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uNDERSTANDING AND TARGETING SENESCENCE IN CLONAL HEMATOPOIESIS

Award Number: K00CA284253
ORGANIZATION: NATIONAL CANCER INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 01/01/2025
PERIOD OF PERFORMANCE END DATE: 06/16/2025

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uNDERSTANDING AND TARGETING SENESCENCE IN CLONAL HEMATOPOIESIS - Clonal hematopoiesis (CH) is characterized by the presence of hematopoietic cells carrying one or more somatic mutations in the absence of overt hematological disease. The prevalence of CH rises with age and has been associated with increased mortality and a higher risk of progression to hematological cancers, as well as agerelated conditions such as cardiovascular and pulmonary events and liver disease. However, the mechanisms underlying the promotion of CH and its connection to age-related sequelae are not fully understood. A prominent feature of aging is the accumulation of senescent cells. Cellular senescence represents a stress response program marked by a halt in proliferation and the release of a proinflammatory Senescence-Associated Secretory Phenotype (SASP). Under normal circumstances, the SASP attracts immune cells, targeting senescent cells and restoring tissue homeostasis. However, increased tissue damage and declining immune function impede this clearance during aging, resulting in a chronic pro-inflammatory milieu. Evidence suggests chronic inflammation promotes CH and alters the balance between quiescence, self-renewal, and lineage commitment in hematopoietic stem and progenitor cells (HSPCs). Preliminary data from our research indicates that CH-mutant clones heavily rely on proinflammatory cytokines, and in aged animal models, they aggregate near senescent cells. The goal of my KOO postdoctoral work is to elucidate the role of cellular senescence in the progression of CH. I aim to explore the interactions between senescent cells and CH-mutant clones and identify key signaling molecules that could be potential biomarkers for disease progression in aging. Additionally, I will utilize uPAR-CAR T cells to eliminate senescent cells and study how this affects CH expansion, thus interrogating the therapeutic potential of targeting senescence to prevent high-risk CH. In conclusion, completing my proposed work will yield new insights into the age-driven progression of CH, as well as the development of novel biomarkers and therapeutic strategies from a senolytic angle.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = -$55,422 )
2026	2025	COLD SPRING HARBOR LABORATORY	1 BUNGTOWN RD	COLD SPG HBR	NY	11724	SUFFOLK	USA	Cancer Research Manpower	000	3	11/28/2025	EXTENSION WITH OR WITHOUT FUNDS	-$55,422
														Subtotal = -$55,422

Issue Date FY: 2025 ( Subtotal = $101,491 )
2025	2025	COLD SPRING HARBOR LABORATORY	1 BUNGTOWN RD	COLD SPG HBR	NY	11724	SUFFOLK	USA	Cancer Research Manpower	001	3	7/4/2025	EXTENSION WITH OR WITHOUT FUNDS	$0
2025	2025	COLD SPRING HARBOR LABORATORY	1 BUNGTOWN RD	COLD SPG HBR	NY	11724	SUFFOLK	USA	Cancer Research Manpower	000	3	1/21/2025	EXTENSION WITH OR WITHOUT FUNDS	$101,491
														Subtotal = $101,491

Grand Total All Awards = $46,069

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uNDERSTANDING AND TARGETING SENESCENCE IN CLONAL HEMATOPOIESIS

Award Number: K00CA284253

ORGANIZATION: NATIONAL CANCER INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 01/01/2025

PERIOD OF PERFORMANCE END DATE: 06/16/2025

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