Opportunity Information: Apply for PAR 16 227
Apply for PAR 16 227
- The HHS-NIH11 in the education, health sector is offering a public funding opportunity titled "The Role of Mobile Genetic Elements in Cancer (R01)" and is now available to receive applicants.
- Interested and eligible applicants and submit their applications by referencing the CFDA number(s): 93.396, 93.866,.
- This funding opportunity was created on May 05, 2016 and posted on May 05, 2016.
- Applicants must submit their applications by Sep 07, 2019. (Agency may still review applications by suitable applicants for the remaining/unused allocated funding in 2026.)
- Eligible applicants include: State governments, County governments, City or township governments, Special district governments, Independent school districts, Public and State controlled institutions of higher education, Native American tribal governments (Federally recognized), Public housing authorities/Indian housing authorities, Native American tribal organizations (other than Federally recognized tribal governments), Nonprofits having a 501(c)(3) status with the IRS, other than institutions of higher education, Nonprofits that do not have a 501(c)(3) status with the IRS, other than institutions of higher education, Private institutions of higher education, For profit organizations other than small businesses, Small businesses, Others (see text field entitled Additional Information on Eligibility for clarification).
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Opportunity Summary:
The funding opportunity titled "The Role of Mobile Genetic Elements in Cancer (R01)" (Funding Opportunity Number PAR-16-227) is a National Institutes of Health (NIH) research grant program under the U.S. Department of Health and Human Services. It uses the standard NIH R01 mechanism, meaning it is intended to support hypothesis-driven, investigator-initiated research projects that can define clear biological mechanisms and generate substantial, generalizable knowledge. The scientific focus is on mobile genetic elements, especially retroelements, and how their expression and activity are controlled in cancer, as well as how their activity may shape tumor behavior over time.
A central theme of the announcement is that many cancers show activation of mobile genetic elements, but the field still lacks a strong mechanistic understanding of what drives that activation and what it actually does to tumors. The FOA highlights two major categories of mobile elements: long terminal repeat (LTR) elements, which include human endogenous retroviruses (HERVs), and non-LTR retroelements, particularly LINE-1 (also called L1). LINE-1 is emphasized because it remains one of the few autonomously active retrotransposons in humans and has been observed to be active in a range of tumor types. Even with evidence of activity, it remains uncertain whether somatic LINE-1 insertions meaningfully contribute to cancer development and progression, for example by creating genetic diversity within a tumor (tumor heterogeneity) or by producing adaptive changes that help cancer cells grow, survive stress, metastasize, or resist therapy.
The FOA also points to the unclear role of HERVs in cancer. HERV sequences are remnants of ancient viral infections embedded in the human genome; while most are no longer capable of forming infectious viruses, they can still be transcribed or produce proteins or regulatory RNAs under certain conditions. In cancer, epigenetic disruption and other regulatory changes can lead to HERV expression, but the consequences are not fully understood. This opportunity encourages projects that go beyond simply cataloging expression and instead test how HERV activity might influence cancer-related processes, including effects on gene regulation, immune signaling, cellular identity, and other pathways relevant to transformation and tumor progression.
In practical terms, the NIH is asking for applications that investigate the mechanisms that regulate when, where, and how mobile genetic elements become expressed and active during cell transformation and in established tumors. That includes studying the cellular and molecular controls that normally silence or restrain these elements, and how those controls are altered in cancer. The FOA is especially interested in work that connects mobile element activity to real functional outcomes in tumors, such as whether mobile element activation drives or reflects genomic instability, whether new insertions or element-derived transcripts create subclones with distinct properties, and whether these processes contribute to cancer evolution over time, including under treatment pressure. A major motivation is to close a knowledge gap between observed retroelement activity in tumors and a causal understanding of its impact on disease trajectory and treatment response.
The opportunity is categorized under Education and Health and is associated with CFDA numbers 93.396 and 93.866. Eligibility is broad and includes many types of U.S. organizations: state, county, city, and special district governments; public and state-controlled institutions of higher education; private institutions of higher education; independent school districts; federally recognized Native American tribal governments and other tribal organizations; public housing authorities/Indian housing authorities; nonprofit organizations with or without 501(c)(3) status (as long as they are not institutions of higher education, where applicable); for-profit organizations other than small businesses; and small businesses. The sponsoring agency is listed as HHS-NIH11. The FOA was posted on May 5, 2016, and the listed closing date was September 7, 2019 (with the original and current closing dates matching in the provided record). The award ceiling and expected number of awards are not specified in the supplied source data.
Overall, this R01 opportunity is designed to push the field toward mechanistic, experimentally grounded answers about mobile genetic elements in cancer. It seeks studies that explain how retroelements such as LINE-1 and HERVs are regulated during tumorigenesis and that directly test how their activation or insertional activity contributes to tumor heterogeneity, cancer evolution, and therapeutic response, with the broader aim of clarifying whether these elements are merely biomarkers of dysregulation or active participants in the biology that makes cancers aggressive and hard to treat.
Frequently Asked Questions (FAQs): The Role of Mobile Genetic Elements in Cancer (R01) - PAR-16-227
What is the title of this funding opportunity?
The funding opportunity is titled "The Role of Mobile Genetic Elements in Cancer (R01)".
What is the Funding Opportunity Number (FOA number)?
The Funding Opportunity Number is PAR-16-227.
Which federal agency sponsors this opportunity?
This opportunity is sponsored by the National Institutes of Health (NIH) under the U.S. Department of Health and Human Services (HHS). The sponsoring agency is listed as HHS-NIH11.
What type of grant mechanism does this program use?
This opportunity uses the standard NIH R01 mechanism, which is intended to support hypothesis-driven, investigator-initiated research projects designed to define clear biological mechanisms and generate substantial, generalizable knowledge.
What scientific topic does this FOA focus on?
The FOA focuses on mobile genetic elements, especially retroelements, and investigates how their expression and activity are controlled in cancer and how that activity may shape tumor behavior over time.
What problem or knowledge gap is this FOA trying to address?
The FOA highlights that many cancers show activation of mobile genetic elements, but there is still a lack of strong mechanistic understanding of what drives that activation and what it does to tumors. The program aims to close the gap between observed retroelement activity in tumors and a causal understanding of how it impacts disease trajectory and treatment response.
Which categories of mobile genetic elements are specifically highlighted?
The FOA highlights two major categories:
- Long terminal repeat (LTR) elements, including human endogenous retroviruses (HERVs)
- Non-LTR retroelements, particularly LINE-1 (L1)
Why is LINE-1 (L1) emphasized in this opportunity?
LINE-1 is emphasized because it remains one of the few autonomously active retrotransposons in humans and has been observed to be active in a range of tumor types. However, it is still uncertain whether somatic LINE-1 insertions meaningfully contribute to cancer development and progression.
What cancer-related outcomes related to LINE-1 does the FOA mention?
The FOA discusses uncertainty about whether somatic LINE-1 insertions contribute to cancer by generating genetic diversity within a tumor (tumor heterogeneity) or by producing adaptive changes that help cancer cells grow, survive stress, metastasize, or resist therapy.
What does the FOA say about the role of HERVs in cancer?
The FOA states that the role of HERVs in cancer remains unclear. HERV sequences are remnants of ancient viral infections embedded in the human genome; most are no longer capable of forming infectious viruses, but they can still be transcribed or produce proteins or regulatory RNAs under certain conditions. In cancer, epigenetic disruption and other regulatory changes can lead to HERV expression, but the consequences are not fully understood.
Does the FOA encourage projects that only catalog mobile element expression?
No. The FOA encourages projects that go beyond simply cataloging expression and instead test how mobile element activity influences cancer-related processes.
What kinds of functional effects of HERV activity are mentioned as areas of interest?
The FOA mentions interest in whether HERV activity may influence cancer-related processes including:
- Gene regulation
- Immune signaling
- Cellular identity
- Other pathways relevant to transformation and tumor progression
What types of mechanistic questions does the NIH want applicants to investigate?
The FOA requests applications that investigate the mechanisms regulating when, where, and how mobile genetic elements become expressed and active during cell transformation and in established tumors. This includes studying the cellular and molecular controls that normally silence or restrain these elements and how those controls are altered in cancer.
How does this FOA connect mobile element activity to tumor evolution?
The FOA is especially interested in studies that connect mobile element activity to functional outcomes such as whether new insertions or element-derived transcripts create subclones with distinct properties, and whether these processes contribute to cancer evolution over time, including under treatment pressure.
What tumor-related processes are specifically referenced as potential consequences of mobile element activation?
The FOA references several possible consequences, including:
- Whether activation drives or reflects genomic instability
- Whether new insertions or transcripts contribute to tumor heterogeneity
- Whether mobile element activity influences disease trajectory and treatment response
Is the FOA trying to determine whether mobile elements are biomarkers or drivers?
Yes. A stated broader aim is to clarify whether mobile genetic elements are primarily biomarkers of dysregulation or active participants in the biology that can make cancers more aggressive and difficult to treat.
What program area/category is this opportunity listed under?
The opportunity is categorized under Education and Health.
What CFDA numbers are associated with this funding opportunity?
The FOA is associated with CFDA numbers 93.396 and 93.866.
Who is eligible to apply?
Eligibility is broad and includes many types of U.S. organizations, including:
- State governments
- County governments
- City or township governments
- Special district governments
- Public and state-controlled institutions of higher education
- Private institutions of higher education
- Independent school districts
- Federally recognized Native American tribal governments
- Other Native American tribal organizations
- Public housing authorities / Indian housing authorities
- Nonprofit organizations with or without 501(c)(3) status (as long as they are not institutions of higher education, where applicable)
- For-profit organizations other than small businesses
- Small businesses
Is this opportunity limited to academic institutions?
No. The eligibility list includes a wide range of entities beyond higher education, including government entities, tribal governments and organizations, nonprofits, for-profits (other than small businesses), and small businesses.
When was this FOA posted?
The FOA was posted on May 5, 2016.
What is the listed closing date for this opportunity?
The listed closing date in the provided record is September 7, 2019. The original and current closing dates match in the supplied source data.
Is the award ceiling provided?
No. The supplied source data does not specify an award ceiling.
Is the expected number of awards provided?
No. The supplied source data does not specify the expected number of awards.
What kinds of studies does this FOA seem designed to promote?
This R01 opportunity is designed to push the field toward mechanistic, experimentally grounded studies of mobile genetic elements in cancer. It emphasizes research that explains how retroelements such as LINE-1 and HERVs are regulated during tumorigenesis and that directly tests how their activation or insertional activity contributes to tumor heterogeneity, cancer evolution, and therapeutic response.
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