Carcinogenesis, Biomarkers & Epidemiology Program

Overview | Leaders | Members | Research | Publications | Activities

 

Program Overview

The Carcinogenesis, Biomarkers and Epidemiology (CBE) Program's mission is to conduct population studies that address new knowledge generated by the program on the causes and possible prevention of cancer. By elucidating the basis of risk, host response, and carcinogenic processes across the cancer spectrum (cancer development, early disease progression and survival), our goal is to understand and ameliorate cancer incidence, morbidity and mortality in the population. This mission is the predominant conceptual model around which the field of environmental cancer epidemiology has coalesced in recent years. We define environmental exposure broadly as that which occurs at the cellular level from exogenous and endogenous exposures, usually at the critical macromolecule, following the concept of the biologically effective dose that Perera and Weinstein (1) first proposed in 1982. Thus, an environmental exposure might be from an exogenous source, such as tobacco smoke, infectious agent, or diet, or an endogenous source, such as hormones or free radical production. The conceptual model further posits that genetic susceptibilities underlie every step from exposure to cancer and outcomes. Thus, nearly every research project in the Program involves the development, validation, and/or application of human cancer biomarkers, with a major focus on gene-environment interactions in populations.

Given this emphasis on gene-environment interactions in the CBE Program's research portfolio, acquired and inherited predispositions are central to most program member's activities. Acquired predisposition is measured by phenotypes (e.g. DNA damage, cytogenetic changes and tumor markers) as the cumulative effects of carcinogen exposure that will then have downstream effects. Behavior (e.g. tobacco smoking and smoking topography) is also included among acquired predispositions. The inherited traits of interest might have a high or low penetrance, and can predict either cancer risk or outcomes.

The Specific Aims are:

Aim 1:To foster an understanding for the mechanisms and pathways of carcinogenesis through laboratory studies that can be readily translated to population investigation and intervention.

Aim 2: To use information gained from carcinogenesis studies to foster the development of biomarkers and molecular epidemiology methods for assessing cancer risk and prevention.

Aim 3: To determine genetic risk factors, phenotypic markers, genotype-phenotype relationships and gene-environment interactions for persons at risk for cancer and cancer progression.

 

Perera, F. P. & Weinstein, I. B. (1982). Molecular epidemiology and carcinogen-DNA adduct detection: new approaches to studies of human cancer causation. J. Chronic. Dis. 35, 581-600.