Cancer Etiology Branch (CEB)
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The Cancer Etiology Branch (CEB) supports research programs dealing with biological, chemical, and physical agents that are known or possible etiological factors or co-factors in cancer.  These research programs also address the control of these etiological agents and their associated diseases and with the contribution of the host genome, proteome and microbiome to the sensitivity of cells, tissues and organs to these agents. Studies supported by the Branch fall into two broad categories. Studies of Biological Carcinogenesis deal with biologic agents (primarily viruses and bacteria) as etiologic agents in malignancy, and include studies of mechanisms of oncogenesis and interactions of these agents with host cells. Studies of Chemical Carcinogenesis encompass studies of cancers caused or promoted by chemical or physical agents, acting separately or together, or in combination with biological agents, and their mechanisms of action, as well as basic studies to identify possible targets for preventive or therapeutic measures.

Program Areas

DNA and RNA Viruses in Carcinogenesis

Evidence suggests viruses and microbes contribute to the etiology of as much as 20% of human cancer, nd the Branch supports research that seeks to elucidate the role played by both DNA and RNA viruses in this process.  These include studies of the structure, infectious process, host immune and inflammatory response, and oncogenic mechanisms of viruses that play a known or suspected role in the carcinogenic process.  Research on human viruses and animal virus models including papilloma viruses (HPV), Epstein-Barr virus (EBV), cytomegalovirus (CMV), Adenoviruses (Ad), hepatitis viruses (HVB and HVC), Polyomaviruses (Py, SV40), and retroviruses are currently supported.  The etiology and etiological mechanisms of hepatocellular carcinoma and the role of the hepatitis virus in these processes is an area of particular Branch involvement.  Emerging areas of particular interest include the identification of new viruses or new roles for existing viruses, in cancer, and further studies of newly identified viruses, such as Merkel Cell carcinoma virus and XMRV, which have been recently linked to human cancer.

Chemical and Physical Carcinogenesis

The role of chemical and physical agents in cancer etiology and the need to understand the mechanisms by which they induce and promote cancer continues to be an important area of basic cancer research.  The Branch supports research that leads to the identification of chemical carcinogens, tumor initiators and promoters, and the characterization of their metabolism, toxicity, activation and deactivation pathways, mechanisms of action, as well as biochemical and molecular markers of chemical carcinogenesis.  Areas of particular interest include the applications of systems genetics and other emerging technologies to variations in carcinogen susceptibility.

HIV and AIDS-Associated Malignancies

While past and current progress in the understanding and treatment of Human Immunodeficiency virus (HIV) infection and  Acquired Immune Deficiency Syndrome (AIDS) has greatly improved patient survival, this increased survival has been coupled with the development of cancer at higher rates than that observed among the HIV/AIDS negative population.  The Branch supports investigations of the role of HIV and other viruses [HHV-8/KSHV), human papillomavirus (HPV), Epstein-Barr virus (EBV), and hepatitis C virus (HCV)] as etiologic agents of AIDS-associated cancers, and how their interactions affect carcinogenesis and progression.

Bacterial Carcinogenesis and the Role of the Microbiome

There steadily increasing evidence that indicating that bacteria play a role in the initiation and progression of cancer, particularly those, such as H. pylori, involving the gastrointestinal tract.  The Branch supports a variety of studies directed at determining the role and mechanism of action of cancer-associated bacterial species in colon and other human cancers, and their interactions with other etiologic agents.  This program also supports studies of the possible etiological role that changes in the microbiome, commensal bacteria, intestinal epithelial cell homeostasis, and the disregulated innate immune response, play in the development of gastrointestinal and other malignancies.