Opportunity Information: Apply for PA 08 140

  • The National Institutes of Health in the education environment health sector is offering a public funding opportunity titled "In Utero Exposure to Bioactive Food Components and Mammary Cancer Risk (R01)" and is now available to receive applicants.
  • Interested and eligible applicants and submit their applications by referencing the CFDA number(s): 93.113 Environmental Health 93.393 Cancer Cause and Prevention Research 93.396 Cancer Biology Research.
  • This funding opportunity was created on Dec 5, 2008 and posted on Apr 10, 2008.
  • Applicants must submit their applications by May 7, 2011. (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 Nonprofits that do not have a 501(c)(3) status with the IRS, other than institutions of higher education Nonprofits having a 501(c)(3) status with the IRS, other than institutions of higher education Others (see text field entitled Additional Information on Eligibility for clarification) Small businesses Private institutions of higher education Public and State controlled institutions of higher education State governments.
  • Other Eligible Applicants include the following Eligible Agencies of the Federal Government Non domestic (non U.S.) Entities (Foreign Organizations) Regional Organizations U.S. Territory or Possession.
Apply for PA 08 140

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Opportunity Summary:

The NIH funding opportunity PA 08 140, titled "In Utero Exposure to Bioactive Food Components and Mammary Cancer Risk (R01)," supports preclinical research aimed at clarifying how exposures during pregnancy can shape breast cancer risk later in life. Sponsored by the National Cancer Institute (NCI) in partnership with the National Institute of Environmental Health Sciences (NIEHS) and the Office of Dietary Supplements (ODS), the FOA is built around the idea that the fetal environment is a critical window of susceptibility. The central goal is to understand how a developing mammary gland responds to in utero exposure to bioactive dietary compounds and certain environmental chemicals, and how those early-life exposures may reprogram biological pathways in ways that either raise or lower mammary cancer susceptibility in adulthood.

Scientifically, the FOA is looking for innovative, mechanistic studies that connect specific prenatal exposures to measurable downstream changes, including altered hormonal and growth factor signaling, shifts in gene expression, and lasting epigenetic modifications. While there is broad evidence that diet can influence cancer risk and that some exposures may be protective, the announcement highlights major gaps: which exact nutrients or food components matter most, where they act in the body, what doses are relevant, and how timing during gestation changes outcomes. On the risk side, it also points to environmental agents suspected of contributing to mammary cancer development, including mycotoxins, heterocyclic amines, and endocrine-active environmental chemicals. For these agents, the FOA emphasizes that the field still needs clearer answers about dose-response relationships, precise windows of susceptibility, and the underlying biological mechanisms linking prenatal exposure to later tumor outcomes.

A major feature of this announcement is its encouragement to use high-throughput and systems-level tools to move the science forward. Applicants are urged to incorporate modern genomic, epigenomic, proteomic, and metabolomic approaches to map how prenatal dietary or chemical exposures can leave long-lasting molecular signatures that influence adult breast cancer susceptibility. The expectation is that these kinds of data-rich approaches will reveal pathways and biomarkers that cannot be captured by narrower, single-endpoint studies, and will help identify causal mechanisms rather than simple correlations. Ultimately, the program is framed as a path toward evidence-based maternal dietary intervention strategies designed to reduce breast cancer risk in offspring, grounded in rigorous preclinical model research.

In terms of funding structure, this FOA uses the NIH R01 research project grant mechanism and runs in parallel with a companion announcement (PA 08 141) that supports smaller, exploratory R21 projects with the same scientific scope. The R01 mechanism is intended for more mature projects with substantial aims, allowing investigators to conduct longer and more comprehensive studies. The maximum project period is five years, and while there is no strict dollar cap for the R01 budget, applicants are expected to request an amount that fits the real needs of the proposed work. The research plan length follows the PHS398 format, with a 25-page limit for the Research Plan section (Items 2-5), including figures and tables.

Eligibility is broad and includes a wide range of domestic and non-domestic organizations. Eligible applicants include public and state-controlled institutions of higher education, private institutions of higher education, nonprofits (including those with and without 501(c)(3) status), for-profit organizations other than small businesses, small businesses, state governments, U.S. territories or possessions, regional organizations, foreign organizations, and eligible federal agencies. On the investigator side, any individual with the necessary expertise and resources may serve as PD/PI, and the NIH specifically notes that individuals from underrepresented racial and ethnic groups and individuals with disabilities are encouraged to apply. The FOA also allows multiple PDs/PIs on a single application, which can be useful for interdisciplinary projects that combine nutrition science, toxicology, developmental biology, omics technologies, and cancer biology.

The application policies are relatively flexible: applicants may submit more than one proposal as long as each is scientifically distinct. Resubmissions are allowed, but they must include an introduction that directly addresses prior peer-review critiques. Renewals are also permitted, which supports longer-term programs of research where ongoing mechanistic work is needed to build on earlier findings. The announcement notes that the number of awards depends on available funds and the quality and volume of applications received, a standard NIH approach that ties funding decisions to both budget conditions and peer-review outcomes.

Administratively, the opportunity was posted April 10, 2008, with a closing date of May 7, 2011, and an archive date of June 7, 2011. It is associated with multiple CFDA program areas reflecting its cross-cutting focus, including environmental health and cancer cause, prevention, and biology research (CFDA 93.113, 93.393, 93.396). Overall, PA 08 140 is best understood as a targeted effort to push the field beyond general claims that "diet matters" or "chemicals matter" by funding well-designed preclinical studies that pinpoint when, how, and through what molecular pathways prenatal exposures alter mammary cancer risk across the life course.

FAQs: NIH PA-08-140 - In Utero Exposure to Bioactive Food Components and Mammary Cancer Risk (R01)

What is NIH PA-08-140?

PA-08-140 is an NIH funding opportunity announcement titled "In Utero Exposure to Bioactive Food Components and Mammary Cancer Risk (R01)." It supports preclinical research that examines how exposures during pregnancy can influence mammary (breast) cancer susceptibility later in life.

What is the main purpose of this funding opportunity?

The central goal is to clarify how the fetal environment, as a critical window of susceptibility, shapes later mammary cancer risk. The FOA focuses on how in utero exposure to bioactive dietary components and certain environmental chemicals can reprogram biological pathways in ways that raise or lower cancer susceptibility in adulthood.

Which NIH institutes or offices sponsor this opportunity?

The FOA is sponsored by the National Cancer Institute (NCI), in partnership with the National Institute of Environmental Health Sciences (NIEHS) and the Office of Dietary Supplements (ODS).

What type of research does this FOA support?

This FOA supports innovative, mechanistic, preclinical studies that connect specific prenatal exposures to measurable downstream biological changes linked to mammary cancer outcomes later in life.

What does "preclinical" mean in the context of this FOA?

Based on the FOA description, the emphasis is on preclinical model research designed to uncover causal mechanisms and molecular pathways, rather than clinical trials or observational human studies.

What kinds of prenatal exposures are of interest?

The FOA highlights two broad exposure categories during gestation: (1) bioactive dietary compounds (including nutrients or food components), and (2) certain environmental chemicals suspected to influence mammary cancer risk.

Which environmental agents are specifically mentioned?

The FOA cites environmental agents suspected of contributing to mammary cancer development, including mycotoxins, heterocyclic amines, and endocrine-active environmental chemicals.

What specific scientific questions or gaps is the FOA trying to address?

The announcement points to major knowledge gaps, including: which specific nutrients or food components matter most, where and how they act in the body, what doses are relevant, and how timing during gestation changes outcomes. For environmental agents, it emphasizes the need for clearer dose-response relationships, precise windows of susceptibility, and underlying biological mechanisms linking prenatal exposure to later tumor outcomes.

What kinds of biological changes or endpoints does the FOA expect applicants to study?

The FOA is interested in downstream changes that can be measured and mechanistically linked to prenatal exposures, including altered hormonal and growth factor signaling, shifts in gene expression, and lasting epigenetic modifications.

Does the FOA encourage systems biology or high-throughput approaches?

Yes. A major feature is the encouragement to use high-throughput and systems-level tools, including genomic, epigenomic, proteomic, and metabolomic approaches, to map long-lasting molecular signatures from prenatal exposures.

Why does the FOA emphasize data-rich approaches like omics?

The FOA frames these approaches as a way to identify pathways and biomarkers that may be missed by single-endpoint studies, and to help establish causal mechanisms rather than simple correlations.

How does this FOA connect to prevention or intervention?

The program is positioned as a pathway toward evidence-based maternal dietary intervention strategies intended to reduce breast cancer risk in offspring, grounded in rigorous preclinical mechanistic research.

What grant mechanism is used for PA-08-140?

This FOA uses the NIH R01 Research Project Grant mechanism, which is intended for more mature projects with substantial aims and longer, more comprehensive studies.

Is there a related or companion funding opportunity?

Yes. The FOA runs in parallel with a companion announcement, PA-08-141, which supports smaller, exploratory R21 projects with the same scientific scope.

What is the maximum project period for an R01 under this FOA?

The maximum project period is five years.

Is there a strict budget cap for this R01?

No strict dollar cap is stated for the R01 budget. Applicants are expected to request an amount appropriate to the actual needs of the proposed work.

What is the research plan page limit?

The research plan follows the PHS398 format, with a 25-page limit for the Research Plan section (Items 2-5), including figures and tables.

Which organizations are eligible to apply?

Eligibility is broad and includes many domestic and non-domestic organization types, including: public and state-controlled institutions of higher education, private institutions of higher education, nonprofits (with or without 501(c)(3) status), for-profit organizations other than small businesses, small businesses, state governments, U.S. territories or possessions, regional organizations, foreign organizations, and eligible federal agencies.

Are foreign (non-U.S.) organizations eligible?

Yes. Foreign organizations are explicitly listed among eligible applicants.

Who is eligible to serve as the PD/PI?

Any individual with the necessary expertise and resources may serve as PD/PI. The FOA specifically encourages applications from individuals from underrepresented racial and ethnic groups and individuals with disabilities.

Can an application include multiple PDs/PIs?

Yes. The FOA allows multiple PDs/PIs on a single application, supporting interdisciplinary approaches.

What kinds of interdisciplinary teams might fit this FOA?

The FOA indicates that projects may benefit from combining expertise in areas such as nutrition science, toxicology, developmental biology, omics technologies, and cancer biology.

Can an applicant submit more than one application?

Yes. Applicants may submit more than one proposal as long as each application is scientifically distinct.

Are resubmissions allowed?

Yes. Resubmissions are allowed, but they must include an introduction that directly addresses prior peer-review critiques.

Are renewals allowed?

Yes. Renewals are permitted, which can support longer-term programs of mechanistic research building on earlier findings.

How many awards will NIH make under this FOA?

The FOA indicates that the number of awards depends on available funds and the quality and volume of applications received.

When was this opportunity posted, and what were the key dates?

The announcement was posted on April 10, 2008. The closing date was May 7, 2011, and the archive date was June 7, 2011.

Which CFDA program areas are associated with this FOA?

The opportunity is associated with multiple CFDA areas reflecting its cross-cutting focus, including CFDA 93.113, 93.393, and 93.396.

What makes PA-08-140 different from broader "diet and cancer" research?

The FOA is framed as a targeted effort to move beyond general statements that diet or chemicals matter, by funding well-designed preclinical studies that pinpoint when, how, and through what molecular pathways prenatal exposures alter mammary cancer risk across the life course.

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