Chromosomal aberrations of malignant pleural effusions of lung adenocarcinoma: Different cytogenetic changes are correlated with genders and smoking habits

Chueh Chuan Yen, Shu Ching Liang, Y. J. Jong, Yann Jang Chen, Chi Hung Lin, Yuh Min Chen, Yu Chung Wu, Wu Chou Su, Chi Ying F. Huang, Szu Wen Tseng, Jacqueline Whang-Peng

Research output: Contribution to journalArticle

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Abstract

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.

Original languageEnglish
Pages (from-to)292-301
Number of pages10
JournalLung Cancer
Volume57
Issue number3
DOIs
Publication statusPublished - Sep 1 2007
Externally publishedYes

Fingerprint

Malignant Pleural Effusion
Cytogenetics
Chromosome Aberrations
Habits
Smoking
Neoplasms
Pleural Effusion
Carcinogenesis
Chromosomes
Adenocarcinoma of lung
lactate dehydrogenase C4
Genes

Keywords

  • Chromosomal aberrations
  • Comparative genomic hybridization
  • Gender
  • LDH
  • Lung neoplasm
  • Quantitative PCR
  • Smoking

ASJC Scopus subject areas

  • Oncology
  • Pulmonary and Respiratory Medicine
  • Cancer Research

Cite this

Chromosomal aberrations of malignant pleural effusions of lung adenocarcinoma : Different cytogenetic changes are correlated with genders and smoking habits. / Yen, Chueh Chuan; Liang, Shu Ching; Jong, Y. J.; Chen, Yann Jang; Lin, Chi Hung; Chen, Yuh Min; Wu, Yu Chung; Su, Wu Chou; Huang, Chi Ying F.; Tseng, Szu Wen; Whang-Peng, Jacqueline.

In: Lung Cancer, Vol. 57, No. 3, 01.09.2007, p. 292-301.

Research output: Contribution to journalArticle

Yen, Chueh Chuan ; Liang, Shu Ching ; Jong, Y. J. ; Chen, Yann Jang ; Lin, Chi Hung ; Chen, Yuh Min ; Wu, Yu Chung ; Su, Wu Chou ; Huang, Chi Ying F. ; Tseng, Szu Wen ; Whang-Peng, Jacqueline. / Chromosomal aberrations of malignant pleural effusions of lung adenocarcinoma : Different cytogenetic changes are correlated with genders and smoking habits. In: Lung Cancer. 2007 ; Vol. 57, No. 3. pp. 292-301.
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abstract = "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.",
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T1 - Chromosomal aberrations of malignant pleural effusions of lung adenocarcinoma

T2 - Different cytogenetic changes are correlated with genders and smoking habits

AU - Yen, Chueh Chuan

AU - Liang, Shu Ching

AU - Jong, Y. J.

AU - Chen, Yann Jang

AU - Lin, Chi Hung

AU - Chen, Yuh Min

AU - Wu, Yu Chung

AU - Su, Wu Chou

AU - Huang, Chi Ying F.

AU - Tseng, Szu Wen

AU - Whang-Peng, Jacqueline

PY - 2007/9/1

Y1 - 2007/9/1

N2 - 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.

AB - 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.

KW - Chromosomal aberrations

KW - Comparative genomic hybridization

KW - Gender

KW - LDH

KW - Lung neoplasm

KW - Quantitative PCR

KW - Smoking

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