近日腫瘤研究者發(fā)現(xiàn),，煙民和非煙民所得的肺癌,，其實有著本質(zhì)區(qū)別。該研究是約翰·霍普金斯大學（JOHNS HOPKINS）的最新研究發(fā)現(xiàn),，該結論表明,，對肺癌的治療也應該有所不同。
約翰·霍普金斯大學金梅爾腫瘤中心，分管臨床研究工作的副主任查爾斯·魯丁說：“不吸煙者得的肺癌在基因,、細胞和分子生物學方面的性質(zhì)與吸煙相關肺癌是不同的,，這一點目前越來越清楚了。同時,，現(xiàn)在也有非常好的證據(jù)表明,，對于不吸煙的人，防治肺癌的策略可能也與吸煙者不同,。”
這里的不吸煙者,，是指那些一生吸煙少于100支的人。對于這些人群,，由于他們沒有吸煙史,，醫(yī)生很少會懷疑他們得了肺癌，而肺癌往往在晚期表現(xiàn)出咳嗽,、胸痛,，經(jīng)常被誤診為呼吸道疾病，使用抗生素或著抗哮喘藥物進行治療,。魯丁補充道,。
“從不吸煙的患者對一類叫表皮生長因子受體抑制劑（EGFR inhibitors）的藥物反應更好，因為這類患者表皮生長因子受體基因（EGFR gene）突變的可能性更大一些,。”魯丁進一步解釋道,。
EGFR通常促進細胞的生長發(fā)育，一旦發(fā)生基因變異,，會使細胞不受控制地生長,。細胞不受控制地生長，這正是癌癥的特征,。
對于臨床前景,，他說：“針對不吸煙者的基因改變進行靶向治療，這有些其它的成功例子,，比如針對有EML4－ALK基因改變的腫瘤進行的治療,。專門對這一人群進行的全基因水平組相關性研究可以告訴我們更多信息。“
在美國人口癌癥相關死因排名中,，不吸煙者所患肺癌排在第六位,。
接觸二手煙和氡氣被認為是造成不吸煙者罹患這種疾病的重要因素。但是,，大約有一半不吸煙者肺癌病例無法用已知的危險因素進行解釋,。這些已知危險因素還包括：石棉、燒薪材的室內(nèi)火爐和油煙,。
南加利福尼亞大學預防醫(yī)學系的喬納森·薩梅特教授和弗洛拉·L·桑頓都表示：“除了二手煙和氡接觸外,，我們?nèi)匀缓茈y解釋不吸煙者得肺癌的原因,。”
魯丁也表示，不吸煙者的肺癌狀況往往在婦女和東亞的一些人群中更為常見,，可能是由于婦女更多地接觸由烹飪油和燃柴火爐等生成的室內(nèi)污染,。
在美國，非吸煙者肺癌占肺癌病例數(shù)的10至15%,，每年約20,000例,。同時，所有類型肺癌患者的生存機率都不高,。
這項研究成果分為三篇論文發(fā)表在在9月15日的《臨床癌癥研究》（Clinical Cancer Research）雜志上,。這項研究由航空乘務員醫(yī)學研究所（Flight Attendant Medical Research Institute）資助。（生物谷Bioon.com）
生物谷推薦原始出處：
Clinical Cancer Research September 15, 2009 15, 5622
Lung Cancer in Never Smokers: A Call to Action
Charles M. Rudin, Erika Avila-Tang and Jonathan M. Samet
Johns Hopkins University, Baltimore, Maryland
The causative association between tobacco use and lung cancer is a well-established fact. However, lung cancer also occurs, at surprisingly high rates, in lifelong never smokers. In fact, lung cancer in never smokers is among the leading causes of cancer-related mortality. This CCR Focus summarizes recent data, identifies knowledge deficits, and suggests future research directions with regard to this critically important subset of lung cancer patients.
Clinical Cancer Research September 15, 2009 15, 5626
Lung Cancer in Never Smokers: Clinical Epidemiology and Environmental Risk Factors
Jonathan M. Samet1, Erika Avila-Tang1, Paolo Boffetta2, Lindsay M. Hannan3, Susan Olivo-Marston4, Michael J. Thun3 and Charles M. Rudin1
1Johns Hopkins University, Baltimore, Maryland;
2International Agency for Research on Cancer, Lyon, France; 3American Cancer Society, Atlanta, Georgia; and 4National Cancer Institute, Bethesda, Maryland
More than 161,000 lung cancer deaths are projected to occur in the United States in 2008. Of these, an estimated 10 to 15% will be caused by factors other than active smoking, corresponding to 16,000 to 24,000 deaths annually. Thus lung cancer in never smokers would rank among the most common causes of cancer mortality in the United States if considered as a separate category. Slightly more than half of the lung cancers caused by factors other than active smoking occur in never smokers. As summarized in the accompanying article, lung cancers that occur in never smokers differ from those that occur in smokers in their molecular profile and response to targeted therapy. These recent laboratory and clinical observations highlight the importance of defining the genetic and environmental factors responsible for the development of lung cancer in never smokers. This article summarizes available data on the clinical epidemiology of lung cancer in never smokers, and several environmental risk factors that population-based research has implicated in the etiology of these cancers. Primary factors closely tied to lung cancer in never smokers include exposure to known and suspected carcinogens including radon, second-hand tobacco smoke, and other indoor air pollutants. Several other exposures have been implicated. However, a large fraction of lung cancers occurring in never smokers cannot be definitively associated with established environmental risk factors, highlighting the need for additional epidemiologic research in this area.
Clinical Cancer Research September 15, 2009 15, 5646
Lung Cancer in Never Smokers: Molecular Profiles and Therapeutic Implications
Charles M. Rudin1, Erika Avila-Tang1, Curtis C. Harris2, James G. Herman1, Fred R. Hirsch3, William Pao4, Ann G. Schwartz5, Kirsi H. Vahakangas6 and Jonathan M. Samet1
1Johns Hopkins University, Baltimore, Maryland;
2National Cancer Institute, Bethesda, Maryland;
3University of Colorado, Denver, Colorado;
4Memorial Sloan-Kettering Cancer Center, New York, New York;
5Wayne State University, Detroit, Michigan; and
6University of Kuopio, Kuopio, Finland
The majority of lung cancers are caused by long term exposure to the several classes of carcinogens present in tobacco smoke. Although a significant fraction of lung cancers in never smokers may also be attributable to tobacco, many such cancers arise in the absence of detectable tobacco exposure, and may follow a very different cellular and molecular pathway of malignant transformation. Recent studies summarized here suggest that lung cancers arising in never smokers have a distinct natural history, profile of oncogenic mutations, and response to targeted therapy. The majority of molecular analyses of lung cancer have focused on genetic profiling of pathways responsible for metabolism of primary tobacco carcinogens. Limited research has been conducted evaluating familial aggregation and genetic linkage of lung cancer, particularly among never smokers in whom such associations might be expected to be strongest. Data emerging over the past several years show that lung cancers in never smokers are much more likely to carry activating mutations of the epidermal growth factor receptor (EGFR), a key oncogenic factor and direct therapeutic target of several newer anticancer drugs. EGFR mutant lung cancers may represent a distinct class of lung cancers, enriched in the never-smoking population, and less clearly linked to direct tobacco carcinogenesis. These insights followed initial testing and demonstration of efficacy of EGFR-targeted drugs. Focused analysis of molecular carcinogenesis in lung cancers in never smokers is needed, and may provide additional biologic insight with therapeutic implications for lung cancers in both ever smokers and never smokers.
