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Last Updated: 11/03/17

Current Funding Opportunities

The Requests for Applications (RFAs) and Program Announcements (PAs) listed below communicate CDP’s current funding opportunities and research interests. CDP staff contacts and published notices are provided in the summary link for each opportunity. We encourage you to discuss your proposed research with a CDP program director before you submit an application. This page updates to reflect the active Funding Opportunities.

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Revision Applications for Validation of Biomarker Assays Developed Through NIH-Supported Research Grants (R01): PAR-17-003

Posted date: October 4, 2016; Expiration date: October 29, 2019
Application receipt dates: February 28, 2017; July 11, 2017; February 27, 2018; July 11, 2018; October 26, 2018; February 27, 2019; July 11, 2019; October 28, 2019, by 5:00 PM local time of applicant organization.

The purpose of this Funding Opportunity Announcement (FOA) is to accelerate the pace of translation of NCI-supported methods/assays/technologies (referred to as "assays") to the clinic. Specifically, the focus of this FOA is on the adaption and clinical validation of molecular/cellular/imaging markers (referred to as "markers" or "biomarkers") for cancer detection, diagnosis, prognosis, monitoring, and prediction of response to treatment, as well as markers for cancer control and prevention. Research applications may support acquisition of well-annotated specimens from NCI-supported or other clinical trials or observational cohorts/consortia for the purpose of clinical validation of the assay. Research projects proposed for this FOA encourage multi-disciplinary interaction among scientific investigators, assay developers, clinicians, statisticians and clinical laboratory staff. Clinical laboratory scientist(s) and statistical experts are highly encouraged to comprise integral parts of the application. This FOA is not intended to support early stage development of technology or the conduct of clinical trials, but rather the adaption and validation of assays to the point where they could be integrated into clinical trials as investigational assays/tools/devices.

CDP contact: Dr. Kelly Kim, 240-276-7811, kimke@mail.nih.gov

Integrating Biospecimen Science Approaches into Clinical Assay Development (U01): PAR-16-166

Posted date: April 5, 2016; Expiration date: June 23, 2018
Application receipt dates: June 22, 2016; February 13, 2017; October 11, 2017, by 5:00 PM local time of applicant organization.

This Funding Opportunity Announcement (FOA) will support extramural research to investigate and mitigate challenges facing clinical assay development due to tissue biopsy biospecimen preanalytical variability. The program will tie in with current efforts to optimize clinical biomarker assays utilized in NCI-sponsored clinical trials. Results from this research program will improve the understanding of how biopsy collection, processing, and storage procedures may affect all aspects of analytical performance for current and emerging clinical biomarkers, as well as expedite clinical biomarker assay development through the evidence-based standardization of biopsy handling practices. Critical information gained through these research awards may increase the reliability of clinical biomarker assays, reduce time requirements for assay development, and decrease assay failure during late-stage testing.

CDP contact: Dr. Abhi Rao, 240-276-5715, abhi.rao@mail.nih.gov

Assay Validation For High Quality Markers For NCI-Supported Clinical Trials: PAR-17-317 (UH2/UH3 Clinical Trial Not Allowed)

Reissue of PAR-15-095. Posted date: October 13, 2017; Expiration date: October 9, 2020.
Application receipt dates: February 14, 2018; July 10, 2018; October 8, 2018; February 13, 2019; July 10, 2019; October 8, 2019; February 13, 2020; July 10, 2020; October 8, 2020, by 5:00 PM local time of applicant organization.

This Funding Opportunity Announcement (FOA) is a phased initiative to improve the development of molecular diagnostics for use in NCI-supported clinical trials in cancer. This FOA includes, but is not limited to, the validation of prognostic, predictive or response markers for treatment and markers for cancer control or prevention trials. Applicants should have an assay that works in human samples and whose importance is well justified for development into a clinical assay.

CDP contact: Dr. Kelly Kim, 240-276-7811, kimke@mail.nih.gov

View the full FOA on Grants.NIH.Gov.

Assay Validation For High Quality Markers For NCI-Supported Clinical Trials: PAR-15-096 (UH3 Clinical Trials Not Allowed)

Reissue of PAR-15-096. Posted date: October 13, 2017; Expiration date: October 9, 2020.
Application receipt dates: February 14, 2018; July 10, 2018; October 8, 2018; February 13, 2019; July 10, 2019; October 8, 2019; February 13, 2020; July 10, 2020; October 8, 2020, by 5:00 PM local time of applicant organization.

Assays proposed for this FOA may be used to validate existing assays for use in other trials, observational studies or populations. Projects proposed for this FOA will require multi-disciplinary interaction and collaboration among scientific investigators, clinicians, statisticians and clinical laboratory scientists and staff. Clinical laboratory staff, technical and other needs must be an integral part of the application. This FOA is not intended to support trials that assess the clinical utility of a marker/assay but is intended to develop assays to the point where their clinical utility could be assessed in other trials.

CDP contact: Dr. Kelly Kim, 240-276-7811, kimke@mail.nih.gov

View the full FOA on Grants.NIH.Gov.

Bioengineering Technologies

The NIH bioengineering program supports basic, applied, and translational bioengineering research that addresses important biological or medical research problems.

CDP contact: Mr. Miguel Ossandon: 240-276-5714, ossandom@mail.nih.gov

Exploratory/Developmental Bioengineering Research Grants [EBRG]: PA-16-040 (R21)

Release/Posted Date: November 20, 2015; Expiration date: January 8, 2019
Application Receipt Dates: February 16, June 16, October 16

The EBRGs support early bioengineering research. EBRG applications may contain minimal or no preliminary data, and may propose hypothesis-driven, discovery-driven or design-directed research.

Bioengineering Research Grants [BRG]: PAR-16-242 (R01)

Posted Date: May 10, 2016; Expiration date: May 8, 2019 (renewal of PAR-13-137)
Application Receipt Dates: February 5, June 5, October 5

The BRGs support multi-disciplinary research performed in in a single laboratory or by multiple organizations. A BRG application may propose hypothesis-driven, discovery-driven, developmental, or design-directed research.

Bioengineering Research Partnerships [BRP]: PA-16-116 (U01)

Release/Posted Date: March 2, 2016; Expiration date: January 8, 2019
Application Receipt Dates: May 18, 2016, September 13, 2016, May 18, 2017, September 13, 2017, May 8, 2018, September 13, 2018

The BRPs support large basic, applied, and translational multi-disciplinary research performed by multiple organizations that applies an integrative approach, which includes bioengineering and biomedical/clinical components.

NCI Provocative Questions (PQ) Initiative

Identifying Perplexing Problems to Drive Progress Against Cancer

Submission Deadlines:

  • Applications due October 30, 2017, June 28, 2018, and October 30, 2018
  • Letter of Intent due 30 days before application due dates

Award Mechanisms: R01 and R21 awards for each Provocative Question (PQ)

Program Contact: Dr. Sean E. Hanlon (Associate Director, Office of the Director, Center for Strategic Scientific Initiatives, NCI) E-mail: hanlonse@mail.nih.gov

Provocative Question Specific Information for R01 & R21 Applications:

  • Research Answers to NCI’s Provocative Questions (R01)
    (RFA-CA-17-017)
    National Cancer Institute
    Application Receipt Date(s): June 28, 2017; October 30, 2017; June 28, 2018; October 30, 2018, by 5:00 PM local time of applicant organization. All types of applications allowed for this funding opportunity announcement are due on these dates. No late applications will be accepted for this Funding Opportunity Announcement.

  • Research Answers to NCI’s Provocative Questions (R21)
    (RFA-CA-17-018)
    National Cancer Institute

    Application Receipt Date(s): June 28, 2017; October 30, 2017; June 28, 2018; October 30, 2018, by 5:00 PM local time of applicant organization. All types of applications allowed for this funding opportunity announcement are due on these dates. No late applications will be accepted for this Funding Opportunity Announcement.

Pediatric PQ FOAs with a receipt date in November 2017:

https://grants.nih.gov/grants/guide/pa-files/PAR-16-218.html
https://grants.nih.gov/grants/guide/pa-files/PAR-16-217.html

Funding Opportunity Purpose:

The purpose of this Funding Opportunity Announcement is to support innovative research projects designed to solve specific problems and paradoxes in cancer research. “Provocative Questions” (PQs) are meant to challenge researchers to elucidate specific problems in key areas of cancer research that are important but have not received sufficient attention.

Some of these PQs stem from intriguing but older, neglected observations that have never been adequately explored. Other PQs are built on more recent findings that are perplexing or paradoxical, revealing important gaps in current knowledge. Finally, some PQs reflect problems that traditionally have been thought to be intractable but that now may be open to investigations using new strategies and recent technical advances.

The current issuance of the PQ Initiative includes an updated set of 12 PQs. Each research project proposed in response to this FOA must be focused on addressing one particular research problem defined by one specific PQ selected from the following list. Projects proposed to address specific PQs may use strategies that incorporate ideas and approaches from multiple disciplines, as appropriate. Transdisciplinary projects are encouraged as long as they serve the scientific focus of the specific PQ chosen. For more information, please visit: https://provocativequestions.nci.nih.gov/

The RFA links and all PQ intent statements and background info are available via this link: https://provocativequestions.nci.nih.gov/pq-funding-opportunity-information/current-rfas-and-pqs

PQ 1: What molecular mechanisms influence disease penetrance in individuals who inherit a cancer susceptibility gene?

Intent: Individuals who carry a mutation in a cancer susceptibility gene, for example individuals with Li-Fraumeni, Cowden, or Lynch Syndrome, have a dramatically increased risk over non-carriers of developing cancer. This Provocative Question calls for research to determine how the rate of disease penetrance is influenced by various life experiences such as environmental exposure, patient natural history (e.g., abnormal changes in hormone levels), or interactions with other genes/biological pathways. The intent of this question is to go beyond association studies, which identify factors that change disease penetrance in individuals with an inherited cancer susceptibility gene, and determine the mechanisms that explain how these changes influence disease occurrence. Mechanistic studies of events that either increase or decrease rates of penetrance are suitable for study. Preclinical or computational models may also be used to understand how disease penetrance may be altered.

Applications that do not explore issues presented in this Intent Statement will be considered nonresponsive to this Provocative Question.

PQ 2: How do variations in immune function caused by comorbidities or observed among different populations affect response to cancer therapy?

Intent: Although the immune system has the potential to detect and eliminate cancer, considerable variability in immune function exists among populations and in response to comorbidities. These variations may help to explain observed differences in response to cancer therapies among patients and different populations. This Provocative Question seeks applications that will identify and/or validate immune response variations among cancer patients (including tumor-associated immune responses and/or host immune responses) and investigate how these variations may positively or negatively affect response to cancer therapy. Successful applications might include mechanistic or epidemiological studies to investigate how population-based differences in immune traits (e.g., across such populations as racial/ethnic groups, age groups, and/or gender) can influence therapeutic outcomes. Furthermore, applications may seek to determine how comorbid conditions (e.g. obesity, heart disease, diabetes, etc.) may influence immune function and elucidate mechanism(s) by which this influence may affect therapeutic responses.

Applications that do not explore issues presented in this Intent Statement will be considered nonresponsive to this Provocative Question.

PQ 3: Do genetic interactions between germline variations and somatic mutations contribute to differences in tumor evolution or response to therapy?

Intent: Cancer is characterized by numerous genetic and epigenetic alterations occurring in both the germline and somatic (i.e., tumor) genomes. Independently, projects focused on characterizing the germline and tumor genomes have led to improved understanding of cancer etiology and biology that will be exceedingly valuable as starting points for the identification of prognostic, diagnostic and therapeutic markers as well as therapeutic targets for the development of new treatments. This Provocative Question seeks research that would integrate germline and somatic genetic data in a systematic manner to gain a comprehensive picture of how the genetics of both the person and the tumor interact to affect tumor evolution, progression, or response to therapy.

Applications that do not explore issues presented in this Intent Statement will be considered nonresponsive to this Provocative Question.

PQ 4: Can we develop tools to directly change the expression or function of multiple chosen genes simultaneously and use these tools to study the range of changes important for human cancer?

Intent: Progression of human cancers is driven by the simultaneous dysregulation of multiple genes and gene products. However, these changes are often studied in isolation or in experimental systems that are not amenable to multiple genetic or epigenetic perturbations. This Provocative Question calls for development of approaches and systems that enable simultaneous, sequential, and/or spatially controlled tuning of the expression or function of multiple chosen genes in cancer-relevant mammalian systems. Applications must be grounded in a context of human cancer, and successful applications should demonstrate that the proposed approach facilitates modulation and quantification of phenotypes relevant to human cancer progression and/or response to treatment, ideally within an in vivo or ex vivo system.

Applications that do not explore issues presented in this Intent Statement will be considered nonresponsive to this Provocative Question.

PQ 5: How does mitochondrial heterogeneity influence tumorigenesis or progression?

Intent: Mitochondria within one cell, among closely related cells, or between different individuals can display heterogeneity in mtDNA sequences, proteome, morphologic and spatial dynamics, and functional capacities. This Provocative Question asks researchers to propose mechanistic studies that will characterize how mitochondrial variation within individual tumor cells, among cells within tumor microenvironment(s), or in the same cell types from different individuals influences tumorigenesis or progression. Successful applications will examine how mitochondria vary over time and how they alter or contribute to tumor development, adaptation, stemness, phenotypic plasticity, resistance, invasion and metastasis. Research that examines whether mitochondrial heterogeneity can be used as a basis for disease monitoring, understanding response to therapy, or in the development of new therapies is also encouraged.

Applications that do not explore issues presented in this Intent Statement will be considered nonresponsive to this Provocative Question.

PQ 6: How do circadian processes affect tumor development, progression, and response to therapy?

Intent: Circadian processes, driven by natural 24-hour rhythms, maintain the internal clocks critical for physiological homeostasis and adapting to a fluctuating environment. On a molecular level, circadian processes are regulated by a core transcription-translation negative feedback loop that drives expression and oscillatory regulation of genes that coordinate processing information from both extrinsic (i.e., light/dark, wake/sleep) and intrinsic (i.e., nutrient/hormone/inflammatory) stimuli. This Provocative Question seeks research to understand the mechanisms by which circadian or other oscillatory processes, and the consequences of their disruption, influence cancer development and outcomes. Such influences likely involve interactions across multiple time scales and levels (molecular to organismal) and involve both circadian and other oscillatory processes. Applications that focus on one scale or bridge multiple scales are equally encouraged, as are applications from researchers across all cancer-related disciplines from cell biologists to biobehavioral and population scientists, oncologists, clinicians, translational scientists, and care givers. Understanding how circadian and other oscillatory processes influence cancer development, progression, and response to therapy should illuminate potential new avenues to manage or treat cancer.

Applications that do not explore issues presented in this Intent Statement will be withdrawn as scientifically nonresponsive to this Provocative Question.

PQ 7: How do cancer-specific subcellular pathognomonic structures develop, what is their function, and can they be a source of novel therapeutic targets?

Intent: Our current understanding of pathognomonic structures characteristic for cancers is limited. Pathologists are trained to recognize and classify cancers based on distinct features and patterns in cells and tissues, most routinely aided by stains and conventional microscopy. This provocative question seeks research applications that expand the concept of pathognomonic figures. Can technologies be advanced to reveal the existence of new pathognomonic forms or features at the subcellular scale or bridging multiple scales? Mechanistically, how are pathognomonic structures formed, what are their cancer biology dynamics and function, and how do they contribute to distinct cancer phenotypes? How might this information be leveraged to improve detection, diagnosis or develop new treatment strategies? One goal of the PQ7 is to encourage interdisciplinary science that fosters innovation and new insights on basic pathognomonic cancer biology and its utility to inform and advance strategies to advance our understanding of cancer biology on a subcellular level.

Applications that do not explore issues presented in this Intent Statement will be considered nonresponsive to this Provocative Question.

PQ 8: What are the predictive biomarkers for the onset of immune-related adverse events associated with checkpoint inhibition, and are they related to markers for efficacy?

Intent: Immune checkpoint inhibitors, including anti-cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) and anti-programmed cell death protein 1 (PD-1) or its ligand 1 (PD-L1) monoclonal antibodies (mAbs), enhance anti-tumor immune responses in multiple cancers through restoration of T-cell function. However, many patients treated with immune checkpoint inhibitors experience variable degrees of immune-related adverse events (irAEs) in diverse organ systems. If these irAEs are identified early, they can be managed properly. It has also been reported that clinical response to anti-CTLA-4 mAb is potentially associated with the presence of irAEs. This Provocative Question (PQ) invites research applications for identification and/or validation of mechanistic biomarkers for prediction of on- or post-treatment irAEs associated with therapies involving immune checkpoint inhibitors. This PQ also encourages unbiased evaluation of the relationship between biomarkers of irAEs and extended survival benefits in cancer patients treated with immune checkpoint inhibitor therapies. The ultimate goals of this PQ are to provide clinically-validated biomarkers that may inform clinical trial designs, and guide physicians to select and sequence therapies involving immune checkpoint inhibitors for the purpose of reducing or avoiding life-threatening irAEs in individual cancer patients.

Applications that do not explore issues presented in this Intent Statement will be considered nonresponsive to this Provocative Question.

PQ 9: Can we develop bifunctional small molecules that will couple oncoproteins or other cancer causing molecules of interest to inactivating processes such as degradation and achieve tissue-specific loss of function?

Intent: Proteolysis Targeting Chimeras, or PROTACs, are heterobifunctional small molecules that link targeted proteins to the E3 ubiquitin ligase system, leading to target protein degradation through the ubiquitin-proteasome system. This Provocative Question seeks to extend the concept of inactivating oncoproteins or cancer-causing molecules through the use of bifunctional molecules, defined as small molecules that include a ligand moiety specific for a target oncoprotein or cancer-causing protein, linked to a second moiety involved in protein inactivation (inactivation moiety). The ultimate goal of this PQ is identification and/or preclinical development of novel bifunctional molecules that lead to tumor-specific loss or inactivation of selected target proteins for therapeutic benefit. Studies that test this concept on currently “undruggable” targets are encouraged as are studies that use novel protein inactivation moieties. Responsive applications may focus on design of bifunctional molecules, and/or testing of the biological functions of new or existing bifunctional molecules.

Applications that do not explore issues presented in this Intent Statement will be considered nonresponsive to this Provocative Question.

PQ 10: How do microbiota affect the response to cancer therapies?

Intent: This Provocative Question seeks grant applications that use our increasing knowledge of the resident human microbiota to understand how these organisms or their secreted products affect cancer therapies. Approaches may include studies that focus on effects of the changing microbiota (i.e. their alteration of host barrier, metabolic, and immune functions) within an individual patient undergoing treatment or among different patients undergoing identical therapy but with different outcomes. Analogous studies in pre-clinical models are also invited. Key aspects of study might include either how the microbiota alter the composition, concentration, stability, or effectiveness of standard or experimental classes of therapies, or the identification and study of microbial regulatory mechanisms that mediate these changes.

Applications that do not explore issues presented in this Intent Statement will be considered nonresponsive to this Provocative Question.

PQ 11: Through what mechanisms do diet and nutritional interventions affect the response to cancer treatment?

Intent: This Provocative Question seeks grant applications that address how diet and nutritional interventions affect the response to cancer treatment, treatment-related adverse events, cancer prognosis and related health outcomes. All types of studies that serve to elucidate the mechanisms of how diet and nutrition effect cancer outcomes are encouraged, including clinical trials, observational studies, and mechanistic studies in animals and humans. Transdisciplinary research and studies which consider multidimensional and/or dynamic dietary patterns (where dynamism includes the timing of meals and circadian rhythms, as well as changing diets over the course of treatment and survival) are also encouraged. Research applications may examine the association of diet and nutritional interventions with a range of outcomes among cancer patients and survivors, but should also address the mechanisms (such as influence of the microbiome, metabolome, immunology, and epigenetics) by which these relationships occur. Proposed studies should take into account other known prognostic factors that may influence cancer and related outcomes, such as weight/body composition, activity levels, and other lifestyle factors.

Applications that do not explore issues presented in this Intent Statement will be considered nonresponsive to this Provocative Question.

PQ 12: What are the molecular and/or cellular mechanisms that underlie the development of cancer therapy-induced severe adverse sequelae?

Intent: While many acute toxicities can be adequately managed during cancer therapy (e.g., febrile neutropenia, acute nausea and vomiting) and will resolve once therapy has been completed (e.g., mucositis), there are other adverse sequelae that persist after completion of therapy and for which there are no effective management strategies. These include, but are not limited to, therapy-induced peripheral neuropathy, neurocognitive impairments, cardiovascular toxicity, pulmonary fibrosis, arthralgias, and immune system-related adverse events. This Provocative Question seeks research that will (1) identify novel mechanisms that induce such chronic sequelae, (2) apply the knowledge gained from understanding these mechanisms to facilitate design of new treatments (or approaches) that may decrease or reverse adverse cancer therapy effects, or (3) facilitate mechanism-based design of new cancer therapies that are expected to show decreased adverse effects when compared with existing therapies. Such studies may be performed in pre-clinical, non-clinical, and/or clinical settings. Successful applications must focus on adverse therapy related sequelae (whether immediate or delayed in onset) for which current management or treatment strategies are limited or ineffective.

Applications that do not explore issues presented in this Intent Statement will be considered nonresponsive to this Provocative Question.

FOR THE LATEST INFORMATION ABOUT NCI INITIATIVES, VISIT
Division of Extramural Activities, National Cancer Institute
http://deainfo.nci.nih.gov/funding.htm

National Institutes of Health
U.S. Department of Health and Human Services