Opportunity Information: Apply for PA 07 069
Apply for PA 07 069
- The National Institutes of Health in the education health sector is offering a public funding opportunity titled "Mechanisms of Alcohol Associated Cancers (R01)" and is now available to receive applicants.
- Interested and eligible applicants and submit their applications by referencing the CFDA number(s): 93.273 Alcohol Research Programs 93.393 Cancer Cause and Prevention Research.
- This funding opportunity was created on Dec 5, 2008 and posted on Nov 20, 2006.
- Applicants must submit their applications by Multiple Receipt Dates See Link to Full Announcement for details.. (Agency may still review applications by suitable applicants for the remaining/unused allocated funding in 2026.)
- Eligible applicants include: For profit organizations other than small businesses Public and State controlled institutions of higher education Native American tribal governments (Federally recognized) Independent school districts Small businesses Nonprofits that do not have a 501(c)(3) status with the IRS, other than institutions of higher education State governments City or township governments Private institutions of higher education Special district governments Public housing authorities/Indian housing authorities Native American tribal organizations (other than Federally recognized tribal governments) County governments Others (see text field entitled Additional Information on Eligibility for clarification) Nonprofits having a 501(c)(3) status with the IRS, other than institutions of higher education.
- Foreign institutions are eligible to apply. Eligible agencies of the Federal Government can apply. Faith based or community based organizations can apply.
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Opportunity Summary:
The Mechanisms of Alcohol Associated Cancers (R01) opportunity (Funding Opportunity Number PA-07-069) is a National Institutes of Health (NIH) Funding Opportunity Announcement led by the National Institute on Alcohol Abuse and Alcoholism (NIAAA) in partnership with the National Cancer Institute (NCI) and the NIH Office of Dietary Supplements (ODS). Its central goal is to fund full-scale research projects that explain, in clear molecular and biochemical terms, how chronic alcohol consumption contributes to the initiation and progression of cancer. The program is specifically aimed at building a more complete mechanistic picture of alcohol-related carcinogenesis by encouraging investigators to use integrative, state-of-the-art approaches rather than focusing on a single isolated pathway.
The scientific scope centers on cancers for which alcohol is a recognized or suspected risk factor across multiple organ sites, including the oral cavity, pharynx, larynx, esophagus, stomach, large intestine (colon/rectum), liver, and breast. Applications are expected to move beyond simple epidemiologic association and instead clarify how alcohol exposure produces cellular and tissue changes that promote malignant transformation, tumor growth, and related processes. The FOA highlights the importance of studying alcohol metabolism and downstream damage, especially the role of acetaldehyde, a reactive and toxic alcohol metabolite that can form DNA adducts and contribute to mutagenesis. It also calls out cytochrome P450 2E1 (CYP2E1), an enzyme induced by alcohol that can generate reactive oxygen species and increase oxidative stress, potentially leading to DNA damage, lipid peroxidation, and altered signaling environments that favor cancer development.
In addition to direct genotoxic and oxidative mechanisms, the announcement emphasizes broader biological systems that alcohol can disrupt in ways that may increase cancer risk. One highlighted area is angiogenesis and tumor-supportive microenvironment changes, including the involvement of vascular endothelial growth factor (VEGF), a key driver of blood vessel formation that can help tumors grow and spread. Another major area is alcohol-related immune impairment, since long-term alcohol use can weaken immune surveillance and modify inflammatory signaling, which may reduce the body’s ability to eliminate abnormal cells early or may foster chronic inflammation that supports tumorigenesis. The FOA also points to alcohol-induced disruption of nutrient and methyl-donor metabolism, naming S-adenosylmethionine (SAMe), folate, betaine, iron, and vitamin A. These metabolic and micronutrient pathways are closely tied to DNA synthesis and repair, epigenetic regulation through methylation, oxidative balance, and tissue differentiation; when dysregulated, they can create conditions that allow precancerous changes to accumulate or persist.
From a funding mechanism standpoint, this FOA uses the NIH Research Project Grant (R01), which is intended for more mature, hypothesis-driven projects with substantial scope, well-developed aims, and strong preliminary rationale. The announcement notes that it runs in parallel with a companion FOA of identical scientific scope that uses the R21 Exploratory/Developmental mechanism (PA-06-270). In practical terms, that parallel structure signals that NIH was seeking both exploratory early-stage ideas (R21) and larger, more definitive mechanistic studies (R01) in the same topic area, with this specific listing focused on the R01 pathway.
Administratively, the opportunity is categorized as discretionary funding and uses the standard grant instrument. It falls under CFDA numbers 93.273 (Alcohol Research Programs) and 93.393 (Cancer Cause and Prevention Research), reflecting the joint alcohol-and-cancer focus. There is no cost sharing or matching requirement. The posting date listed is November 20, 2006, and the announcement uses multiple receipt dates rather than a single deadline, meaning applicants were expected to apply on standard NIH cycles or specified rolling dates referenced in the full announcement. The program is now archived (archive date April 5, 2009), but the summary captures what the FOA supported during its active period.
Eligibility is broad and includes many organization types across the public, private, nonprofit, and for-profit sectors. Eligible applicants include public and private institutions of higher education, nonprofit organizations (including those with and without 501(c)(3) status, with some distinctions), small businesses, independent school districts, and multiple levels of government (state, county, city/township, special district), as well as tribal governments and tribal organizations. Importantly, the eligibility statement explicitly allows foreign institutions to apply, allows eligible federal agencies to apply, and indicates that faith-based and community-based organizations may apply as well. The administering agency is NIH, and the full announcement was hosted on the NIH grants guide site.
Overall, the opportunity is best understood as an NIH initiative to push the field toward mechanistic clarity on how long-term alcohol exposure drives cancer across diverse tissues, using modern technologies and integrative designs that connect alcohol metabolism, cellular damage pathways, immune and microenvironment effects, and nutrition-related metabolic disruptions into coherent, testable models of carcinogenesis.
FAQs: Mechanisms of Alcohol Associated Cancers (R01) - PA-07-069
What is the Mechanisms of Alcohol Associated Cancers (R01) funding opportunity?
It is a National Institutes of Health (NIH) Funding Opportunity Announcement (FOA) that supported full-scale R01 research projects focused on explaining, in molecular and biochemical terms, how chronic alcohol consumption contributes to the initiation and progression of cancer. The FOA number is PA-07-069.
Which NIH institutes and offices lead and partner on this FOA?
The FOA is led by the National Institute on Alcohol Abuse and Alcoholism (NIAAA), in partnership with the National Cancer Institute (NCI) and the NIH Office of Dietary Supplements (ODS).
What is the central scientific goal of this program?
The central goal is to build a more complete mechanistic picture of alcohol-related carcinogenesis by funding integrative, state-of-the-art studies that clarify how alcohol exposure produces cellular and tissue changes that promote malignant transformation, tumor growth, and related processes.
Is this FOA focused on epidemiology or mechanism?
The scientific emphasis is mechanistic. Applications were expected to move beyond simple epidemiologic association and instead explain causal pathways and biological processes linking chronic alcohol consumption to cancer initiation and progression.
Which cancer sites are within scope?
The FOA highlights cancers where alcohol is a recognized or suspected risk factor across multiple organ sites, including the oral cavity, pharynx, larynx, esophagus, stomach, large intestine (colon/rectum), liver, and breast.
What kinds of research approaches does the FOA encourage?
The FOA encourages integrative, state-of-the-art approaches rather than studies limited to a single isolated pathway. The intent is to connect multiple mechanisms into coherent, testable models of alcohol-related carcinogenesis.
What role does alcohol metabolism play in the FOA's scientific priorities?
Alcohol metabolism and downstream damage are emphasized as key mechanistic areas. The FOA specifically highlights acetaldehyde, a reactive and toxic metabolite, as well as alcohol-induced enzymatic pathways that can create damaging cellular environments.
Why is acetaldehyde specifically called out?
Acetaldehyde is noted as a reactive and toxic alcohol metabolite that can form DNA adducts and contribute to mutagenesis, making it a plausible driver of cancer-related genetic damage.
What is CYP2E1 and why is it relevant to alcohol-associated cancers?
Cytochrome P450 2E1 (CYP2E1) is an enzyme induced by alcohol. The FOA notes that CYP2E1 can generate reactive oxygen species and increase oxidative stress, potentially leading to DNA damage, lipid peroxidation, and altered signaling that may favor cancer development.
Does the FOA include oxidative stress and DNA damage mechanisms?
Yes. Oxidative stress is a highlighted theme, including reactive oxygen species generation, DNA damage, lipid peroxidation, and downstream signaling changes that may contribute to carcinogenesis.
Does the FOA address tumor microenvironment or angiogenesis?
Yes. The FOA emphasizes angiogenesis and tumor-supportive microenvironment changes, including the role of vascular endothelial growth factor (VEGF), a key driver of blood vessel formation that can support tumor growth and spread.
How does immune function fit into the FOA's scope?
Alcohol-related immune impairment is explicitly highlighted. The FOA notes that long-term alcohol use can weaken immune surveillance and alter inflammatory signaling, potentially reducing early elimination of abnormal cells or fostering chronic inflammation that supports tumorigenesis.
Are nutrition and methyl-donor pathways considered within scope?
Yes. The FOA points to alcohol-induced disruption of nutrient and methyl-donor metabolism and names several pathways and factors tied to DNA synthesis/repair and epigenetic regulation.
Which specific nutrients or metabolites are named in the FOA?
The FOA specifically names S-adenosylmethionine (SAMe), folate, betaine, iron, and vitamin A as relevant to alcohol-related disruptions that may influence cancer risk.
Why are SAMe, folate, and betaine mentioned in a cancer mechanism FOA?
These factors are closely tied to methyl-donor availability and methylation processes involved in epigenetic regulation, as well as pathways supporting DNA synthesis and repair. The FOA highlights that disruption of these systems may create conditions that allow precancerous changes to accumulate or persist.
What grant mechanism does this FOA use?
This FOA uses the NIH Research Project Grant (R01) mechanism, which is intended for more mature, hypothesis-driven projects with substantial scope, well-developed aims, and strong preliminary rationale.
Is there a companion opportunity for exploratory projects?
Yes. The FOA notes a companion announcement with identical scientific scope using the R21 Exploratory/Developmental mechanism (PA-06-270). This parallel structure indicates NIH interest in both exploratory early-stage concepts (R21) and larger mechanistic studies (R01).
What type of funding is this categorized as?
The opportunity is categorized as discretionary funding and uses the standard grant instrument.
What CFDA numbers are associated with this FOA?
The FOA is associated with CFDA 93.273 (Alcohol Research Programs) and 93.393 (Cancer Cause and Prevention Research), reflecting its joint alcohol-and-cancer focus.
Is cost sharing or matching required?
No. The FOA states there is no cost sharing or matching requirement.
When was this FOA posted, and is it still active?
The posting date listed is November 20, 2006. The FOA is archived, with an archive date of April 5, 2009, meaning it is no longer active as described in the summary.
Did the FOA have a single deadline or multiple receipt dates?
It uses multiple receipt dates rather than a single deadline. Applicants were expected to apply on standard NIH cycles or specified rolling dates referenced in the full announcement.
Who is eligible to apply?
Eligibility is broad and includes a wide range of organization types across public, private, nonprofit, and for-profit sectors, including institutions of higher education, nonprofit organizations (with and without 501(c)(3) status, with distinctions), small businesses, independent school districts, and multiple levels of government.
Are tribal governments or tribal organizations eligible?
Yes. The eligibility statement includes tribal governments and tribal organizations.
Are foreign institutions eligible to apply?
Yes. The eligibility statement explicitly allows foreign institutions to apply.
Can U.S. federal agencies apply?
Yes. The eligibility statement indicates that eligible federal agencies may apply.
Are faith-based and community-based organizations eligible?
Yes. The eligibility statement indicates that faith-based and community-based organizations may apply.
Which agency administers this opportunity?
The administering agency is NIH, and the full announcement was hosted on the NIH Grants Guide site.
What kind of projects fit best under this R01 FOA?
Projects that are mature, hypothesis-driven, and designed to provide mechanistic clarity on how long-term alcohol exposure drives cancer across tissues, ideally integrating alcohol metabolism (including acetaldehyde and CYP2E1-related effects), cellular damage pathways, immune and microenvironment effects (including angiogenesis/VEGF), and nutrition-related metabolic disruptions into coherent models.
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