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Evaluating genetic, clinical, and environmental risk factors for second primary lung cancer

Principal Investigator
Name
Summer Han
Degrees
PhD
Institution
Stanford University
Position Title
Assistant Professor
Email
About this CDAS Project
Study
NLST (Learn more about this study)
Project ID
NLST-498
Initial CDAS Request Approval
Apr 13, 2019
Title
Evaluating genetic, clinical, and environmental risk factors for second primary lung cancer
Summary
Lung cancer (LC) is a leading cause of cancer deaths in the U.S. The widespread adoption of computed tomography (CT) screening enables the early detection of lung cancer and is expected to increase the number of long-term LC survivors. Recent studies show that LC survivors have a high risk of developing second primary lung cancer (SPLC), the incidence of which is around 4-6 times higher than that of initial primary lung cancer (IPLC) in the general population. While national lung screening guidelines have been established for IPLC by the U.S. Preventive Services Task Force (USPSTF), no such consensus guidelines exist for LC survivors who are exposed to a high risk of SPLC. Furthermore, the factors that contribute to the development of SPLC have not yet been established. Our long-term goal is to reduce the overall LC mortality in the U.S. population by focusing on SPLC. The overall objectives of this application are to identify the genetic, clinical, and environmental determinants for SPLC, to assess an individual’s risk of developing SPLC, and to evaluate efficient lung screening strategies for SPLC to help inform the development of consensus screening guidelines for LC survivors.
Aims

Our specific aims are to identify clinical, environmental risk factors for for SPLC and build a statistical model for predicting SPLC risk based on environmental, clinical and genetic risk factors including smoking, radiation exposure, family history of lung cancer, COPD (Chronic Obstructive Pulmonary Disease), race, tumor characteristics of IPLC (tumor size, stage, extent, histology, age at diagnosis, etc.), and polygenic risk score.

Collaborators

Rayjean Hung, Chris Amos, David Christiani, Iona Cheng, Neal Freedman

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