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 permanent 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.
The membership panel is a list of chartered members only.
- 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
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 Molecular Oncogenesis (MONC) in studies of post-translational modifications such as ubiquitylation or sumoylation. Applications that investigate post-translational modification of components of DNA damage/repair may be assigned to CE. Applications aiming to investigate post-translational modification processes that contribute to cellular transformation and early oncogenesis may be assigned to MONC.
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 with Molecular Genetics A (MGA) and Molecular Genetics B (MGB) in genome stability and molecular mechanisms of human DNA damage and repair. Applications aiming to investigate molecular genetic mechanisms contributing to carcinogenesis should be assigned to CE. Applications aiming to investigate normal, noncarcinogenic molecular genetic mechanisms may be assigned to MGA or MGB.
There are shared interests with Arthritis, Connective Tissue and Skin (ACTS) in skin interactions with the environment, skin carcinogenesis, melanoma, and UV radiation. Applications that focus on DNA damage and repair mechanisms in skin cell transformation and neoplasia may be assigned to CE. Applications that focus on cellular factors and signaling cascades involved in skin response to UV and photobiology may be assigned to ACTS.