H. LEE MOFFITT CANCER CENTER AND RESEARCH INSTITUTE HOSPITAL, INC. - Florida Company Profile

DVHKP4N619V9

1X4B9

2025-12-05

2024-12-06

2002-04-18

1X4B9

Active

Non-Manufacturer

2024-12-06

2029-12-06

2025-12-05

REBECCA NICKLESON

1073339412

2024-12-02

View on NPI website

JOANNA C WEISS

EVP, CHIEF FINANCIAL OFFICER

8137451188

332B00000X - Durable Medical Equipment & Medical Supplies

Yes

+1 813-745-4673

36C24823N0028

View Award on USAspending website

AWARD

DELIVERY ORDER

48000.00

48000.00

48000.00

Department of Veterans Affairs

2022-10-01

PATHOLOGY CONSULTATIONS

621111: OFFICES OF PHYSICIANS (EXCEPT MENTAL HEALTH SPECIALISTS)

Q515: MEDICAL- PATHOLOGY

75N92019F00074

View Award on USAspending website

AWARD

DELIVERY ORDER

-82308.77

-82308.77

-82308.77

Department of Health and Human Services

2019-06-03

PRODUCTION ASSISTANCE FOR CELLULAR THERAPIES (PACT)- CELL PROCESSING FACILITIES CELL MANUFACTURING AND PROCESS DEVELOPMENT SERVICES FOR PCT0025-01: FVIII TCR-ENGINEERED TREG CELL PRODUCT

541712: RESEARCH AND DEVELOPMENT IN THE PHYSICAL, ENGINEERING, AND LIFE SCIENCES (EXCEPT BIOTECHNOLOGY)

AN12: HEALTH R&D SERVICES; HEALTH CARE SERVICES; APPLIED RESEARCH

75N92019F00036

View Award on USAspending website

AWARD

DELIVERY ORDER

-30868.55

-30868.55

-30868.55

Department of Health and Human Services

2018-12-03

PRODUCTION ASSISTANCE FOR CELLULAR THERAPIES (PACT)- CELL PROCESSING FACILITIES CELL MANUFACTURING AND PROCESS DEVELOPMENT SERVICES FOR PCT0005-02: CRYOPRESERVATION TECHNICAL STUDY

541712: RESEARCH AND DEVELOPMENT IN THE PHYSICAL, ENGINEERING, AND LIFE SCIENCES (EXCEPT BIOTECHNOLOGY)

AN12: HEALTH R&D SERVICES; HEALTH CARE SERVICES; APPLIED RESEARCH

2025-05-12

View on USAspending

Department of Health and Human Services

MYC-ALARMIN AXIS AS A NOVEL THERAPEUTIC VULNERABILITY IN MYELOFIBROSIS - PROJECT SUMMARY MYELOFIBROSIS (MF) IS A HEMATOLOGIC MALIGNANCY THAT IS CHARACTERIZED BY CONSTITUTIONAL SYMPTOMS, SPLENOMEGALY, BONE MARROW (BM) FIBROSIS, AND HIGH RISK OF TRANSFORMATION TO ACUTE MYELOID LEUKEMIA (AML). MF IS AMONG THE MOST AGGRESSIVE CHRONIC MYELOID NEOPLASMS, WITH A MEDIAN OVERALL SURVIVAL (OS) LESS THAN 4 YEARS. SOMATIC MUTATIONS IN THE JAK2, CALR, AND MPL GENES ARE COMMON IN ~85% OF MF PATIENTS, AND PRECLINICAL STUDIES HAVE SHOWN THAT THESE MUTATIONS RESULT IN CONSTITUTIVE ACTIVATION OF THE JAK/STAT PATHWAY, LEADING TO CHRONIC INFLAMMATION AND BM FIBROSIS. ACCORDINGLY, THE FDA HAS APPROVED THREE JAK2 INHIBITORS, RUXOLITINIB, FEDRATINIB, AND PACRITINIB, BASED ON THEIR CLINICAL IMPROVEMENTS IN CONSTITUTIONAL SYMPTOMS, SPLENOMEGALY AND OS. HOWEVER, A SUBSTANTIAL FRACTION OF MF PATIENTS LACK JAK2-ACTIVATING MUTATIONS. MOREOVER, JAK2-ACTIVATING MUTATIONS PERSIST IN PATIENTS UNDERGOING JAK2 INHIBITOR THERAPIES AND A SUBGROUP OF PATIENTS HAVE SUBOPTIMAL RESPONSE TO JAK2 INHIBITORS, UNDERSCORING THE URGENT NEED FOR DEVELOPING NEW THERAPEUTIC STRATEGIES TO IMPROVE CLINICAL OUTCOMES. MYC IS A TRANSCRIPTION FACTOR THAT CONTROLS CELL PROLIFERATION, SURVIVAL, AND METABOLISM. ALTHOUGH MYC PLAYS IMPORTANT ONCOGENIC ROLES IN MYELOID MALIGNANCIES SUCH AS AML, ITS ROLE IN THE MF PATHOGENESIS IS UNKNOWN. NOTABLY, OUR RECENT STUDIES REVEALED THAT MYC COPY NUMBER GAIN FREQUENTLY OCCURS IN MF PATIENTS AND THAT THIS IS ASSOCIATED WITH INCREASED LEVELS OF MYC PROTEIN EXPRESSION IN PATIENT BM CELLS. IMPORTANTLY, WE HAVE SHOWN THAT ACTIVATION OF MYC EXPRESSION IN MOUSE HEMATOPOIETIC STEM CELLS (HSCS) IS SUFFICIENT TO PROVOKE MF INDEPENDENT OF JAK2, CALR, AND MPL MUTATIONS, AND THAT THIS REQUIRES UPREGULATION OF S100A9, AN ALARMIN OR DANGER ASSOCIATED MOLECULAR PATTERNS (DAMPS) PROTEIN THAT PLAYS PIVOTAL ROLES IN INFLAMMATION AND INNATE IMMUNITY. ACCORDINGLY, THE MYC-S100A9 AXIS UNDERLIES COMPLEX NETWORK OF INFLAMMATORY SIGNALING THAT INVOLVES VARIOUS HEMATOPOIETIC CELL TYPES IN THE BM NICHE. FINALLY, WE DISCOVERED THAT MYC ALSO INDUCES EXPANSION OF MESENCHYMAL STROMAL CELLS (MSCS) THAT ARE KNOWN AS MYOFIBROBLASTS CONTRIBUTING TO THE MF PATHOGENESIS. THESE FINDINGS SUPPORT THE HYPOTHESES THAT ACTIVATION OF MYC-ALARMIN PATHWAY DRIVES MF INDEPENDENT OF JAK2/CALR/MPL MUTATIONS AND THAT INHIBITING MYC OR ITS TARGET ALARMINS WILL IMPROVE CLINICAL OUTCOMES IN MF PATIENTS HAVING INCREASED MYC EXPRESSION. TO TEST THESE HYPOTHESES, WE WILL ASSESS THE PRECLINICAL ACTIVITY OF PHARMACOLOGIC AGENTS TARGETING THE MYC-S100A9 AXIS IN MF AND DETERMINE THE MECHANISMS OF MYC-DIRECTED UPREGULATION OF S100A9 (AIM 1). FURTHER, WE WILL ASSESS THE ROLES OF MYC-S100A9 CIRCUIT IN ACTIVATION AND EXPANSION OF MYOFIBROBLASTS AND THEIR CONTRIBUTION TO MF DEVELOPMENT (AIM 2). FINALLY, WE WILL DEFINE THE ROLES OF MYC AND ITS TARGET ALARMINS IN MF DRIVEN BY JAK2 PATHWAY MUTATIONS (AIM 3). COLLECTIVELY, THIS RESEARCH WILL PROVIDE IMPORTANT INSIGHTS INTO A NEW MOLECULAR CIRCUIT CONNECTING MYC AND ALARMIN-MEDIATED INFLAMMATION, AND WILL TEST IF THE MYC-ALARMIN AXIS REPRESENTS A NOVEL THERAPEUTIC VULNERABILITY THAT CAN BE TARGETED TO IMPROVE CLINICAL OUTCOMES IN MF.

1106082.00

0.00

0.00

2025-05-19

View on USAspending

Department of Health and Human Services

DUAL E3 LIGASE FUNCTION OF TRIM25 IN MODULATING INNATE IMMUNITY - PROJECT SUMMARY/ABSTRACT INNATE IMMUNITY IS CRUCIAL FOR HUMAN HEALTH AND IS PRIMARILY REGULATED BY POST-TRANSLATIONAL MODIFICATIONS, SUCH AS UBIQUITIN AND UBIQUITIN-LIKE (UBL) MODIFIERS. SPECIFICALLY, TRIPARTITE MOTIF-CONTAINING PROTEIN 25 (TRIM25), IS AN E3 LIGASE THAT ENZYMATICALLY MODIFIES SUBSTRATES WITH UBIQUITIN AND THE UBL PROTEIN ISG15 AND PARTICIPATES IN MODULATING INNATE IMMUNITY THROUGH THE IMMUNORECEPTORS RETINOIC ACID-INDUCIBLE GENE I-LIKE RECEPTORS (RLRS). DESPITE A GENERAL UNDERSTANDING OF THE ROLE TRIM25 PLAYS IN THE UBIQUITINATION OF RIG-I, LITTLE IS KNOWN ABOUT THE ROLE TRIM25 PLAYS IN ISGYLATION OF RLRS AND HOW TRIM25 SELECTS BETWEEN EITHER PROCESS. FURTHER, A NEW VIRAL MODE OF ANTAGONISM OF TRIM25 BY THE HUMAN PAPILLOMA VIRUS HAVE BEEN DISCOVERED BUT HAVE NOT BEEN DEFINED AT THE MOLECULAR LEVEL. IN THIS PROPOSAL, IN THE K99 PHASE OF THIS AWARD (AIM 1), I WILL INVESTIGATE THE MECHANISM OF THE VIRAL E6 ANTAGONISM OF TRIM25 AND HOW THIS INHIBITION EFFECTS THE DUAL FUNCTIONS OF TRIM25 TO UBIQUITINATE AND ISGYLATE RLRS. IN THE R00 PHASE OF THIS AWARD (AIM 2, I WILL DISSECT THE FUNCTIONAL SELECTIVITY OF TRIM25 AND THE EFFECTS THIS HAS ON SUBSTRATE MODIFICATION. THIS RESEARCH WILL PROVIDE ME WITH TRAINING IN YEAST DISPLAY SYSTEMS, DIRECTED EVOLUTION AND BIOCHEMISTRY AND RESEARCH ON TRIM25 BIFUNCTIONALITY WILL BE CARRIED OVER TO MY OWN LAB. THIS AWARD WILL ENABLE ME TO TAKE ADVANTAGE OF PROTEIN ENGINEERING AND IMMUNOLOGY EXPERTISE VIA MY ADVISORY COMMITTEE (DR. BINNING AND DR. PILON-THOMAS), AS WELL AS CAREER DEVELOPMENT OPPORTUNITIES AT THE MOFFITT CANCER CENTER. I WILL ALSO BOLSTER MY PREVIOUS EXPERIENCE IN DIVERSITY, EQUITY AND INCLUSION (DEI) ADVOCACY WITH NEW TRAINING TO BEST POSITION MYSELF TO FURTHER DEI EFFORTS THROUGHOUT MY INSTITUTION AND COMMUNITY. I WILL ATTEND CONFERENCES AND PARTICIPATE IN MOFFITT-SPONSORED AND MOSAIC UE5 INITIATIVES FOCUSED ON LAB MANAGEMENT AND LEADERSHIP. THIS WILL AID ME TRANSITION TO AN INDEPENDENT SCIENTIST SPECIALIZING IN UBIQUITIN BIOLOGY AND INNATE IMMUNITY, WHICH IS A RAPIDLY GROWING AND IMPORTANT AREA OF SCIENTIFIC RESEARCH.

110335.00

0.00

0.00

2025-05-07

View on USAspending

Department of Health and Human Services

SAMBAI - ESTABLISHING A COMPREHENSIVE ASSESSMENT OF CONTRIBUTORS TO CANCER INEQUITIES ACROSS THE AFRICAN DIASPORA - SAMBAI: SOCIETAL, ANCESTRY, MOLECULAR AND BIOLOGICAL ANALYSES OF INEQUALITIES RESEARCH ABSTRACT BACKGROUND PROSTATE, BREAST, AND PANCREATIC CANCERS ALL HAVE A DISPROPORTIONATELY HIGHER RATE OF AGGRESSIVE TUMOR GRADE AND EARLY ONSET IN BLACK PATIENTS, WITH RECENT SPIKES OF HIGH INCIDENCE IN WEST AFRICAN NATIONS COMPARED TO OTHER AFRICAN REGIONS. THE GENETIC BACKGROUND CORRELATIONS IMPLICATE PREDISPOSITIONS. MEMBERS OF OUR SAMBAI TEAM OF INVESTIGATORS HAVE PIONEERED GENOMICS IN CANCER DISPARITIES RESEARCH, AND OVER THE PAST TWO DECADES, WE HAVE UNCOVERED COMPELLING EVIDENCE OF DISTINCT IMMUNOLOGICAL MECHANISMS ASSOCIATED WITH GENETIC ANCESTRY. OUR SAMBAI TEAM MEMBERS HAVE DEVELOPED METHODS TO QUANTIFY ENVIRONMENTAL EXPOSURES AND INTERROGATE THE LIVED EXPERIENCES OF MARGINALIZED POPULATIONS, INCLUDING EPIGENETIC RESPONSES TO RACISM. AIMS WE WILL PARTNER WITH SCIENTISTS ACROSS THE US, AFRICA, AND THE UK TO BUILD AN UNPRECEDENTED RESOURCE, THE SAMBAI BIOBANK AND DATA REPOSITORY FOR CANCER EQUITY RESEARCH. WE WILL GENERATE A COMPREHENSIVE, ACCURATE, AND RELEVANT MEASUREMENT OF SOCIAL, ENVIRONMENTAL, GENETIC, AND IMMUNOLOGICAL FACTORS TO COMPLETE AN INTEGRATED SET OF ANALYSES TO DEFINE THE CAUSAL VS. MODIFIER RELATIONSHIPS OF DISPARATE OUTCOMES IN DIVERSE UNDERSERVED POPULATIONS. WE WILL ESTABLISH A SUSTAINABLE FRAMEWORK FOR TEAM SCIENCE APPROACHES WITH UNDER-REPRESENTED PARTNERS AND ESTABLISH BEST PRACTICES FOR COORDINATING CANCER EQUITY RESEARCH ON A GLOBAL SCALE. METHODS WE PROPOSE TO UTILIZE MULTIPLE METHODS ACROSS OUR DIFFERENT WORK PACKAGES. SOCIAL DETERMINANTS INCLUDE SELF- REPORTING SURVEYS AND DATABASE ABSTRACTIONS. EXPOSOMES UTILIZE MASS SPECTROMETRY OF PLASMA. GENOMICS WILL UTILIZE THREE SEQUENCING METHODS ON GERMLINE AND TUMOR TISSUE, INCLUDING LONG READ, SHORT/DEEP, AND ULTRA-LOW PASS WHOLE GENOME SEQUENCING. LASTLY, IMMUNOLOGICAL PROFILES WILL BE MEASURED WITH SPATIAL TRANSCRIPTOMICS AND CIRCULATING MULTIPLEX IMMUNOASSAYS. THESE DATA REQUIRE NOVEL COMPUTATIONAL FRAMEWORKS, INCLUDING CLOUD- BASED VIRTUALIZATION AND THE USE OF MACHINE LEARNING TECHNOLOGIES TO IDENTIFY NOVEL ASSOCIATIONS ACROSS THE STRATA OF SOCIAL TO SPATIAL DATA ELEMENTS AND ACROSS OUR DIVERSE GEOGRAPHIC AND ANCESTRAL SAMBAI COHORTS. UTILITY AND IMPACT WE WILL IMPROVE RESEARCH CAPACITY IN UNDER-RESOURCED ENVIRONMENTS FOR LARGE-SCALE CANCER RESEARCH AND EQUITABLE ACCESS TO DATA WITH EQUITABLE FEASIBILITY TO IMPROVE TREATMENT AND OUTCOMES. WE WILL DEFINE INTERACTIONS OF ENVIRONMENTAL EXPOSURES, SOCIAL DETERMINANTS, AND GENETIC ANCESTRY THAT DETERMINE IMMUNOLOGICAL LANDSCAPES OF PRIMARY TUMORS AND/OR CIRCULATING IMMUNOLOGICAL PROFILES IN PATIENTS OF AFRICAN DESCENT. OUR PROJECT WILL CONTRIBUTE A DATA REPOSITORY WITH 100K FEATURES/PATIENT, FOR 40,000 PATIENTS. THE IMPACT ON THIS POPULATION INCLUDES A NOVEL TRIAL DESIGN, IN COLLABORATION WITH OUR PATIENT ADVOCACY PARTNERS, TO ENSURE THAT THE SPECIFIC GENOMIC AND IMMUNOLOGICAL FEATURES WE UNCOVER BECOME PART OF TARGETED PRECISION ONCOLOGY THERAGNOSTIC OPTIONS.

142189.00

0.00

0.00

2025-05-22

View on USAspending

Department of Health and Human Services

DEVELOPMENT OF BIFUNCTIONAL CDK2 INHIBITORS FOR TREATMENT OF CCNE1-DRIVEN CANCERS - PROJECT SUMMARY OVARIAN CANCER IS AMONG THE FIVE LEADING CAUSES OF CANCER DEATH IN THE US WITH ESTIMATED 20,000 NEW CASES AND MORE THAN 13,000 DEATHS IN 2023. HIGH-GRADE SEROUS OVARIAN CANCER (HGSOC) IS THE MOST COMMON AND DEADLY SUBTYPE AND ACCOUNTS FOR ~75% OF OVARIAN CANCER DEATHS. AMPLIFICATION AND OVEREXPRESSION OF CCNE1, THE GENE ENCODING CYCLIN E1, LEADS TO HYPERACTIVATION OF THE COGNATE KINASE CDK2 AND OCCURS IN ~50% OF HGSOC PATIENTS. DYSREGULATED CCNE1 EXPRESSION IS ALSO FREQUENTLY OBSERVED IN AGGRESSIVE SUBTYPES OF ENDOMETRIAL CANCER AND TRIPLE-NEGATIVE BREAST CANCER. IN OVARIAN CANCER. CCNE1 AMPLIFICATION IS ASSOCIATED WITH POOR PROGNOSIS AND RESISTANCE TO CHEMOTHERAPY, AND MOST PATIENTS WITH ADVANCED HGSOC (>80%) EXPERIENCE RECURRENCE AND ULTIMATELY SUCCUMB TO THEIR DISEASE. THE PAUCITY OF THERAPEUTIC OPTIONS FOR CCNE1-DRIVEN TUMORS MAKES THE DEVELOPMENT OF NOVEL DRUGS THAT COUNTERACT THIS ABERRATION A CRITICAL UNMET NEED. CDK2 IS A VALIDATED DRUG TARGET, AND STUDIES BY MANY LABORATORIES IN ACADEMIA AND THE PHARMACEUTICAL INDUSTRY HAVE SHOWN THAT TARGETING CDK2 IS A VIABLE AND PERHAPS IDEAL APPROACH TO COMBAT CANCERS CHARACTERIZED BY CCNE1 AMPLIFICATION. HOWEVER, CONVENTIONAL ATP-SITE (TYPE I) INHIBITORS HAVE LARGELY FAILED IN THE CLINIC DUE TO INSUFFICIENT SELECTIVITY, PARTICULARLY OFF TARGET INHIBITION OF THE CLOSELY RELATED AND COMMON ESSENTIAL KINASE CDK1. WE HAVE PREVIOUSLY IDENTIFIED AN ALLOSTERIC SITE UNIQUE TO CDK2 AND DEMONSTRATED THAT SMALL MOLECULE LIGANDS OCCUPYING THIS SITE STABILIZE A CDK2 CONFORMATIONAL STATE THAT IS LESS FAVORABLE FOR INTERACTION WITH CYCLINS. WHILE SUCH MONOVALENT ALLOSTERIC (TYPE III) LIGANDS LACK THE HIGH BINDING AFFINITY REQUIRED TO EFFECTIVELY DISRUPT THE INTERACTION OF CDK2 WITH CYCLIN E1, OUR RECENT STRUCTURAL AND COMPUTATIONAL STUDIES PROVIDE STRONG EVIDENCE THAT JOINING AN ALLOSTERIC LIGAND WITH A HIGH-AFFINITY ATP-SITE (TYPE I) INHIBITOR PRESENTS A NEW MEANS TO SUPPRESS THE HYPERACTIVATION OF CDK2 CAUSED BY ELEVATED CYCLIN E1 LEVELS. THE OVERALL OBJECTIVE OF THIS PROJECT IS TO DEVELOP FIRST-IN-CLASS BIFUNCTIONAL ALLOSTERIC INHIBITORS THAT STABILIZE CDK2 IN A CONFORMATIONAL STATE INCOMPATIBLE WITH CYCLIN E1 BINDING. WE HYPOTHESIZE THAT SUCH INHIBITORS POTENTLY AND SELECTIVELY DISRUPT THE CDK2-CYCLIN E1 COMPLEX, THEREBY COUNTERACTING THE ONCOGENIC ACTIVITY OF ELEVATED CCNE1 EXPRESSION. THE RATIONALE UNDERLYING THIS RESEARCH IS THAT IT WILL PROVIDE GENERAL INSIGHTS INTO THE FEASIBILITY OF BIVALENT ALLOSTERIC CDK2 INHIBITORS IN THE CONTEXT OF CCNE1-DRIVEN CANCERS AND BUILD A STRONG SCIENTIFIC FRAMEWORK WHEREBY NEW THERAPEUTIC STRATEGIES CAN BE DEVELOPED.

433255.00

0.00

0.00

2025-04-24

View on USAspending

Department of Health and Human Services

THE DELTA ECOLOGY OF NSCLC TREATMENT - SUMMARY – MOFFITT CSBC PROPOSAL OVERVIEW THE MOFFITT CSBC PROPOSAL IS FOCUSED ON THE ESSENTIAL AND HIGHLY DYNAMICAL INTERPLAY BETWEEN CANCER CELL EVOLUTION AND THE CONSTANTLY CHANGING ECOLOGY OF THE LUNG MICROENVIRONMENT. TUMORS ARE NOT SIMPLY COLLECTIONS OF MUTATED CELLS THAT GROW IN ISOLATION. RATHER, THEY RESPOND TO AND MODIFY BOTH THE PHYSICAL MICROENVIRONMENT AND A VARIETY OF HOST CELLS, AND THESE CHANGES IN ECOLOGY (“∆-ECOLOGY”) ARE KEY TO UNDERSTANDING TUMOR PROGRESSION AND THE RESPONSE TO THERAPY – PARTICULARLY THE DEVELOPMENT OF RESISTANCE. CENTRAL TO THIS PROPOSAL IS QUANTIFYING, UNDERSTANDING, AND ACTIONING THE CHANGE THAT OCCURS DURING TREATMENT TO BOTH THE TUMOR AND NON-TUMOR ECOLOGY IN NON-SMALL CELL LUNG CANCER (NSCLC), WHICH IS THE MOST COMMON AND AMONG THE MOST LETHAL OF HUMAN CANCERS. WE WILL DEFINE THE ECOLOGICAL AND EVOLUTIONARY DYNAMICS THAT GOVERN NSCLC PROGRESSION AND TREATMENT SUCCESS OR FAILURE THROUGH 2 PROJECTS AND 2 SHARED RESOURCE CORES. EACH PROJECT WILL FOCUS ON DIFFERENT D-ECOLOGY DYNAMICS IN THE PRESENCE OF DIFFERENT DRIVER MUTATIONS (RAS, EGFR, ALK) FOR WHICH TARGETED THERAPY IS AVAILABLE. EACH PROJECT DEMONSTRATES OUR UNIFYING THEME OF TIGHT EMPIRICAL/MATHEMATICAL INTEGRATION THROUGH THE SEQUENCE OF DEVELOP, PREDICT, CALIBRATE, TEST, OPTIMIZE, AND VALIDATE. THUS, EACH PROJECT BEGINS WITH AVAILABLE CLINICAL DATA FOLLOWED BY IN SILICO (PREDICT AND OPTIMIZE), IN VITRO (CALIBRATE AND TEST) AND IN VIVO (VALIDATE) MODEL SYSTEMS LEADING TO READILY TRANSLATABLE TREATMENT OPTIONS. THE MATHEMATICAL AND ECOLOGICAL CORES INCORPORATE THE MATHEMATICAL AND COMPUTATIONAL METHODS NEEDED FOR BRIDGING THE PROJECTS. THE MATH CORE WILL SERVE AS THE MECHANISTIC MODEL ENGINE OF THE CENTER, FACILITATING BOTH SPATIAL AND NON-SPATIAL MODELS OF ECO-EVOLUTIONARY PROCESSES TO GENERATE AND TEST HYPOTHESES REGARDING ∆- ECOLOGY. THE ECOLOGY CORE SERVES AS DATA REPOSITORY AND ECOLOGICAL ANALYSIS ENGINE WORKING IN LOCKSTEP WITH THE THREE PROJECTS FOCUSED ON DIFFERENT ASPECTS OF NSCLC ∆-ECOLOGY (IMMUNE AND STROMAL) TO DEVELOP AND APPLY SPATIAL ECOLOGICAL MODELS. THESE CORES WILL SERVE OUR TWO PROJECTS: PROJECT 1: DELTA IMMUNE ECOLOGY OF NSCLC 1.1 QUANTIFY THE ∆-ECOLOGY OF PATIENT SAMPLES PRE- AND ON- TREATMENT TO PREDICT OUTCOMES; 1.2 IMPACT OF KRAS INHIBITOR THERAPY WITH IMMUNOTHERAPY ON LUNG TUMOR ECOLOGY; 1.3 USE PREDICTIVE MODELING TO GENERATE EVOLUTIONARY INSPIRED MULTI-AGENT TREATMENT STRATEGIES. PROJECT 2: DELTA STROMAL ECOLOGY OF NSCLC 2.1 DECIPHER, IN VIVO, THE ∆-ECOLOGY OF ACQUIRED RESISTANCE TO TARGETED THERAPIES IN NSCLC; 2.2 DEFINE THE IMPACT OF STROMAL SHELTERING ON THE EMERGENCE OF RESISTANCE AND TUMOR GROWTH RELAPSE; 2.3 DISCOVER OPTIMAL THERAPEUTIC STRATEGIES TO SUPPRESS RESISTANCE.

4149708.00

0.00

0.00

2022-11-04

Complaint

12902 USF MAGNOLIA DRIVE, TAMPA, FL, 33612

Safety

Partial

59-3238634

% YVETTE M LYONS TREMONTI

Government Instrumentality, Title-Holding Corporation, Charitable Organization, Agricultural Organization, Board of Trade, Pleasure, Recreational, or Social Club, Fraternal Beneficiary Society, Order or Association, Voluntary Employees' Beneficiary Association (Non-Govt. Emps.), Domestic Fraternal Societies and Associations, Teachers Retirement Fund Assoc., Benevolent Life Insurance Assoc., Burial Association, Credit Union, Mutual Insurance Company or Assoc. Other Than Life or Marine, Corp. Financing Crop Operations, Supplemental Unemployment Compensation Trust or Plan, Employee Funded Pension Trust (Created Before 6/25/59), Post or Organization of War Veterans, Legal Service Organization, Black Lung Trust, Multiemployer Pension Plan, Veterans Assoc. Formed Prior to 1880, Trust Described in Sect. 4049 of ERISA, Title Holding Co. for Pensions, etc., State-Sponsored High Risk Health Insurance Organizations, State-Sponsored Workers' Compensation Reinsurance, ACA 1322 Qualified Nonprofit Health Insurance Issuers, Apostolic and Religious Org. (501(d)), Cooperative Hospital Service Organization (501(e)), Cooperative Service Organization of Operating Educational Organization (501(f)), Child Care Organization (501(k)), Charitable Risk Pool, Qualified State-Sponsored Tuition Program, 4947(a)(1) - Private Foundation (Form 990PF Filer)

1994-07

Type of organization and use of contribution: A public charity. Deductibility Limitation: 50% (60% for cash contributions)