SLOAN-KETTERING INSTITUTE FOR CANCER RESEARCH

KUKXRCZ6NZC2

6X133

2026-05-14

2025-05-16

2002-02-25

6X133

Active

Non-Manufacturer

2024-06-18

2029-06-18

2025-06-14

MATTHEW WARSHAW

+1 646-227-3092

+1 212-639-8207

75N91022P00804

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AWARD

PURCHASE ORDER

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0.00

Department of Health and Human Services

2022-09-26

EXTEND SERVICES FOR THE PURCHASE ORDER: PURCHASE ORDER - SAMPLES FOR NCI'S MULTI-ANCESTRY GENOME-WIDE ASSOCIATION STUDY.

541380: TESTING LABORATORIES AND SERVICES

Q301: REFERENCE LABORATORY TESTING

75N92019P00092

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AWARD

PURCHASE ORDER

-0.04

-0.04

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Department of Health and Human Services

2019-04-04

NIAMS' AUTOIMMUNITY BRANCH (AB) IS IN NEED OF A SCIENTIFIC INVESTIGATOR WITH A PHD IN BIO-SCIENCES TO CONCLUDE THE STUDY ON FAS MODULATION, CELL FATE AND ITS RELATION TO HUMAN DISEASE.

541990: ALL OTHER PROFESSIONAL, SCIENTIFIC, AND TECHNICAL SERVICES

R499: SUPPORT- PROFESSIONAL: OTHER

75N92018P00076

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AWARD

PURCHASE ORDER

246768.00

246768.00

246768.00

Department of Health and Human Services

2018-09-18

177LU-EB-DOTATATE IND ENABLEMENT PROJECT, SEE ATTACHED STATEMENT OF WORK FOR DETAILS.

621511: MEDICAL LABORATORIES

B504: SPECIAL STUDIES/ANALYSIS- CHEMICAL/BIOLOGICAL

2025-04-15

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Department of Defense

SYSTEMATIC FUNCTIONAL DISSECTION OF CANCER CELL STATES IN LUNG TUMORS

923805.00

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0.00

2025-04-22

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Department of Health and Human Services

DECODING DISEASE-CRITICAL GENOMIC ARCHITECTURE USING MULTIMODAL SINGLE-CELL OMICS DATA - PROJECT SUMMARY/ABSTRACT UNDERSTANDING THE FUNCTIONAL ARCHITECTURE OF HUMAN DISEASES AND TRAITS AT A CELLULAR RESOLUTION IS CRITICAL FOR INFORMING FOLLOW-UP FUNCTIONAL CHARACTERIZATION EXPERIMENTS AND NOMINATING GENES AND PATHWAYS FOR DEVELOPING DRUG TARGETS. LARGE SCALE OMICS DATA ENCOMPASSING MULTIPLE MODALITIES (RNA-SEQ, ATAC-SEQ, CHIP-SEQ), A BROAD RANGE OF TISSUES AND CELL TYPES, AND DIVERSE BIOLOGICAL CONTEXTS, SUCH AS DISEASE STAGES, DEVELOPMENTAL TRAJECTORIES, AND GENE PERTURBATIONS, OFFER SIGNIFICANT NEW RESOURCES TO GAIN A DEEPER UNDERSTANDING OF THE GENETIC ARCHITECTURE OF COMPLEX DISEASES. IN THIS PROPOSAL, WE PLAN TO DEVELOP STATISTICAL AND MACHINE LEARNING APPROACHES THAT BRIDGE THE GAPS BETWEEN HUMAN GENETICS AND SINGLE-CELL OMICS DATA TO DECODE THE REGULATORY ACTIVITY UNDERLYING DISEASE VARIANTS, LINK VARIANTS TO GENES ACCURATELY IN RELEVANT CELL TYPES OF ACTION, AND IDENTIFY DISEASE-CRITICAL CO-OPERATIVE PROGRAMS OF GENES AND GENOMIC ELEMENTS ACTIVATED IN SPECIFIC BIOLOGICAL CONTEXTS . THE PROPOSED AIMS ARE TARGETED AT UNCOVERING NEW INSIGHTS INTO COMPLEX DISEASE ETIOLOGY BY ADVANCING OUR UNDERSTANDING OF GENE REGULATION AND EXPLORING THE SYNERGIES AND CONTRASTS IN EPIGENOMIC ACTIVITY AND DOWNSTREAM CELLULAR PROCESSES OR BIOLOGICAL PATHWAYS. A KEY GOAL OF THIS APPLICATION IS TO PRODUCE A SET OF COMPUTATIONAL TOOLS AND WORKFLOWS THAT CAN IDENTIFY AND RANK FUNCTIONALLY DISEASE-CRITICAL VARIANTS, GENES, AND PATHWAYS, ALONG WITH A DETAILED UNDERSTANDING OF THEIR PUTATIVE CELL TYPE AND BIOLOGICAL CONTEXT OF ACTION. THIS CAN GREATLY INFORM DOWNSTREAM DISEASE-FOCUSED INTERVENTION STRATEGIES LIKE DRUG PERTURBATION, AND SINGLE-GUIDE OR COMBINATORIAL CRISPR SCREENING EXPERIMENTS. IN THE FIRST AIM OF THIS PROPOSAL, WE WILL LEVERAGE SINGLE-CELL RNA+ATAC MULTIOME DATA TO LEARN IMPROVED STRATEGIES OF LINKING ENHANCERS TO GENES IN A CELL TYPE, EXPLORE THE CO-OPERATIVE EFFECTS OF MULTIPLE ENHANCERS ON GENE REGULATION, AND IDENTIFY SETS OF ENHANCERS AND LINKED GENES THAT TOGETHER CONSTITUTE DISTINCT DISEASE-CRITICAL FUNCTIONAL UNITS. IN THE SECOND AIM, WE WILL USE QUANTITATIVE TRAIT LOCI (XQTL) DATA SPANNING A BROAD RANGE OF MOLECULAR PHENOTYPES TO MAP THE CIS AND TRANS-REGULATORY ARCHITECTURE OF GWAS VARIANTS, AND BETTER PINPOINT CAUSAL VARIANTS FOR THESE PHENOTYPES THROUGH INTEGRATION WITH BASE-PAIR RESOLUTION VARIANT FUNCTION ASSAYS AND MODELS, SUCH AS SEQUENCE-BASED DEEP LEARNING MODELS. IN THE THIRD AIM, WE WILL LEVERAGE MULTIMODAL OMICS DATA OBSERVED ACROSS MULTIPLE BIOLOGICAL CONTEXTS TO IDENTIFY PROGRAMS OF GENES AND ELEMENTS ACTIVATED UNDER SPECIFIC CONTEXTS AND ASSESS THEIR IMPACT ON COMPLEX DISEASE GWAS SIGNALS. WE WILL ALSO DEMONSTRATE HOW DISEASE-RELATED BENCHMARKING OF GENE PROGRAMS ACTIVATED UPON ENHANCER AND GENE PERTURBATIONS CAN INFORM A COST-EFFICIENT EXPERIMENTAL PLAN OF A DOWNSTREAM PERTURBATION EXPERIMENT WITH MULTI-OMICS READOUTS. ALL VARIANT- LEVEL FUNCTIONAL ANNOTATIONS, VARIANT-GENE LINKS, AND GENE PROGRAMS, TOGETHER WITH A QUANTITATIVE AND QUALITATIVE ASSESSMENT OF THEIR IMPACT ON HUMAN DISEASES, AND ALL RELEVANT COMPUTATIONAL SOFTWARE AND PIPELINES WILL BE SHARED PUBLICLY WITH THE SCIENTIFIC COMMUNITY.

470580.00

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0.00

2025-04-18

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Department of Health and Human Services

RSMI HEALS - PROJECT SUMMARY/ABSTRACT THERE ARE 26 MILLION LIMITED ENGLISH PROFICIENT (LEP) PEOPLE IN THE U.S. POPULATION (THOSE WHO SPEAK ENGLISH LESS THAN “VERY WELL”); THE TWO MOST FREQUENTLY SPOKEN LANGUAGES ARE SPANISH (63%) AND CHINESE (7%). THE LEP POPULATION FACES DISPARITIES IN CANCER OUTCOMES, IN PART DUE TO COMMUNICATION BARRIERS AND LACK OF ACCESS TO LANGUAGE INTERPRETATION SERVICES. TECHNOLOGY HOLDS GREAT PROMISE FOR EFFICIENT, SCALABLE REMOTE INTERPRETING SOLUTIONS TO BRIDGE THE LANGUAGE BARRIER. HOWEVER, THERE IS STILL NO EVIDENCE-BASED GOLD STANDARD FOR TECHNOLOGY-BASED INTERPRETING. CURRENTLY, THERE ARE 3 TECHNOLOGY-BASED, PEOPLE-RENDERED METHODS EMPLOYED FOR REMOTE INTERPRETING: 1) REMOTE CONSECUTIVE MEDICAL INTERPRETING (RCMI; “AUDIO CONSECUTIVE”), THE MOST COMMONLY UTILIZED, 2) REMOTE CONSECUTIVE VIDEO MEDICAL INTERPRETING (RCVI; “VIDEO CONSECUTIVE”), A GROWING RESOURCE, AND 3) REMOTE SIMULTANEOUS MEDICAL INTERPRETING (RSMI), “UN-STYLE” SIMULTANEOUS INTERPRETING APPLIED TO THE MEDICAL ENCOUNTER, WHICH HOLDS TREMENDOUS PROMISE FOR CLOSELY APPROXIMATING A SAME LANGUAGE ENCOUNTER, DECREASING INTERPRETING ERRORS, AND IMPROVING OUTCOMES. FURTHER, WITH THE RAPID ADVANCE OF ARTIFICIAL INTELLIGENCE (AI) SOLUTIONS, THERE IS AI POTENTIAL FOR LESS EXPENSIVE, MORE SCALABLE INTERPRETING SERVICES DELIVERY. RSMI HEALS WILL USE A HYBRID TYPE 2 DESIGN, COMBINING A RANDOMIZED CONTROLLED TRIAL (RCT), CONDUCTED ACROSS 3 DIVERSE CANCER CLINICS, WITH A CONSOLIDATED FRAMEWORK FOR IMPLEMENTATION RESEARCH (CFIR) PROCESS EVALUATION, TO GATHER BOTH CLINICAL EFFICACY AND REAL-WORLD IMPLEMENTATION EVIDENCE ON THE OPTIMAL TECHNOLOGY- ENABLED MEDICAL INTERPRETATION MODALITY. THE RCT WILL ENROLL 576 SPANISH- AND MANDARIN-SPEAKING LEP PATIENTS WITH STAGES II AND III BREAST CANCER TO COMPARE RSMI (UN-STYLE) WITH RCMI (AUDIO CONSECUTIVE) AND WITH RCVI (VIDEO CONSECUTIVE) INTERPRETING. SPECIFIC AIM 1 IS TO COMPARE ACROSS ARMS (A) THE PROPORTION OF INTERPRETING ERRORS OF CLINICAL SIGNIFICANCE (PRIMARY OUTCOME), AND B) I) APPOINTMENT ADHERENCE, II) PATIENT KNOWLEDGE OF TREATMENT/INSTRUCTIONS, III) THE PATIENT-PROVIDER RELATIONSHIP (USING THE PEPPI), AND IV) EFFICIENCY BY INTERPRETED MEDICAL FACT. SPECIFIC AIM 2 IS TO UTILIZE THE CFIR PROCESS ANALYSIS TO GATHER DATA ON A) INTEGRATING HOST INSTITUTION AND SYSTEMS FACTORS/POLICIES INTO THE INTERVENTION, AND B) IMPLEMENTATION POTENTIAL, THROUGH THE EXPLORATION OF THE FOLLOWING: I) FACILITATORS OF AND BARRIERS TO A) INTERVENTION DELIVERY, AND B) INTERVENTION SUSTAINABILITY AFTER STUDY COMPLETION; AND II) HOW THE INTERVENTIONS AND THEIR DELIVERY COULD BE REFINED TO IMPROVE FUTURE ADOPTION AND SUSTAINABILITY. SPECIFIC AIM 3 IS TO UTILIZE EVIDENCE FROM THE RCT AND THE CFIR PROCESS EVALUATION TO OUTLINE POLICY AND FUNDING IMPLICATIONS. OUR EXPLORATORY AIM IS TO CONDUCT ERROR AND EFFICIENCY ANALYSES OF RSMI VS AI-RSMI, AND TO GAUGE THE POTENTIAL ACCEPTABILITY OF AI-RSMI WITH PATIENT AND FACILITY SURVEYS. THESE FINDINGS WILL INFORM FUTURE MULTISITE LARGE-SCALE R01 AND/OR PCORI-LIKE STUDIES TO FURTHER ADDRESS EQUITABLE CANCER CARE FOR LEP POPULATIONS ACROSS A VARIETY OF LANGUAGES, SETTINGS, AND DISEASES.

1503249.00

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2025-04-18

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Department of Health and Human Services

THE CROSSTALK BETWEEN OBESITY-INDUCED FATTY LIVER AND LIVER METASTASIS - PROJECT SUMMARY/ABSTRACT CANDIDATE: AS A POSTDOCTORAL FELLOW IN DR. SCOTT LOWE’S LAB AT MSKCC, MY RESEARCH FOCUSES ON THE CONTRIBUTION OF OBESITY-INDUCED NON-ALCOHOLIC FATTY LIVER DISEASE (NAFLD), PARTICULARLY HEPATIC LIPID ACCUMULATION, TO LIVER METASTASIS FROM PANCREATIC DUCTAL ADENOCARCINOMA (PDAC). MY LONG-TERM GOAL IS TO ESTABLISH AN INDEPENDENT RESEARCH PROGRAM THAT AIMS TO DISSECT THE INTERACTIONS BETWEEN OBESITY/NAFLD AND METASTASIS, WITH THE ULTIMATE GOAL OF EXPLOITING THIS KNOWLEDGE FOR THERAPEUTIC BENEFIT. THE PROPOSED RESEARCH WILL FORM A SOLID FOUNDATION, ON WHICH I CAN ESTABLISH MY OWN RESEARCH GROUP BY THE END OF THE K99 PHASE. RESEARCH: LIVER IS A FREQUENT METASTATIC SITE FOR MANY CANCERS INCLUDING PDAC, AND LIVER METASTASIS IS TYPICALLY ASSOCIATED WITH POOR PROGNOSIS. OBESITY-ASSOCIATED NAFLD IS THE MOST PREVALENT CHRONIC LIVER DISEASE THAT AFFECTS ~25% OF THE POPULATION WORLDWIDE, AND WILL BECOME A PREDOMINANT FACTOR IN SHAPING THE NICHE FOR METASTATIC CANCERS. HOWEVER, HOW CANCER MECHANISTICALLY TAKES ADVANTAGE OF THE LIPID-RICH AND INFLAMMATORY ENVIRONMENT OF NAFLD REMAINS LARGELY UNKNOWN. MY EARLY POSTDOCTORAL WORK SHOW THAT LIVER METASTASIS FREQUENTLY CO-OCCURS WITH HEPATIC LIPID ACCUMULATION IN PATIENTS, AND FATTY ACID IS A CAUSAL DRIVER OF PDAC LIVER METASTASIS IN MOUSE MODELS OF NAFLD. MOREOVER, IN OBESE MICE, THE KEY LIPOLYSIS ENZYME IS UNCONVENTIONALLY ELEVATED IN HEPATOCYTES ADJACENT TO METASTASES, WHICH ACCUMULATE FATTY ACID CATABOLITE Β-HYDROXYBUTYRATE (ΒOHB) AND UPREGULATE INTERFERON-Γ (IFNΓ) RESPONSES. THIS PROPOSAL WILL TEST THE HYPOTHESIS THAT METASTASIS INDUCES LIPOLYSIS IN NEIGHBORING HEPATOCYTES TO PROVIDE FATTY ACIDS, WHICH CREATES A MULTIFACETED PRO-METASTATIC PROGRAM. I WILL LEVERAGE FUNCTIONAL GENETICS IN MOUSE MODELS TO INTERROGATE LIPOLYSIS IN THE NICHE HEPATOCYTES (AIM 1), AND TO DETERMINE THE CONTRIBUTIONS OF FATTY ACID-ΒOHB TO EPIGENOME (AIM 2) AND IFNΓ SIGNALING TO THE IMMUNE NICHE (AIM 3) IN NAFLD-DRIVEN METASTASIS, WITH SPATIAL ANALYTICS TO VALIDATE THESE RESULTS IN HUMAN SAMPLES. THESE STUDIES WILL ILLUMINATE THE MECHANISMS THAT DRIVE LIVER METASTASIS IN OBESITY AND NAFLD, WHICH COULD INFORM NEW STRATEGIES FOR THERAPEUTIC INTERVENTION IN A GROWING POPULATION OF PATIENTS. ENVIRONMENT: MSKCC PROVIDES AN IDEAL ENVIRONMENT FOR ME TO ACCOMPLISH MY TRAINING AND RESEARCH GOALS, AND SUCCESSFULLY TRANSITION TO AN INDEPENDENT FACULTY POSITION AT AN ACADEMIC INSTITUTION. MY MENTOR DR. LOWE IS A WORLD LEADER IN CANCER BIOLOGY, WITH EXPERTISE ON CANCER GENETICS AND MOUSE MODELS. IN ADDITION, I HAVE ASSEMBLED AN ADVISORY COMMITTEE OF ESTABLISHED SCIENTISTS WITH RELEVANT EXPERTISE AND STRONG COMMITMENT TO MENTORING (DRS. FARESE, LI, AND SHERMAN). TOGETHER, ALL MENTORS WILL SUPPORT MY TRANSITION TO INDEPENDENCE BY PROVIDING VALUABLE RESEARCH EXPERIENCE AND CAREER GUIDANCE. WITH THE COLLABORATIVE ENVIRONMENT AND BROAD SPECTRUM OF RESOURCES AT MSKCC, THIS SUPPORT NETWORK CREATES OPTIMAL CONDITIONS FOR THE SUCCESSFUL COMPLETION OF THE PROPOSED RESEARCH AND CAREER DEVELOPMENT PLANS.

6306.32

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0.00

2025-04-14

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Department of Health and Human Services

DISSECTING FOSL1-MEDIATED LINEAGE PLASTICITY AND RESISTANCE TO ANDROGEN RECEPTOR SIGNALING INHIBITION IN PROSTATE CANCER - PROJECT SUMMARY/ABSTRACT CANDIDATE: I AM A POSTDOCTORAL RESEARCH ASSOCIATE IN THE LABORATORY OF DR. YU CHEN IN THE HUMAN ONCOLOGY AND PATHOGENESIS PROGRAM (HOPP) AT MEMORIAL SLOAN KETTERING CANCER CENTER. MY PHD TRAINING AT BOSTON UNIVERSITY SCHOOL OF MEDICINE UNDER THE SUPERVISION OF DR. SAM THIAGALINGAM ALLOWED ME TO DEVELOP CELLULAR AND MOLECULAR BIOLOGICAL SKILLS TO FUNCTIONALLY CHARACTERIZE CANDIDATE GENES INVOLVED IN CANCER PROGRESSION AND INVESTIGATE THERAPEUTIC VULNERABILITIES. MY CURRENT RESEARCH FOCUSES ON UTILIZING PATIENT-DERIVED ORGANOID MODELS TO DEFINE EPIGENETIC SUBTYPES OF CASTRATION RESISTANT PROSTATE CANCER (CRPC) AND DETERMINING THE DEPENDENCY ON TRANSCRIPTION FACTORS TO MEDIATE GROWTH AND LINEAGE IDENTITY. MY PROPOSED RESEARCH AND MENTORING PLAN WILL PROVIDE ME WITH A STRONG FOUNDATION TOWARDS BECOMING AN INDEPENDENT INVESTIGATOR IN ACADEMIA. MY LONG-TERM CAREER GOAL IS TO ADVANCE PERSONALIZED CANCER MEDICINE, WITH SPECIFIC INTERESTS IN DISEASE MODELING, FUNCTIONAL CHARACTERIZATION OF DRIVERS OF LINEAGE PLASTICITY, AND EVALUATION OF THERAPEUTICS TO TARGET ONCOGENIC DEPENDENCY. TO ACHIEVE THIS GOAL, I HAVE DEVELOPED A CAREER PLAN THAT WILL ENSURE MY SUCCESS TO BECOMING AN INDEPENDENT INVESTIGATOR BY: 1) BOLSTERING MY SCIENTIFIC KNOWLEDGE AND TECHNICAL EXPERTISE, 2) ASSEMBLING AN ADVISORY COMMITTEE TO OVERSEE MY TRAINING PROGRESS, 3) IMPROVING MY COMMUNICATION SKILLS, 4) EXPANDING MY PROFESSIONAL NETWORK, AND 4) PREPARING ME FOR LEADING AND MENTORING FUTURE TRAINEES. RESEARCH: PROSTATE CANCER DEPENDS ON ANDROGEN RECEPTOR (AR) SIGNALING FOR GROWTH AND SURVIVAL. THE ADVENT OF THERAPIES TARGETING AR SIGNALING HAS DRIVEN THE DISEASE TOWARDS AR-INDEPENDENCE. USING A FUNCTIONAL GENOMICS APPROACH, WE HAVE IDENTIFIED A NEW EPIGENETIC SUBTYPE OF CRPC CALLED STEM CELL-LIKE (SCL), WHICH IS DRIVEN BY FOSL1 AND LACKS THERAPEUTIC OPTIONS. GENETIC PERTURBATION OF FOSL1 AND ITS COOPERATING FACTORS YAP/TAZ LEADS TO IMPAIRED CELL GROWTH AND LOSS OF SCL LINEAGE, SUGGESTING THAT CRPC- SCL CELLS ARE DEPENDENT ON FOSL1 FOR SURVIVAL. BUILDING ON THESE DISCOVERIES, IN THIS PROPOSAL, I AIM TO: 1) DEFINE THE ROLE OF FOSL1 IN MEDIATING LINEAGE PLASTICITY AND RESISTANCE TO ENZALUTAMIDE IN PROSTATE CANCER AND 2) EVALUATE THERAPEUTICS TO TARGET THE YAP/TAZ/TEAD/FOSL1 PATHWAY IN THE STEM CELL-LIKE SUBTYPE OF PROSTATE CANCER. ENVIRONMENT: THE YU CHEN LABORATORY IS A PART OF THE HOPP UNDER THE LEADERSHIP OF DR. CHARLES SAWYERS AT MEMORIAL SLOAN KETTERING CANCER CENTER, A TOP-TIER INSTITUTE IN CANCER RESEARCH. THE PRIMARY MENTOR IS DR. YU CHEN, A PIONEER IN DEVELOPING PROSTATE CANCER ORGANOIDS FROM PATIENTS AND AN EXPERT IN THE STUDY OF EPIGENETICS AND ABERRANTLY ACTIVATED TRANSCRIPTIONAL PROGRAMS. FURTHERMORE, MY ADVISORY COMMITTEE AND COLLABORATOR WILL PROVIDE ADDITIONAL SUPPORT FOR THE PROPOSED RESEARCH AND CAREER DEVELOPMENT PLANS.

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