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Genome-wide chromatin structure and function in Kaposi Sarcoma tissue

Award Number: R15CA306651
ORGANIZATION: NATIONAL CANCER INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 07/11/2025
PERIOD OF PERFORMANCE END DATE: 06/30/2028

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Genome-wide chromatin structure and function in Kaposi Sarcoma tissue - Project Summary/Abstract The Kaposi sarcoma-associated herpesvirus (KSHV) is an etiological agent of cancer. Among these malignancies, Kaposi sarcoma (KS) is particularly prevalent in people living with HIV. Central to identifying potential points of therapeutic intervention is a fundamental understanding of how the virus drives cancer progression at the molecular level. Since its discovery decades ago, the field has excelled at laboratory studies of KSHV infection. Particular challenges remain, however, in studying actual tissue. This proposal attempts to bridge this gap with a focused project that connects key collaborators in the greatest areas of need. By building on established relationships with a biorepository and leveraging resources at an advanced core facility, this project aims to study hard-to-find specimens with frontline genomics methods. All experiments will be performed by undergraduate students. Specific Aim 1 will identify virus-associated host enhancers and regulated genes in KS tissue. The project will obtain clinical specimens of KS from the AIDS and Cancer Specimen Resource. Skin lesions will be brought to and processed at the Mount Sinai School of Medicine Center for Advanced Genomics Technology for multiome single-cell ATAC-seq and single-cell RNA-seq experiments. The sequencing data of open chromatin and gene expression will be analyzed by a team of undergraduates from Barnard College. The goal is to identify enhancers and regulated genes modulated by the presence of viral infection. This will provide a map of chromatin interactions from actual cancer tissue and represents a transformative step beyond cell culture studies. Specific Aim 2 will identify host super-enhancers in KS tissue. To complement the open chromatin experiments of Aim 1, Aim 2 will use ChIP-seq to identify super-enhancers for KS. The same frozen tumor tissue from the AIDS and Cancer Specimen Resource in Aim 1 will be processed. ChIP-seq will be performed using antibodies against BRD4, a host regulator of super- enhancer activity. The goal is to identify active super-enhancers. This will provide a map of key oncogene regulatory elements from actual cancer tissue and represents a transformative step beyond cell culture studies. The AREA Impact Strategy emphasizes student peer mentorship and leadership. This proposal will designate three students to serve as laboratory mentors and leaders. Along with the principal investigator, the peer leaders will coordinate experiments and data analysis with other students on the team. This intertwines mentorship training with the research experience and provides opportunities at multiple levels of engagement. The overall impact will be identification of potential drivers of KS. Elucidating regulatory architecture and circuitry will identify enhancers and transcription factors that may be essential for growth and potential targets in future treatments.


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: 2025 ( Subtotal = $476,754 )
2025	2025	BARNARD COLLEGE	3009 BROADWAY	NEW YORK	NY	10027	NEW YORK	USA	Cancer Biology Research	000	1	7/11/2025	NEW	$476,754
														Subtotal = $476,754

Grand Total All Awards = $476,754

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Genome-wide chromatin structure and function in Kaposi Sarcoma tissue

Award Number: R15CA306651

ORGANIZATION: NATIONAL CANCER INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

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

PERIOD OF PERFORMANCE START DATE: 07/11/2025

PERIOD OF PERFORMANCE END DATE: 06/30/2028

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