© 2017           

By Keith S. Wexler, MBA, Maternal Fetal Medicine, Prenatal Diagnosis and Biotech/Life Sciences Consultant, GENASSIST, Inc.

Paul Wexler, M.D., F.A.C.O.G., Medical Director, GENASSIST, Inc.

Clinical Professor, Department of OB/GYN, University of Colorado Health Sciences Center

Clinical Professor, Division of Genetics/Dept. of Pediatrics, Univ. of Colorado/The Children’s Hospital

Lung Cancer is the leading cause of cancer deaths for men and women in the United States, and is directly related to cigarette and/or cigar smoking.

Lung Cancer accounts for 28% of all cancer deaths annually in men (approximately 85,000) and 26% of all cancer deaths in women (approximately 71,000).

(Reference: Cancer Statistics 2013 – A Presentation from the American Cancer Society © 2013 American Cancer Society).


Although there has been a significant decrease in the number of men and women who smoke, the recent legalization of marijuana in several states in the Unites States and the creation of E-cigarettes may result in the resurgence of smoking, especially among young adults.

One of the healthcare criticisms with the legalization of marijuana and E-cigarettes is the lack of information and warnings regarding the possible increased risks for Lung Cancer.

It has been suspected for a long time that there may be an inherited susceptibility to the development of lung cancer.

It has been shown in several studies that some individuals exposed to toxic agents like:

  • Silicates
  • Asbestos
  • Coal mine dust
  • Cigarettes and other inhaled teratogens fail to develop lung cancer and other individuals with little or no toxic exposures develop lung cancer.

Also, individuals exposed to the same toxic agents may develop different types of lung cancer with varying severity and response to treatment. Small cell lung cancer is much more difficult to treat than squamous cell carcinoma, adenocarcinoma and large cell undifferentiated types.

In one study, mutations in the EGFR gene (chromosome 7: 7p11.2) appeared to be more common in people with lung cancer who never smoked, in women, in Asians and in adenocarcinoma.

Mutations in the KRAS gene (chromosome 12: 12p12.1) were more common in Caucasians, males and former smokers.

More recent studies have suggested the EGFR activation may lead to increased activity of a fibroblast growth factor gene Fn14 which can accelerate growth and spread of non-small cell lung cancer.

Also, acquired changes in the p53 gene (chromosome 9: 9p21.3) and p16 (chromosome 9: 9p21.3) tumor suppressor genes, perhaps induced by environmental exposures, may also be involved in non-small cell lung cancer.

(Reference: Dr. Adi Gazdar, Journal of the National Cancer Institute, 1 March 2005).