Opportunity Information: Apply for PA 08 211
Apply for PA 08 211
- The National Institutes of Health in the education health sector is offering a public funding opportunity titled "Diet Induced Changes in Inflammation as Determinants of Colon Cancer (R21)" and is now available to receive applicants.
- Interested and eligible applicants and submit their applications by referencing the CFDA number(s): 93.393 Cancer Cause and Prevention Research 93.396 Cancer Biology Research 93.399 Cancer Control.
- This funding opportunity was created on Dec 5, 2008 and posted on Jul 18, 2008.
- Applicants must submit their applications by Sep 7, 2011. (Agency may still review applications by suitable applicants for the remaining/unused allocated funding in 2026.)
- Each selected applicant is eligible to receive up to $200,000.00 in funding.
- Eligible applicants include: Small businesses 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 Private institutions of higher education Public and State controlled 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) State governments.
- Other Eligible Applicants include the following Eligible Agencies of the Federal Government Hispanic serving Institutions Regional Organizations U.S. Territory or Possession.
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Opportunity Summary:
Diet Induced Changes in Inflammation as Determinants of Colon Cancer (R21) is a National Cancer Institute (NCI) funding opportunity announcement that aims to support early stage, exploratory research on how diet can shift inflammatory processes in ways that influence colon cancer risk. The main scientific emphasis is on identifying and characterizing diet driven changes in inflammation that either promote or protect against colon carcinogenesis. Rather than focusing broadly on diet and cancer associations, the opportunity is oriented toward mechanistic and translational questions about specific inflammatory mediators, how they are altered by dietary components, and how those changes could plausibly modify cancer risk at the level of colon cells and relevant biological pathways.
The FOA highlights three priority research directions. First, it encourages studies that map and define diet induced changes in anti-inflammatory and pro-inflammatory mediators that modulate colon cancer risk. This could include work that clarifies which signaling molecules, cytokines, lipid mediators, or related inflammatory pathways are influenced by particular dietary patterns or bioactive food components, and how those shifts affect processes like epithelial injury and repair, immune cell recruitment, and tumor promoting microenvironment changes. Second, it calls for research on genetic polymorphisms that modify an individuals response to specific bioactive food components in the context of colon cancer inhibition. In practical terms, this points to gene diet interaction research grounded in biology, where inherited variation could help explain why certain dietary constituents reduce risk for some people but not others, or why inflammatory responses to the same compound differ across genotypes. Third, the FOA seeks studies assessing the physiological effectiveness of dietary components by taking seriously real-world biological constraints such as achievable tissue concentrations, bioactivity, duration of exposure, stability in the gut environment, chemical form, and receptor binding affinity within inflammatory colonocytes. This is essentially a call to move beyond nominal dietary exposure and instead quantify what is actually present at the target site, in what form, for how long, and with what functional impact.
A key limitation is that the FOA explicitly does not support epidemiological studies based on diet related risks of colon cancer. Applications centered on observational diet-cancer correlations, population level association analyses, or similar epidemiologic designs are not responsive. The intent is to stimulate mechanistic, hypothesis generating, and development oriented projects that can clarify causal biology and inform later definitive studies, including work that could eventually translate into targeted dietary interventions or biomarker development tied to inflammatory mechanisms.
The mechanism used is the NIH Exploratory/Developmental Grant (R21), which is typically suited for early, high risk/high reward concepts, pilot studies, and foundational work needed to open new research directions. The award ceiling listed is $200,000, and cost sharing or matching is not required. The FOA notes that awards depend on the availability of funds and the number of meritorious applications received, so the number of awards is not pre-specified. The announcement also runs in parallel with a companion opportunity of identical scientific scope using the R01 mechanism (PA 08 210), which would be more appropriate for mature, fully developed projects with extensive preliminary data and a larger, longer research plan.
Eligibility is broad and includes small businesses, for-profit organizations (including those other than small businesses), nonprofit organizations with or without 501(c)(3) status (with the usual distinctions around higher education), public and private institutions of higher education, and state governments. Additional eligible applicants include certain federal government agencies, Hispanic serving institutions, regional organizations, and U.S. territories or possessions, as indicated in the eligibility information. The sponsoring agency is the National Institutes of Health, specifically NCI, and the program aligns with cancer cause and prevention research, cancer biology research, and cancer control categories (CFDA 93.393, 93.396, and 93.399).
Administratively, the opportunity is identified as PA 08 211, was posted July 18, 2008, and had an original and current closing date of September 7, 2011, with an archive date of October 8, 2011. The full announcement link provided is http://grants.nih.gov/grants/guide/pa-files/PA-08-211.html, and the NIH Office of Extramural Research webmaster contact is provided for access or linking issues (FBOWebmaster@OD.NIH.GOV).
Frequently Asked Questions (FAQs)
What is the "Diet Induced Changes in Inflammation as Determinants of Colon Cancer (R21)" funding opportunity?
This is a National Cancer Institute (NCI) funding opportunity announcement (FOA) that supports early-stage, exploratory research on how diet-driven changes in inflammation may influence colon cancer risk. The focus is on mechanistic and translational studies that explain how specific dietary components affect inflammatory mediators and related pathways in ways that could plausibly promote or protect against colon carcinogenesis.
Which agency is sponsoring this FOA?
The sponsoring agency is the National Institutes of Health (NIH), specifically the National Cancer Institute (NCI).
What is the FOA number for this opportunity?
The opportunity is identified as PA-08-211.
What grant mechanism does this FOA use?
This FOA uses the NIH Exploratory/Developmental Grant mechanism (R21), which is generally intended for early, high-risk/high-reward concepts, pilot studies, and developmental work that can open new research directions.
What is the main scientific emphasis of the FOA?
The main emphasis is on identifying and characterizing diet-driven changes in inflammation that either promote or protect against colon carcinogenesis. The FOA is oriented toward specific inflammatory mediators and biological mechanisms rather than broad associations between diet and cancer.
What types of research questions are most aligned with this FOA?
Research questions that fit best are mechanistic and translational, such as: which inflammatory signaling molecules are altered by specific dietary patterns or bioactive food components; how those changes affect colon epithelial injury/repair and immune cell recruitment; and how inflammation-related microenvironment shifts could modify colon cancer risk at the level of colon cells and relevant pathways.
What are the priority research directions highlighted in the FOA?
The FOA highlights three priorities: (1) mapping and defining diet-induced changes in anti-inflammatory and pro-inflammatory mediators that modulate colon cancer risk; (2) studying genetic polymorphisms that modify an individual's response to bioactive food components relevant to colon cancer inhibition (gene-diet interaction grounded in biology); and (3) assessing the physiological effectiveness of dietary components using real-world constraints such as achievable tissue concentrations, stability in the gut, chemical form, duration of exposure, and receptor binding affinity in inflammatory colon cells.
Does the FOA support studies that identify specific cytokines, lipid mediators, or signaling pathways influenced by diet?
Yes. One priority area explicitly encourages studies that clarify which signaling molecules, cytokines, lipid mediators, or related inflammatory pathways are influenced by particular dietary patterns or bioactive components, and how those shifts connect to colon cancer-relevant processes.
Does the FOA support gene-diet interaction research?
Yes, when it is focused on genetic polymorphisms that modify responses to specific bioactive food components in the context of colon cancer inhibition, with a clear biological rationale for how inherited variation influences inflammatory responses and cancer-related mechanisms.
What does the FOA mean by evaluating "physiological effectiveness" of dietary components?
It refers to studying dietary components in a way that reflects biological reality at the target site. This includes considering whether the relevant compound reaches the tissue in achievable concentrations, remains stable in the gut environment, exists in the correct chemical form, persists for a meaningful duration, binds receptors with sufficient affinity, and has measurable functional impact in inflammatory colon cells.
Are epidemiological studies responsive to this FOA?
No. The FOA explicitly does not support epidemiological studies based on diet-related risks of colon cancer. Applications centered on observational correlations, population-level association analyses, or similar epidemiologic designs are described as non-responsive.
If a project is mainly about diet-cancer associations in populations, is it a good fit?
No. The stated intent is not to fund broad association studies. The FOA is designed to stimulate mechanistic, hypothesis-generating, and development-oriented research that clarifies causal biology and supports future definitive studies.
What kind of outcomes is the FOA trying to enable for future work?
The FOA aims to generate mechanistic insights that could inform later definitive studies. It also notes the potential to eventually translate findings into targeted dietary interventions or biomarker development tied to inflammatory mechanisms.
What is the award ceiling for this R21 opportunity?
The award ceiling listed is $200,000.
Is cost sharing or matching required?
No. Cost sharing or matching is not required.
How many awards will be made under this FOA?
The number of awards is not pre-specified. Awards depend on the availability of funds and the number of meritorious applications received.
Is there a companion funding opportunity for more mature projects?
Yes. The announcement runs in parallel with a companion opportunity of identical scientific scope using the R01 mechanism (PA-08-210). The R01 is described as more appropriate for mature, fully developed projects with extensive preliminary data and a larger, longer research plan.
Who is eligible to apply?
Eligibility is broad and includes small businesses, for-profit organizations (including those other than small businesses), nonprofit organizations with or without 501(c)(3) status (with typical distinctions involving higher education), public and private institutions of higher education, and state governments. Additional eligible applicants include certain federal government agencies, Hispanic-serving institutions, regional organizations, and U.S. territories or possessions, as indicated in the eligibility information.
What research areas or program categories does this FOA align with?
The FOA aligns with cancer cause and prevention research, cancer biology research, and cancer control categories. It is associated with CFDA numbers 93.393, 93.396, and 93.399.
When was this FOA posted?
The FOA was posted on July 18, 2008.
What were the closing and archive dates listed for this FOA?
The original and current closing date listed is September 7, 2011, and the archive date is October 8, 2011.
Where can I find the full FOA text?
The full announcement is available at: http://grants.nih.gov/grants/guide/pa-files/PA-08-211.html
Who should be contacted for access or linking issues related to the FOA webpage?
The NIH Office of Extramural Research webmaster contact is provided for access or linking issues: FBOWebmaster@OD.NIH.GOV
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