (25.8%), 9p (22.6%), 9q (29.0%), 10q (22.6%), 13q (22.6%), 16p (19.4%), 16q (22.6%), 17p (29.0%), 18q (16.1%), 19p (41.9%), 19q (32.3%), 20p (19.4%) and 22q (29%). These genomic changes were generally found consistent with previous reports of CGH analysis of primary tumors of lung adenocarcinoma. Loss of 19q and 22q were more frequently found in our studies (32.3% and 29.0%, respectively) than studies of primary tumors (less than 7% for both genetic changes). Gain of 11p, although not a frequent finding, was relatively more common in this (16%) than other studies (range, 2.9-11.8%). Interestingly, occurrences of 3p loss and 11p gain were higher in smokers than non-smokers, and deletion of 3p and increased copy number of 11p and Xp appeared more often in male than female patients. Among 17 male patients, gain of chromosomal 11p was a frequent aberration in tumors of smokers, while gain of Xp was more easily found in tumors of non-smokers. One candidate gene located within 11p15, lactate dehydrogenase C (LDHC), was selected for further study. Three cases with 11p gain had amplified FISH signals of LDHC. Also tumors from smokers or male had significantly higher transcript level of LDHC than non-smokers or female, respectively. The results demonstrate that different cytogenetic changes of malignant pleural effusions from lung adenocarcinoma are correlated with genders and smoking habits. The role of LDHC in the carcinogenesis of smoking-related lung adenocarcinoma, especially in male patients with pleural effusions, deserves further investigations.
Yen
Chueh-Chuan
CC
Division of Hematology and Oncology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
Liang
Shu-Ching
SC
Jong
Yiin-Jeng
YJ
Chen
Yann-Jang
YJ
Lin
Chi-Hung
CH
Chen
Yuh-Min
YM
Wu
Yu-Chung
YC
Su
Wu-Chou
WC
Huang
Chi-Ying F
CY
Tseng
Szu-Wen
SW
Whang-Peng
Jacqueline
J
D000230:Adenocarcinoma / Q000209:etiology / Q000235:genetics* / Q000473:pathology; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002869:Chromosome Aberrations; D005260:Female; D005784:Gene Amplification; D006801:Humans; D042844:L-Lactate Dehydrogenase (Cytochrome) / Q000235:genetics*; D008175:Lung Neoplasms / Q000209:etiology / Q000235:genetics* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009693:Nucleic Acid Hybridization; D016066:Pleural Effusion, Malignant / Q000235:genetics* / Q000473:pathology; D012737:Sex Factors; D012907:Smoking
D042844:L-Lactate Dehydrogenase (Cytochrome)