Diet, Epigenetic Events, and Cancer Prevention (R01) | Apply Online

Frequently Asked Questions (FAQs): Diet, Epigenetic Events, and Cancer Prevention (R01) - PA-07-175

1) What is the focus of Funding Opportunity PA-07-175?

PA-07-175 supports NIH research on how diet, specific dietary factors, and dietary supplements influence epigenetic biology in ways that may reduce or increase cancer risk. The emphasis is on linking nutritional exposures to measurable epigenetic changes and then to cancer-relevant biological outcomes.

2) What type of grant mechanism is used for this opportunity?

This opportunity uses the NIH R01 mechanism, which is intended for full-scale, hypothesis-driven research projects.

3) What kinds of studies are encouraged (clinical vs. preclinical)?

The announcement supports both clinical and preclinical studies, as long as the work clarifies plausible biological pathways connecting diet-related exposures to epigenetic events and cancer-relevant consequences.

4) What epigenetic mechanisms are specifically mentioned?

The FOA highlights epigenetic mechanisms including DNA methylation and histone post-translational modifications, along with related epigenetic processes tied to cancer prevention and cancer development.

5) What does the FOA mean by moving beyond diet-cancer associations?

Rather than stopping at observational links between diet and cancer, the FOA prioritizes projects that map a biologically plausible chain from nutritional exposure to a measurable epigenetic change and then to outcomes such as tumor incidence, tumor behavior, or cancer-relevant cellular changes.

6) What kinds of outcomes or biological endpoints does NIH want to see connected to epigenetic changes?

The FOA points to outcomes such as tumor incidence, tumor behavior, and cancer-relevant cellular changes. It also highlights cancer-relevant processes including carcinogen metabolism, cell division, cellular differentiation, and apoptosis.

7) Are dietary supplements included within the scope of this opportunity?

Yes. The scope explicitly includes diet, specific dietary factors, and dietary supplements, particularly where they can be tied to specific epigenetic events relevant to cancer prevention or development.

8) What is the role of cross-disciplinary collaboration in this FOA?

A major emphasis is stronger cross-disciplinary work between nutrition scientists and epigenetics researchers. Competitive applications are expected to integrate expertise across these areas to study bioactive food components and connect them to cancer-relevant epigenetic events.

9) What are examples of cancer-relevant processes highlighted in the announcement?

Examples named in the FOA include carcinogen metabolism, cell division, cellular differentiation, and apoptosis.

10) Which NIH institutes are noted as having particular interests within this FOA?

The National Institute on Alcohol Abuse and Alcoholism (NIAAA) and the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) are called out for particular interests within the overall scope.

11) What specific topics is NIAAA especially interested in?

NIAAA is especially interested in studies examining chronic alcohol consumption and its impacts on one-carbon metabolism related factors (S-adenosylmethionine (SAM), betaine, and folate), and how changes in these factors may relate to DNA methylation patterns and cancer.

12) Why is chronic alcohol consumption relevant to epigenetics in this FOA?

The FOA reflects the idea that long-term alcohol intake can disrupt methyl-donor availability and methylation capacity, potentially altering DNA methylation and epigenetic regulation in ways that could influence carcinogenesis.

13) What specific topics is NIDDK especially interested in?

NIDDK highlights interest in normal and neoplastic conditions of the gastrointestinal tract and related organs, focusing on how epigenetic mechanisms affect core cellular behaviors such as division, differentiation, and apoptosis.

14) Are gastrointestinal (GI) tissues and related organs a good fit for this opportunity?

Yes. The FOA specifically notes NIDDK interest in GI tract and related organs, especially where the project examines epigenetic control of fundamental tissue biology and tumor-relevant transitions.

15) Is this FOA intended for pilot projects only?

No. The R01 mechanism is described as supporting full-scale, hypothesis-driven research projects rather than small pilot efforts alone.

16) Are there related NIH opportunities for smaller or earlier-stage studies?

Yes. The FOA is part of a coordinated set of opportunities with the same scientific scope offered through additional mechanisms: an R03 (small grant) and an R21 (exploratory/developmental grant).

17) Is cost sharing or matching required?

No cost sharing or matching requirement is indicated in the information provided.

18) When was this funding opportunity posted?

The opportunity was posted on December 15, 2006.

19) How do submission or receipt dates work for this FOA?

The FOA used multiple receipt dates, and applicants were expected to submit according to NIH standard cycles and the dates listed in the full announcement during the active period.

20) Who is eligible to apply?

Eligibility is broad and includes many types of domestic organizations, including higher education institutions (public and private), state and local governments, tribal governments and tribal organizations, nonprofits (with and without 501(c)(3) status), for-profit organizations, and small businesses, among others.

21) Are foreign institutions eligible to apply?

Yes. Foreign institutions are explicitly eligible, allowing international applicants and collaborations to compete for support.

22) Which agency is offering this opportunity?

The agency is the National Institutes of Health (NIH).

23) What are the CFDA programs associated with this FOA?

The CFDA programs associated with the announcement include alcohol research programs and cancer cause, prevention, and biology research: 93.273, 93.393, and 93.396.

24) What kinds of projects are considered especially aligned with the overall intent of the FOA?

Projects that rigorously connect diet-related exposures to specific epigenetic alterations and then to cancer-relevant biological consequences are strongly aligned. The FOA encourages designs that combine strong nutritional assessment or intervention expertise with state-of-the-art epigenetic measurement and cancer biology.

25) Does the FOA treat epigenetic changes as sufficient on their own?

No. The FOA emphasizes establishing clearer, evidence-based linkages between dietary exposures, epigenetic signatures (such as methylation patterns), and cancer outcomes or tumor characteristics, rather than treating epigenetic changes as purely descriptive findings.