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Ann Schwartz, PhD
AnnSchwartzPhD (Researcher (Verified) )| Communities: All Cancers | Answers: 8 |
| Member Since: Jun. 2012 |
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Professional Statement
Dr. Schwartz is the Deputy Director and Executive Vice President for Research and Academic Affairs at the Karmanos Cancer Institute and a Professor in the Department of Oncology at Wayne State University School of Medicine.
In 2009, she served as Interim President and CEO of the Karmanos Cancer Institute. Dr. Schwartz has been continuously funded by the National Cancer Institute for 20 years, has over 115 publications, and serves as a reviewer for numerous journals and NIH grants, including a recent term on Subcommittee A, the parent committee for Comprehensive Cancer Center Support Grants. Her lung cancer studies have focused on familial aggregation of lung cancer, producing the first estimates of lung cancer risk to relatives in African Americans, evaluation of candidate genes in smoking and estrogen metabolism pathways, and gene discovery using admixture mapping in African Americans. Most recently she has published in the area of inflammation and lung cancer risk, showing 1) increased risk of lung cancer with a history of chronic obstructive lung diseases collectively, and emphysema and chronic bronchitis separately, 2) decreased risk associated with NSAID use, 3) variation in risk and survival associated with SNPs in inflammatory genes, and 4) decreased survival associated with COX-2 but not with EGFR expression in lung tumors in both white and African Americans. Dr. Schwartz has also conducted gene expression studies in prostate cancer using custom array panels for a study of racial disparities in prostate cancer aggressiveness. She is an active participant in two lung cancer consortiums, the Genetic Epidemiology of Lung Cancer Consortium (GELCC) and the International Lung Cancer Consortium (ILCCO), and a pancreatic cancer gene discovery consortium (PacGene).
In 2009, she served as Interim President and CEO of the Karmanos Cancer Institute. Dr. Schwartz has been continuously funded by the National Cancer Institute for 20 years, has over 115 publications, and serves as a reviewer for numerous journals and NIH grants, including a recent term on Subcommittee A, the parent committee for Comprehensive Cancer Center Support Grants. Her lung cancer studies have focused on familial aggregation of lung cancer, producing the first estimates of lung cancer risk to relatives in African Americans, evaluation of candidate genes in smoking and estrogen metabolism pathways, and gene discovery using admixture mapping in African Americans. Most recently she has published in the area of inflammation and lung cancer risk, showing 1) increased risk of lung cancer with a history of chronic obstructive lung diseases collectively, and emphysema and chronic bronchitis separately, 2) decreased risk associated with NSAID use, 3) variation in risk and survival associated with SNPs in inflammatory genes, and 4) decreased survival associated with COX-2 but not with EGFR expression in lung tumors in both white and African Americans. Dr. Schwartz has also conducted gene expression studies in prostate cancer using custom array panels for a study of racial disparities in prostate cancer aggressiveness. She is an active participant in two lung cancer consortiums, the Genetic Epidemiology of Lung Cancer Consortium (GELCC) and the International Lung Cancer Consortium (ILCCO), and a pancreatic cancer gene discovery consortium (PacGene).
Professional Info
Credential: PhD
Research interests:
Epidemiologic studies of cancer risk and progression
Focus on genetic and molecular epidemiology
Hospital or other affiliation: Karmanos Cancer Institute, Wayne State University School of Medicine
City: Detroit
State: MI
Zip: 48201
AnnSchwartzPhD Activities
Incidence rates of lung cancer in different populations reflect variation in the proportion of smokers, dose and duration of smoking, family history, history of COPD, and history of exposures associated with increased lung cancer risk, such as asbestos exposure, and exposures potentially associated with reduced risk, such as NSAIDs or diet. Smoking patterns 30-40 years ago are most relevant to lung cancer rates today given the long latency period from first exposure to diagnosis. African Americans tend to smoke fewer cigarettes per day and start smoking at an older age than whites, but the proportion of African American men who smoke has been higher in the past than the proportion of white men who smoke contributing to higher lung cancer rates today in African American men. There are also reports that demonstrate increased susceptibility in African Americans given a family history of cancer. Additional research is needed to better identify what other environmental exposures and genetic variation contribute to racial disparities in lung cancer incidence. Research is now underway to identify genetic changes associated with risk specifically in African Americans, comparable to work that has already been conducted in white populations.
New answer by AnnSchwartzPhD (Researcher (Verified))
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9 months ago
A family history of lung cancer in a first-degree relative is associated with a 1.5 to 2-fold increased risk of developing lung cancer after taking into consideration shared smoking patterns among family members. This association is seen for all histologic types of lung cancer, and among smokers and never smokers. Slightly higher risks associated with a family history have been shown when the relative is diagnosed with lung cancer under age 50, in African Americans, and when multiple relatives are affected. These findings suggest that there is inherited genetic susceptibility to lung cancer. While a “lung cancer gene” has not yet been identified, reported family history is used clinically to help determine risk. The magnitude of risk associated with having a family history of lung cancer is similar to that associated with familial aggregation of other cancers including breast, colon, and prostate cancer.
New answer by AnnSchwartzPhD (Researcher (Verified))
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9 months ago
80-90% of all lung cancers are attributable to smoking.
New answer by AnnSchwartzPhD (Researcher (Verified))
1
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9 months ago
Smoking is the strongest risk factor for lung cancer. All types of lung cancer are associated with smoking and while there are studies that distinguish gradations of risk due to smoking by histologic type, smoking is the strongest risk factor for both small cell and non-small cell lung cancer.
New answer by AnnSchwartzPhD (Researcher (Verified))
1
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9 months ago
Cigarette smoking increases risk of both lung cancer and chronic obstructive lung disease (COPD) which is defined by airflow limitation from both emphysema and chronic bronchitis. In addition, COPD is an independent risk factor for lung cancer. Once COPD is diagnosed, risk of developing lung cancer increases 2 to 3-fold, even among never smokers. Lung cancer occurrence is linked differentially to specific COPD phenotypes, with highest risk associated with a history of emphysema. A family history of COPD also increases risk of lung cancer development approximately 2-fold. The question remains as to whether COPD is in the causal pathway in the development of lung cancer or a variation in manifestation from the same exposures. Studies that incorporate clinical, inflammatory, genetic and imaging parameters are being conducted that will be of particular interest in furthering lung cancer risk assessment in the presence of COPD.
New answer by AnnSchwartzPhD (Researcher (Verified))
1
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9 months ago
A number of studies have been conducted examining whether aspirin and NSAIDs are associated with reduced risk of lung cancer. Of the studies conducted to date, results have been mixed showing either reduced lung cancer risk or no change in lung cancer risk with NSAID use. These studies are observational in nature and have methodologic limitations that include the potential misclassification in the measures of dose and duration of use, dependence on recall of past use, and limited availability of a detailed smoking history to include in the analyses. Large, prospective studies are needed to better understand the impact of NSAID use on lung cancer risk.
New answer by AnnSchwartzPhD (Researcher (Verified))
1
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9 months ago
Exposure to environmental tobacco smoke (ETS) or second hand smoke is associated with an approximately 30% increased risk of lung cancer. Estimates of risk have come from observational studies where accurate measurement of the extent and timing of ETS exposure is often difficult, but results have been consistent. In addition, studies have shown tobacco metabolites in the serum and urine in children demonstrating exposure to ETS. Both high levels of serum cotinine, a metabolite of nicotine in tobacco smoke, and urinary 4-(mehtylnirosamino)-1-(3-pyridyl)-1-butanol, a biomarker of second hand smoke exposure, have been measured in children. ETS exposure also contributes to increased risk of other lung diseases such as asthma and lower respiratory infections.
New answer by AnnSchwartzPhD (Researcher (Verified))
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9 months ago
Over the last decade, non-small cell lung cancer (NSCLC) has been further described by mutational profiling. A number of the identified mutations are seen more often in never smokers than smokers with NSCLC. Epidermal growth factor receptor (EGFR) mutations and anaplastic lymphoma kinase (ALK) gene rearrangements most often occur in never smokers with adenocarcinoma of the lung. Some literature suggests that KRAS mutations tend to be seen more often in smokers with NSCLC than in never smokers. These mutations tend to occur independently; rarely are they found in the same tumor. Small molecule inhibitors are currently available or under development to molecularly target these and other mutations.
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9 months ago
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