Cancer Etiology Study Section – CE
Ends after February/March 2023 review meetings. This study section was evaluated as part of CSR’s ENQUIRE process which functions to align study sections with advances in science. Learn more about ENQUIRE.
The Cancer Etiology Study Section reviews grant application related to the causal agents, processes, and cells involved in early events in carcinogenesis. The emphasis is on linking disciplines of chemistry and pathology to the etiology of cancer in animal models, with more translational studies in human cells.
The Cancer Etiology Study Section reviews grant applications related to the causal agents, processes, and cells involved in early events in carcinogenesis. Focus areas include the role of DNA damage, DNA replication stress and DNA repair defects in carcinogenesis. The emphasis is on linking disciplines of chemistry, pathology, and molecular genetics to the etiology of cancer modeled in human cells and animals.
The List of Reviewers lists all present, whether standing members or temporary, to provide the full scope of expertise present on that date. Lists are posted 30 days before the meeting and are tentative, pending any last minute changes.
Review Dates
Topics
- DNA damage/repair and chromosomal stability in carcinogenesis
- Repair of DNA adducts/damage caused by carcinogens
- Chemical and environmental carcinogenesis, including endogenous and exogenous compounds that modulate early events in carcinogenesis
- Chemical stress, mitochondrial stress, oxidative stress, free radicals, reactive species that modulate early events in carcinogenesis
- Non-HIV/AIDs viral carcinogenesis
Shared Interests
There are shared interests with Cancer Genetics (CG) in studies of genomic instability, epigenetics and telomeres. Applications aiming to investigate genomic instability and telomeres with a focus on DNA damage repair and environment interactions may be assigned to CE. Applications that focus on genetic and epigenetic aspects of genomic instability and telomere regulation may be assigned to CG.
There are shared interests with Biochemical and Cellular Oncogenesis (BCO) in the in the investigation of post-translational modifications. Applications that focus on post-translational modification processes that contribute to cellular transformation and early oncogenesis may be reviewed in BCO. Applications that focus on post-translational modifications in the context of DNA damage/repair may be reviewed in CE.
There are shared interests with Cancer Prevention Study Section (CPSS) related to chemical carcinogenesis and diet in oxidative stress. Applications aiming to investigate how chemical carcinogenesis and oxidative stress initiate carcinogenesis may be assigned to CE. Applications aiming to determine how to prevent carcinogenesis using diet, antioxidants or other chemical interventions may be assigned to CPSS.
There are shared interests with Radiation Therapeutics and Biology (RTB) related to DNA damage and repair, basic molecular biology of radiation-induced genomic instability and oxidative stress. Applications that focus on the role of DNA damage associated with initiation of carcinogenesis may be assigned to CE. Applications that focus on DNA damage responses and DNA repair associated with UV and radiation carcinogenesis may be assigned to RTB.
There are shared interests with Systemic Injury by Environmental Exposure (SIEE) related to environmental and pharmacological induced toxicity. Applications aiming to investigate environmental or xenobiotic factors contributing the initiation of carcinogenesis may be assigned to CE. Applications where the focus is on environmental or xenobiotic factors that contribute to other chronic diseases in addition to cancer may be assigned to SIEE.
There are shared interests in genome stability and molecular mechanisms of DNA damage and repair with Molecular Genetics (MG). Applications that emphasize the study of aberrant molecular genetic mechanisms to understand the process of carcinogenesis are reviewed in CE. Applications that use cancer-associated alterations to understand normal noncarcinogenic molecular genetic mechanisms are reviewed in MG.
