Research ExplorerPublicationsMolecular alterations at 9q33.1 and polyploidy in asbestos-r...

Molecular alterations at 9q33.1 and polyploidy in asbestos-related lung cancer.

Standard

Molecular alterations at 9q33.1 and polyploidy in asbestos-related lung cancer. / Nymark, Penny; Kettunen, Eeva; Aavikko, Mervi; Ruosaari, Salla; Kuosma, Eeva; Vanhala, Esa; Salmenkivi, Kaisa; Pirinen, Risto; Karjalainen, Antti; Knuutila, Sakari; Wikman, Harriet; Anttila, Sisko.

In: CLIN CANCER RES, Vol. 15, No. 2, 2, 2009, p. 468-475.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Nymark, P, Kettunen, E, Aavikko, M, Ruosaari, S, Kuosma, E, Vanhala, E, Salmenkivi, K, Pirinen, R, Karjalainen, A, Knuutila, S, Wikman, H & Anttila, S 2009, 'Molecular alterations at 9q33.1 and polyploidy in asbestos-related lung cancer.', CLIN CANCER RES, vol. 15, no. 2, 2, pp. 468-475. <http://www.ncbi.nlm.nih.gov/pubmed/19147751?dopt=Citation>

APA

Nymark, P., Kettunen, E., Aavikko, M., Ruosaari, S., Kuosma, E., Vanhala, E., Salmenkivi, K., Pirinen, R., Karjalainen, A., Knuutila, S., Wikman, H., & Anttila, S. (2009). Molecular alterations at 9q33.1 and polyploidy in asbestos-related lung cancer. CLIN CANCER RES, 15(2), 468-475. [2]. http://www.ncbi.nlm.nih.gov/pubmed/19147751?dopt=Citation

Vancouver

Nymark P, Kettunen E, Aavikko M, Ruosaari S, Kuosma E, Vanhala E et al. Molecular alterations at 9q33.1 and polyploidy in asbestos-related lung cancer. CLIN CANCER RES. 2009;15(2):468-475. 2.

Bibtex

@article{ce8a6889c28543deb41c0bc3e294dc31,
title = "Molecular alterations at 9q33.1 and polyploidy in asbestos-related lung cancer.",
abstract = "PURPOSE: Asbestos causes DNA damage and the fibers, together with tobacco smoke, have a synergistic effect on lung cancer risk. We recently identified 18 chromosomal regions that showed differences in DNA copy number between the lung tumors of asbestos-exposed and nonexposed patients. One of the previously identified asbestos-associated chromosomal regions at 9q was further analyzed for allelic imbalance and DNA copy number alterations (CNA) in the lung tumors of asbestos-exposed and nonexposed patients. In addition, the ploidy level of the tumors was studied. EXPERIMENTAL DESIGN: Allelic imbalance was analyzed at 9q31.3-34.3 with 15 microsatellite markers in 52 lung tumor samples from asbestos-exposed and nonexposed patients. CNA at 9q32-34.3 were characterized by fluorescent in situ hybridization (FISH) with six bacterial artificial chromosome probes in 95 lung tumors. The ploidy level was analyzed in 100 lung tumors with FISH using three to five centromere probes. RESULTS: Allelic imbalance at 9q31.3-q34.3 was found in all asbestos-exposed patient tumors (100%, 17 of 17) compared with 64% (14 of 22) in the nonexposed cases (P = 0.005). The most significant difference was detected at 9q33.1 (P = 0.002). FISH results showed that also CNA were more frequent at 9q33.1 in the three major histologic types of non-small-cell lung tumors of exposed patients, and the association showed a dose-dependent trend (P = 0.03). Furthermore, we detected more frequent polyploidy among the exposed (48%, 28 of 58) than among the nonexposed (29%, 12 of 42) patient tumors (P <0.05). CONCLUSIONS: These results provide a basis for the development of a method to identify asbestos-related lung cancer on a molecular level.",
author = "Penny Nymark and Eeva Kettunen and Mervi Aavikko and Salla Ruosaari and Eeva Kuosma and Esa Vanhala and Kaisa Salmenkivi and Risto Pirinen and Antti Karjalainen and Sakari Knuutila and Harriet Wikman and Sisko Anttila",
year = "2009",
language = "Deutsch",
volume = "15",
pages = "468--475",
journal = "CLIN CANCER RES",
issn = "1078-0432",
publisher = "American Association for Cancer Research Inc.",
number = "2",

}

RIS

TY - JOUR

T1 - Molecular alterations at 9q33.1 and polyploidy in asbestos-related lung cancer.

AU - Nymark, Penny

AU - Kettunen, Eeva

AU - Aavikko, Mervi

AU - Ruosaari, Salla

AU - Kuosma, Eeva

AU - Vanhala, Esa

AU - Salmenkivi, Kaisa

AU - Pirinen, Risto

AU - Karjalainen, Antti

AU - Knuutila, Sakari

AU - Wikman, Harriet

AU - Anttila, Sisko

PY - 2009

Y1 - 2009

N2 - PURPOSE: Asbestos causes DNA damage and the fibers, together with tobacco smoke, have a synergistic effect on lung cancer risk. We recently identified 18 chromosomal regions that showed differences in DNA copy number between the lung tumors of asbestos-exposed and nonexposed patients. One of the previously identified asbestos-associated chromosomal regions at 9q was further analyzed for allelic imbalance and DNA copy number alterations (CNA) in the lung tumors of asbestos-exposed and nonexposed patients. In addition, the ploidy level of the tumors was studied. EXPERIMENTAL DESIGN: Allelic imbalance was analyzed at 9q31.3-34.3 with 15 microsatellite markers in 52 lung tumor samples from asbestos-exposed and nonexposed patients. CNA at 9q32-34.3 were characterized by fluorescent in situ hybridization (FISH) with six bacterial artificial chromosome probes in 95 lung tumors. The ploidy level was analyzed in 100 lung tumors with FISH using three to five centromere probes. RESULTS: Allelic imbalance at 9q31.3-q34.3 was found in all asbestos-exposed patient tumors (100%, 17 of 17) compared with 64% (14 of 22) in the nonexposed cases (P = 0.005). The most significant difference was detected at 9q33.1 (P = 0.002). FISH results showed that also CNA were more frequent at 9q33.1 in the three major histologic types of non-small-cell lung tumors of exposed patients, and the association showed a dose-dependent trend (P = 0.03). Furthermore, we detected more frequent polyploidy among the exposed (48%, 28 of 58) than among the nonexposed (29%, 12 of 42) patient tumors (P <0.05). CONCLUSIONS: These results provide a basis for the development of a method to identify asbestos-related lung cancer on a molecular level.

AB - PURPOSE: Asbestos causes DNA damage and the fibers, together with tobacco smoke, have a synergistic effect on lung cancer risk. We recently identified 18 chromosomal regions that showed differences in DNA copy number between the lung tumors of asbestos-exposed and nonexposed patients. One of the previously identified asbestos-associated chromosomal regions at 9q was further analyzed for allelic imbalance and DNA copy number alterations (CNA) in the lung tumors of asbestos-exposed and nonexposed patients. In addition, the ploidy level of the tumors was studied. EXPERIMENTAL DESIGN: Allelic imbalance was analyzed at 9q31.3-34.3 with 15 microsatellite markers in 52 lung tumor samples from asbestos-exposed and nonexposed patients. CNA at 9q32-34.3 were characterized by fluorescent in situ hybridization (FISH) with six bacterial artificial chromosome probes in 95 lung tumors. The ploidy level was analyzed in 100 lung tumors with FISH using three to five centromere probes. RESULTS: Allelic imbalance at 9q31.3-q34.3 was found in all asbestos-exposed patient tumors (100%, 17 of 17) compared with 64% (14 of 22) in the nonexposed cases (P = 0.005). The most significant difference was detected at 9q33.1 (P = 0.002). FISH results showed that also CNA were more frequent at 9q33.1 in the three major histologic types of non-small-cell lung tumors of exposed patients, and the association showed a dose-dependent trend (P = 0.03). Furthermore, we detected more frequent polyploidy among the exposed (48%, 28 of 58) than among the nonexposed (29%, 12 of 42) patient tumors (P <0.05). CONCLUSIONS: These results provide a basis for the development of a method to identify asbestos-related lung cancer on a molecular level.

M3 - SCORING: Zeitschriftenaufsatz

VL - 15

SP - 468

EP - 475

JO - CLIN CANCER RES

JF - CLIN CANCER RES

SN - 1078-0432

IS - 2

M1 - 2

ER -