Re: Just because you never smoked, don't think you won't get lung cancer.

J wrote:

<http://www.boston.com/news/globe/editorial_opinion/oped/articles/2006/05/07/lung_cancer_its_not_just_for_smokers/>

MERYL L. BRALOWER AND PASI A. JÄNNE
Lung cancer: It's not just for smokers

By Meryl L. Bralower and Pasi A. Jänne | May 7, 2006

JUST BECAUSE you never smoked, don't think you won't get lung cancer.

Lung cancer is the leading cancer killer of both men and women in the
United States, accounting for 30 percent of all cancer deaths. It takes
more lives than breast, ovarian, prostate, and colon cancer combined. Its
link to smoking has made lung cancer an underdiagnosed and underfunded
disease. With 15 percent of these 160,000 annual deaths attributed to
nonsmokers, it is time for that to change.

The recent death of Dana Reeve has brought attention to the fact that
there is an increase of lung cancer in nonsmokers, especially in women.
Eighty percent of all nonsmoking lung cancer patients are women.

Up until now there has been an inextricable link between lung cancer and
smoking in the minds of the public and for many doctors as well. There was
an assumption that if you never smoked or smoked a minimal amount, you
would be immune from lung cancer. This connection linking smoking and lung
cancer created a stigma around the disease.

http://www.4walc.org/grants.cfm
Joan's Legacy Research Grants
Submission Deadline: Friday, June 30, 2006

Joan's Legacy invites grant applications for institutional research that studies lung cancer. The foundation is
particularly interested in the genetic basis and biology of bronchoalveolar carcinoma as well as novel therapeutic
approaches for the treatment of this disease.

This funding is intended primarily as seed money for promising new work. It is not for supporting research where
funding has either lapsed or has been previously disapproved. Preference will be given to applications where indirect
costs are minimal or nonexistent.

Details
American Cancer Society Grants
Submission Deadline: Sunday, October 15, 2006

The American Cancer Society provides many grants for independent investigators, postdoctoral fellows, master's and
doctoral candidates. Deadlines are April 1 and October 15 of each year.
Details

Women Against Lung Cancer/
Lung Cancer Online Foundation
Career Development Award
Awarded 9/1/2005 to Hayley McDaid, Ph.D. of Albert Einstein College of Medicine

This award is for junior clinical and basic investigators involved in lung cancer etiology, prevention, and treatment.
Women Against Lung Cancer and The Lung Cancer Online Foundation are co-sponsoring this program to create a critical
mass of lung cancer researchers to ensure effective translation of basic and behavioral research discoveries into
patient therapies to reduce lung cancer incidence, morbidity and mortality. Applicants will be judged on the merits of
their career development plan, research proposal, and research environment, among other factors. For 2005, one 2-year
award of $100,000 will be given.
Details

Women Against Lung Cancer
Research Grant
Awarded 9/1/2005 to Christoph Plass, Ph.D. of The Ohio State University

This grant is for the promotion of understanding sex differences in the molecular, cellular, and environmental
underpinnings of lung cancer, as well as differences in response to treatment. Generously funded by a gift from
Genentech, these awards are designed to provide seed money for promising novel research on sex differences in lung
cancer for faculty members at any point in their careers. For 2005, one 2-year award of $100,000 will be given.

Details


http://www.joanslegacy.org/mu_abstract.html
David Mu, Ph.D., Cold Spring Harbor Laboratory: Discovery and Characterization of Novel Amplified Lung Cancer Genes in
Women

Gain of chromosomes and amplification of genes are genetic hallmarks of cancers. Given the alarming rise of number of
women diagnosed with lung cancer, we wish to examine female lung cancer genome for novel amplified genes, using a whole
genome method termed ?Representational Oligonucleotide Microarray Analysis (ROMA)? developed by Wigler and coworkers
(Lucito et al. 2003). We will systematically catalog each event of chromosomal gain with ROMA in 25 female primary lung
tumor DNA samples and will compare with data already collected in ROMA analyses performed on 34 male primary lung tumor
DNA samples, with the ultimate goal of identifying novel causal genes that drive the female-prone gene amplification in
lung cancer. In a pilot study involving four female NSCLC tumors, two tumors were found to contain an amplified region
on the sex chromosome X, in which a kinase gene is hypothesized to be the target of amplification. We will further
characterize this kinase gene in the realm of lung cancer genetics. Simultaneously, we will perform ROMA analyses on
female lung tumor samples to identify additional amplified genes for further investigation. A clear precedent of
female-prone gene amplification event is the target gene of Herceptin? therapy - the HER2 oncogene. HER2 gene is
amplified in approximately 25-30% of female breast cancer patients, but is only gained very rarely (1-2%) in male
breast cancer patients (Barlund et al. 2004). With novel female-prone lung cancer genes identified, new windows of
opportunities will be presented for creating diagnostic methods and therapies that are potentially more suitable for
women with lung cancer.

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12826030&dopt=Abstract>
1: J Environ Sci Health C Environ Carcinog Ecotoxicol Rev. 2003 May;21(1):1-28. Related Articles, Links
Environmental exposure and lung cancer among nonsmokers: an example of Taiwanese female lung cancer.

Wen Cheng Y, Lee H.

Institute of Medicine and Toxicology, Lung Cancer Research Center, Chung Shan Medical University, Taiwan, ROC.

Lung cancer is the leading cause of cancer death worldwide and in Taiwan. Cigarette smoking is considered to be the
most important risk factor, since about 90% of lung cancer can be related to cigarette smoking. Despite the recent
decrease of cigarette smoking, lung cancer is still the leading cause of cancer death in the United States. In Taiwan,
only around 50% of lung cancer incidence could be associated with cigarette smoking, particularly less than 10% of
Taiwanese women are smokers. Thus, the aetiology of lung cancer for nonsmokers remains unknown. DNA damages including
bulky and oxidative damage may be related with mutation of tumor suppressor genes, such as p53 gene. The high DNA
adduct levels in female may be associated with frequent exposure to indoor cooking oil fumes (COF) and outdoor heavy
air pollution. Oxidative stress induced by COF was also discussed. Different p53 mutation spectra and mutation
frequency between genders reflected that different environmental factors may be involved in nonsmoking male and female
lung cancer development. Most importantly, our recent report has demonstrated that human papillomavirus (HPV) infection
was associated with nonsmoking female lung cancer. Based on our studies with Taiwanese nonsmoking lung cancer as the
model, the possible aetiological factors of lung cancer incidence in Taiwanese nonsmokers were elucidated. PMID:
12826030 [PubMed - indexed for MEDLINE]

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15455389&dopt=Abstract>
Int J Cancer. 2005 Jan 20;113(3):440-5.
Frequent p16INK4a promoter hypermethylation in human papillomavirus-infected female lung cancer in Taiwan.

Wu MF, Cheng YW, Lai JC, Hsu MC, Chen JT, Liu WS, Chiou MC, Chen CY, Lee H.

Department of Internal Medicine, Chung Shan Medical University Hospital, Taichung, Taiwan.

Inactivation of p16INK4a gene through promoter hypermethylation has been frequently observed in non small cell lung
cancer; however, various studies have shown a controversial correlation between p16INK4a hypermethylation and cigarette
smoking. Our recent report showed that human papillomarvirus (HPV) 16/18 infections were associated with the
development of nonsmoking female lung cancer in Taiwan and we further speculated that HPV infection may be linked with
p16INK4a hypermethylation. To verify the influence of environmental exposure, including cigarette smoking,
environmental carcinogen exposure and HPV infections on p16INK4a hypermethylation, tumors from 162 lung patients,
including 67 smoking males, 41 nonsmoking males and 58 nonsmoking females, were subjected to p16INK4a hypermethylation
analysis by methylation-specific PCR. As the results showed, p16INK4a hypermethylation was detected in 40 (59.7%) of 67
smoking male, 15 (36.6%) of 41 nonsmoking male and 35 (60.3%) of 58 nonsmoking female lung tumors. This result seemed
to reveal that gender and cigarette smoking both possess an equal influence on p16INK4a hypermethylation. This result
also led to a speculation that HPV infection may promote p16INK4a hypermethylation in nonsmoking female lung cancer
patients. From our data, p16INK4a hypermethylation frequency in nonsmoking female lung tumors with HPV infection was as
high as 70% (30 of 43) compared to those without HPV infection (33%; 5 of 15). In fact, the correlation between HPV
infection and p16INK4a hypermethylation was only observed in nonsmoking female lung tumors (p = 0.017), but not in
smoking male or nonsmoking male lung tumors. Moreover, the reverse correlation between p16INK4a immunostaining and
p16INK4a promoter hypermethylation was also only observed in nonsmoking female lung tumors. These results strongly
suggested that the involvement of HPV infection in lung tumorigenesis of nonsmoking female cancer patients in Taiwan
may be mediated at least in part through the increase of hypermethylation to cause p16INK4a inactivation. PMID:
15455389 [PubMed - indexed for MEDLINE]


http://jama.ama-assn.org/cgi/content/abstract/291/14/1763
Vol. 291 No. 14, April 14, 2004 TABLE OF CONTENTS
CLINICIAN'S CORNER
Lung Cancer in US Women

A Contemporary Epidemic

Jyoti D. Patel, MD; Peter B. Bach, MD; Mark G. Kris, MD

JAMA. 2004;291:1763-1768.

Lung cancer is the leading cause of cancer death in US women and is responsible for as many deaths as breast cancer and
all gynecological cancers combined. Most lung cancer is caused by cigarette smoke. Despite all that is known about the
devastating effects of cigarettes, one quarter of women in the United States continue to smoke. Women are targeted in
tobacco advertising, and teenage girls are often drawn to cigarette smoking under a variety of social pressures.

Following the increase in smoking, the death rate from lung cancer in US women rose 600% from 1930 to 1997. Women may
be more susceptible than men to the carcinogenic properties of cigarette smoke. In addition, differences in the biology
of lung cancer exist between the 2 sexes with higher levels of DNA adduct formation, increased CYP1A1 expression,
decreased DNA repair capacity, and increased incidence of K-ras gene mutations in women. The novel estrogen receptor
{beta} has also been detected in lung tumors and suggests that estrogen signaling may have a biological role in
tumorigenesis. Given these differences and given the enormous toll this disease has on US women, undertaking
sex-specific research in lung cancer is crucial. Finally, disseminating information about this epidemic may prevent a
similar epidemic in other parts of the world where women are just now becoming addicted to tobacco.

Author Affiliations: Division of Hematology/Oncology, Feinberg School of Medicine, Northwestern University, and the
Robert H. Lurie Comprehensive Cancer Center, Chicago, Ill (Dr Patel); The Health Outcomes Research Group, Department of
Epidemiology and Biostatistics (Dr Bach) and Thoracic Oncology Service, Division of Solid Tumor Oncology, Department of
Medicine, Memorial Sloan-Kettering Cancer Center (Dr Kris) and Department of Medicine, Weill Medical College of Cornell
University (Dr Kris), New York, NY.

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