The Impact of Smoking and TP53 Mutations in Lung Adenocarcinoma Patients with Targetable Mutations--The Lung Cancer Mutation Consortium (LCMC2)

Publication Date:
2018-03-06
Publisher:
The American Association for Cancer Research (AACR)
Print ISSN:
1078-0432
Electronic ISSN:
1557-3265
Topics:
Medicine
Published by:
http://www.aacr.org/
_version_ 1836398818317303809
autor Aisner, D. L., Sholl, L. M., Berry, L. D., Rossi, M. R., Chen, H., Fujimoto, J., Moreira, A. L., Ramalingam, S. S., Villaruz, L. C., Otterson, G. A., Haura, E., Politi, K., Glisson, B., Cetnar, J., Garon, E. B., Schiller, J., Waqar, S. N., Sequist, L. V., Brahmer, J., Shyr, Y., Kugler, K., Wistuba, I. I., Johnson, B. E., Minna, J. D., Kris, M. G., Bunn, P. A., Kwiatkowski, D. J., for the LCMC2 investigators
beschreibung Purpose: Multiplex genomic profiling is standard of care for patients with advanced lung adenocarcinomas. The Lung Cancer Mutation Consortium (LCMC) is a multi-institutional effort to identify and treat oncogenic driver events in patients with lung adenocarcinomas. Experimental Design: Sixteen U.S. institutions enrolled 1,367 patients with lung cancer in LCMC2; 904 were deemed eligible and had at least one of 14 cancer-related genes profiled using validated methods including genotyping, massively parallel sequencing, and IHC. Results: The use of targeted therapies in patients with EGFR, ERBB2, or BRAF p.V600E mutations, ALK, ROS1 , or RET rearrangements, or MET amplification was associated with a survival increment of 1.5 years compared with those with such mutations not receiving targeted therapy, and 1.0 year compared with those lacking a targetable driver. Importantly, 60 patients with a history of smoking derived similar survival benefit from targeted therapy for alterations in EGFR / ALK / ROS1 , when compared with 75 never smokers with the same alterations. In addition, coexisting TP53 mutations were associated with shorter survival among patients with EGFR, ALK , or ROS1 alterations. Conclusion: Patients with adenocarcinoma of the lung and an oncogenic driver mutation treated with effective targeted therapy have a longer survival, regardless of prior smoking history. Molecular testing should be performed on all individuals with lung adenocarcinomas irrespective of clinical characteristics. Routine use of massively parallel sequencing enables detection of both targetable driver alterations and tumor suppressor gene and other alterations that have potential significance for therapy selection and as predictive markers for the efficacy of treatment. Clin Cancer Res; 24(5); 1038–47. ©2017 AACR .
citation_standardnr 6182350
datenlieferant ipn_articles
feed_id 9363
feed_publisher The American Association for Cancer Research (AACR)
feed_publisher_url http://www.aacr.org/
insertion_date 2018-03-06
journaleissn 1557-3265
journalissn 1078-0432
publikationsjahr_anzeige 2018
publikationsjahr_facette 2018
publikationsjahr_intervall 7984:2015-2019
publikationsjahr_sort 2018
publisher The American Association for Cancer Research (AACR)
quelle Clinical Cancer Research
relation http://clincancerres.aacrjournals.org/cgi/content/short/24/5/1038?rss=1
search_space articles
shingle_author_1 Aisner, D. L., Sholl, L. M., Berry, L. D., Rossi, M. R., Chen, H., Fujimoto, J., Moreira, A. L., Ramalingam, S. S., Villaruz, L. C., Otterson, G. A., Haura, E., Politi, K., Glisson, B., Cetnar, J., Garon, E. B., Schiller, J., Waqar, S. N., Sequist, L. V., Brahmer, J., Shyr, Y., Kugler, K., Wistuba, I. I., Johnson, B. E., Minna, J. D., Kris, M. G., Bunn, P. A., Kwiatkowski, D. J., for the LCMC2 investigators
shingle_author_2 Aisner, D. L., Sholl, L. M., Berry, L. D., Rossi, M. R., Chen, H., Fujimoto, J., Moreira, A. L., Ramalingam, S. S., Villaruz, L. C., Otterson, G. A., Haura, E., Politi, K., Glisson, B., Cetnar, J., Garon, E. B., Schiller, J., Waqar, S. N., Sequist, L. V., Brahmer, J., Shyr, Y., Kugler, K., Wistuba, I. I., Johnson, B. E., Minna, J. D., Kris, M. G., Bunn, P. A., Kwiatkowski, D. J., for the LCMC2 investigators
shingle_author_3 Aisner, D. L., Sholl, L. M., Berry, L. D., Rossi, M. R., Chen, H., Fujimoto, J., Moreira, A. L., Ramalingam, S. S., Villaruz, L. C., Otterson, G. A., Haura, E., Politi, K., Glisson, B., Cetnar, J., Garon, E. B., Schiller, J., Waqar, S. N., Sequist, L. V., Brahmer, J., Shyr, Y., Kugler, K., Wistuba, I. I., Johnson, B. E., Minna, J. D., Kris, M. G., Bunn, P. A., Kwiatkowski, D. J., for the LCMC2 investigators
shingle_author_4 Aisner, D. L., Sholl, L. M., Berry, L. D., Rossi, M. R., Chen, H., Fujimoto, J., Moreira, A. L., Ramalingam, S. S., Villaruz, L. C., Otterson, G. A., Haura, E., Politi, K., Glisson, B., Cetnar, J., Garon, E. B., Schiller, J., Waqar, S. N., Sequist, L. V., Brahmer, J., Shyr, Y., Kugler, K., Wistuba, I. I., Johnson, B. E., Minna, J. D., Kris, M. G., Bunn, P. A., Kwiatkowski, D. J., for the LCMC2 investigators
shingle_catch_all_1 The Impact of Smoking and TP53 Mutations in Lung Adenocarcinoma Patients with Targetable Mutations--The Lung Cancer Mutation Consortium (LCMC2)
Purpose: Multiplex genomic profiling is standard of care for patients with advanced lung adenocarcinomas. The Lung Cancer Mutation Consortium (LCMC) is a multi-institutional effort to identify and treat oncogenic driver events in patients with lung adenocarcinomas. Experimental Design: Sixteen U.S. institutions enrolled 1,367 patients with lung cancer in LCMC2; 904 were deemed eligible and had at least one of 14 cancer-related genes profiled using validated methods including genotyping, massively parallel sequencing, and IHC. Results: The use of targeted therapies in patients with EGFR, ERBB2, or BRAF p.V600E mutations, ALK, ROS1 , or RET rearrangements, or MET amplification was associated with a survival increment of 1.5 years compared with those with such mutations not receiving targeted therapy, and 1.0 year compared with those lacking a targetable driver. Importantly, 60 patients with a history of smoking derived similar survival benefit from targeted therapy for alterations in EGFR / ALK / ROS1 , when compared with 75 never smokers with the same alterations. In addition, coexisting TP53 mutations were associated with shorter survival among patients with EGFR, ALK , or ROS1 alterations. Conclusion: Patients with adenocarcinoma of the lung and an oncogenic driver mutation treated with effective targeted therapy have a longer survival, regardless of prior smoking history. Molecular testing should be performed on all individuals with lung adenocarcinomas irrespective of clinical characteristics. Routine use of massively parallel sequencing enables detection of both targetable driver alterations and tumor suppressor gene and other alterations that have potential significance for therapy selection and as predictive markers for the efficacy of treatment. Clin Cancer Res; 24(5); 1038–47. ©2017 AACR .
Aisner, D. L., Sholl, L. M., Berry, L. D., Rossi, M. R., Chen, H., Fujimoto, J., Moreira, A. L., Ramalingam, S. S., Villaruz, L. C., Otterson, G. A., Haura, E., Politi, K., Glisson, B., Cetnar, J., Garon, E. B., Schiller, J., Waqar, S. N., Sequist, L. V., Brahmer, J., Shyr, Y., Kugler, K., Wistuba, I. I., Johnson, B. E., Minna, J. D., Kris, M. G., Bunn, P. A., Kwiatkowski, D. J., for the LCMC2 investigators
The American Association for Cancer Research (AACR)
1078-0432
10780432
1557-3265
15573265
shingle_catch_all_2 The Impact of Smoking and TP53 Mutations in Lung Adenocarcinoma Patients with Targetable Mutations--The Lung Cancer Mutation Consortium (LCMC2)
Purpose: Multiplex genomic profiling is standard of care for patients with advanced lung adenocarcinomas. The Lung Cancer Mutation Consortium (LCMC) is a multi-institutional effort to identify and treat oncogenic driver events in patients with lung adenocarcinomas. Experimental Design: Sixteen U.S. institutions enrolled 1,367 patients with lung cancer in LCMC2; 904 were deemed eligible and had at least one of 14 cancer-related genes profiled using validated methods including genotyping, massively parallel sequencing, and IHC. Results: The use of targeted therapies in patients with EGFR, ERBB2, or BRAF p.V600E mutations, ALK, ROS1 , or RET rearrangements, or MET amplification was associated with a survival increment of 1.5 years compared with those with such mutations not receiving targeted therapy, and 1.0 year compared with those lacking a targetable driver. Importantly, 60 patients with a history of smoking derived similar survival benefit from targeted therapy for alterations in EGFR / ALK / ROS1 , when compared with 75 never smokers with the same alterations. In addition, coexisting TP53 mutations were associated with shorter survival among patients with EGFR, ALK , or ROS1 alterations. Conclusion: Patients with adenocarcinoma of the lung and an oncogenic driver mutation treated with effective targeted therapy have a longer survival, regardless of prior smoking history. Molecular testing should be performed on all individuals with lung adenocarcinomas irrespective of clinical characteristics. Routine use of massively parallel sequencing enables detection of both targetable driver alterations and tumor suppressor gene and other alterations that have potential significance for therapy selection and as predictive markers for the efficacy of treatment. Clin Cancer Res; 24(5); 1038–47. ©2017 AACR .
Aisner, D. L., Sholl, L. M., Berry, L. D., Rossi, M. R., Chen, H., Fujimoto, J., Moreira, A. L., Ramalingam, S. S., Villaruz, L. C., Otterson, G. A., Haura, E., Politi, K., Glisson, B., Cetnar, J., Garon, E. B., Schiller, J., Waqar, S. N., Sequist, L. V., Brahmer, J., Shyr, Y., Kugler, K., Wistuba, I. I., Johnson, B. E., Minna, J. D., Kris, M. G., Bunn, P. A., Kwiatkowski, D. J., for the LCMC2 investigators
The American Association for Cancer Research (AACR)
1078-0432
10780432
1557-3265
15573265
shingle_catch_all_3 The Impact of Smoking and TP53 Mutations in Lung Adenocarcinoma Patients with Targetable Mutations--The Lung Cancer Mutation Consortium (LCMC2)
Purpose: Multiplex genomic profiling is standard of care for patients with advanced lung adenocarcinomas. The Lung Cancer Mutation Consortium (LCMC) is a multi-institutional effort to identify and treat oncogenic driver events in patients with lung adenocarcinomas. Experimental Design: Sixteen U.S. institutions enrolled 1,367 patients with lung cancer in LCMC2; 904 were deemed eligible and had at least one of 14 cancer-related genes profiled using validated methods including genotyping, massively parallel sequencing, and IHC. Results: The use of targeted therapies in patients with EGFR, ERBB2, or BRAF p.V600E mutations, ALK, ROS1 , or RET rearrangements, or MET amplification was associated with a survival increment of 1.5 years compared with those with such mutations not receiving targeted therapy, and 1.0 year compared with those lacking a targetable driver. Importantly, 60 patients with a history of smoking derived similar survival benefit from targeted therapy for alterations in EGFR / ALK / ROS1 , when compared with 75 never smokers with the same alterations. In addition, coexisting TP53 mutations were associated with shorter survival among patients with EGFR, ALK , or ROS1 alterations. Conclusion: Patients with adenocarcinoma of the lung and an oncogenic driver mutation treated with effective targeted therapy have a longer survival, regardless of prior smoking history. Molecular testing should be performed on all individuals with lung adenocarcinomas irrespective of clinical characteristics. Routine use of massively parallel sequencing enables detection of both targetable driver alterations and tumor suppressor gene and other alterations that have potential significance for therapy selection and as predictive markers for the efficacy of treatment. Clin Cancer Res; 24(5); 1038–47. ©2017 AACR .
Aisner, D. L., Sholl, L. M., Berry, L. D., Rossi, M. R., Chen, H., Fujimoto, J., Moreira, A. L., Ramalingam, S. S., Villaruz, L. C., Otterson, G. A., Haura, E., Politi, K., Glisson, B., Cetnar, J., Garon, E. B., Schiller, J., Waqar, S. N., Sequist, L. V., Brahmer, J., Shyr, Y., Kugler, K., Wistuba, I. I., Johnson, B. E., Minna, J. D., Kris, M. G., Bunn, P. A., Kwiatkowski, D. J., for the LCMC2 investigators
The American Association for Cancer Research (AACR)
1078-0432
10780432
1557-3265
15573265
shingle_catch_all_4 The Impact of Smoking and TP53 Mutations in Lung Adenocarcinoma Patients with Targetable Mutations--The Lung Cancer Mutation Consortium (LCMC2)
Purpose: Multiplex genomic profiling is standard of care for patients with advanced lung adenocarcinomas. The Lung Cancer Mutation Consortium (LCMC) is a multi-institutional effort to identify and treat oncogenic driver events in patients with lung adenocarcinomas. Experimental Design: Sixteen U.S. institutions enrolled 1,367 patients with lung cancer in LCMC2; 904 were deemed eligible and had at least one of 14 cancer-related genes profiled using validated methods including genotyping, massively parallel sequencing, and IHC. Results: The use of targeted therapies in patients with EGFR, ERBB2, or BRAF p.V600E mutations, ALK, ROS1 , or RET rearrangements, or MET amplification was associated with a survival increment of 1.5 years compared with those with such mutations not receiving targeted therapy, and 1.0 year compared with those lacking a targetable driver. Importantly, 60 patients with a history of smoking derived similar survival benefit from targeted therapy for alterations in EGFR / ALK / ROS1 , when compared with 75 never smokers with the same alterations. In addition, coexisting TP53 mutations were associated with shorter survival among patients with EGFR, ALK , or ROS1 alterations. Conclusion: Patients with adenocarcinoma of the lung and an oncogenic driver mutation treated with effective targeted therapy have a longer survival, regardless of prior smoking history. Molecular testing should be performed on all individuals with lung adenocarcinomas irrespective of clinical characteristics. Routine use of massively parallel sequencing enables detection of both targetable driver alterations and tumor suppressor gene and other alterations that have potential significance for therapy selection and as predictive markers for the efficacy of treatment. Clin Cancer Res; 24(5); 1038–47. ©2017 AACR .
Aisner, D. L., Sholl, L. M., Berry, L. D., Rossi, M. R., Chen, H., Fujimoto, J., Moreira, A. L., Ramalingam, S. S., Villaruz, L. C., Otterson, G. A., Haura, E., Politi, K., Glisson, B., Cetnar, J., Garon, E. B., Schiller, J., Waqar, S. N., Sequist, L. V., Brahmer, J., Shyr, Y., Kugler, K., Wistuba, I. I., Johnson, B. E., Minna, J. D., Kris, M. G., Bunn, P. A., Kwiatkowski, D. J., for the LCMC2 investigators
The American Association for Cancer Research (AACR)
1078-0432
10780432
1557-3265
15573265
shingle_title_1 The Impact of Smoking and TP53 Mutations in Lung Adenocarcinoma Patients with Targetable Mutations--The Lung Cancer Mutation Consortium (LCMC2)
shingle_title_2 The Impact of Smoking and TP53 Mutations in Lung Adenocarcinoma Patients with Targetable Mutations--The Lung Cancer Mutation Consortium (LCMC2)
shingle_title_3 The Impact of Smoking and TP53 Mutations in Lung Adenocarcinoma Patients with Targetable Mutations--The Lung Cancer Mutation Consortium (LCMC2)
shingle_title_4 The Impact of Smoking and TP53 Mutations in Lung Adenocarcinoma Patients with Targetable Mutations--The Lung Cancer Mutation Consortium (LCMC2)
timestamp 2025-06-30T23:33:06.898Z
titel The Impact of Smoking and TP53 Mutations in Lung Adenocarcinoma Patients with Targetable Mutations--The Lung Cancer Mutation Consortium (LCMC2)
titel_suche The Impact of Smoking and TP53 Mutations in Lung Adenocarcinoma Patients with Targetable Mutations--The Lung Cancer Mutation Consortium (LCMC2)
topic WW-YZ
uid ipn_articles_6182350