The leading cancer killer in women: lung cancer
More women die of lung cancer each year than of any other cancer. Over 72,000 women will die of lung cancer in 2012, nearly twice the number who will die of breast cancer, and nearly three times the number who will die of colorectal cancer. Lung cancer will kill more women than breast, ovarian, and uterine cancers combined. We can’t ignore the facts: lung cancer is a woman’s disease.
Lung cancer surpassed breast cancer as the leading cause of cancer death in women in 1987. Incidence of lung cancer in women has jumped over 600% since 1950, and doubled since 1975, largely due to a dramatic increase in the number of female smokers. But risk from smoking isn’t the whole story - there are differences between men and women that affect lung cancer risk and prognosis:
The data points to specific factors making lung cancer a different disease in women than men, even more so when we take smoking out of the picture. Women, especially neversmokers, are more likely to get certain types of lung cancer (adenocarcinoma) with different mutated genes driving cancer growth (EGFR and ALK), and are more likely to be younger. Lung cancer in neversmokers is estimated to be the 6th leading cause of cancer death in the US - and the majority of those patients are women.
The role of estrogen in lung cancer: There are two major types of estrogen receptors, the proteins that sit on the outside of cells and relay ‘grow’ signals from estrogen. One type of estrogen receptor is found in breast, ovarian and endometrial tissues, and we know estrogen can promote those types of cancer. However, the other estrogen receptor is present in lung tissue and involved in lung development in both men and women. This estrogen receptor is also found in 45-70% of lung tumors (meaning they can be sensitive to estrogen), and laboratory studies have linked both estrogen and progesterone to lung cancer growth.
Researchers are developing a number ways to target estrogen, including antiestrogen therapy (preventing estrogen receptors from sending 'grow' signals), and aromatase inhibitors (preventing estrogens from being made in the body). A recent laboratory study presented this month at the American Association for Cancer Research Annual Meeting showed that estrogen metabolites (the products of estrogen being broken down in the body) can be toxic in the lungs of mice. When exposed to tobacco smoke, the amount of estrogen metabolites increased - indicating that preventing estrogen metabolism may be a way to treat lung cancer.
UALC has funded a few projects studying estrogen in lung cancers, including Drs. Laura Stabile, Carolyn Klinge, Rafaella Sordella, John Heymach, and William Young, Jr. A number of these projects looked at how estrogen works with the EGFR receptor to promote lung cancer growth. There are a few ongoing clinical trials investigating the antiestrogen Faslodex (fulvestrant) in combination with the EGFR-targeted drugs Iressa (gefitinib) or Tarceva (erlotinib).
Researchers are continuing to investigate how estrogen can promote lung cancer and are developing new ways of targeting this process on multiple fronts. Women have already shown how powerful our voices can be in the fight against cancer - with our voices behind lung cancer, we can help researchers develop new treatments for the thousands of women battling this disease.
Donington JS and Colson YL. Sex and Gender Differences in Non-Small Cell Lung Cancer. Semin Thorac Cardiovasc Surg. 2011 Summer;23(2):137-45.
Henschke CL and Miettinen OS. Women’s susceptibility to tobacco carcinogens. Lung Cancer 43:1-5, 2004.
Nakamura H,et al. Female gender is an independent prognostic factor in non-small-cell lung cancer: a meta-analysis. Ann Thorac Cardiovasc Surg. 2011 Oct 25;17(5):469-80.
Siegel R, et al., Cancer Stastics, 2012. CA Cancer J Clin. 2012 Jan-Feb;62(1):10-29.
Wakelee HA, et al., Lung Cancer Incidence in Never Smokers. J Clin Oncol. 2007. Feb 10; 25(7):472-478.
Women and smoking: a report of the Surgeon General. Executive Summary. MMWR Recomm Rep 2002; 51:i-iv, 1-13.