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Mechanisms of epigenetic disruption due to DNA damage and replication stress

Award Number: F31CA310572
ORGANIZATION: NATIONAL CANCER INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 07/01/2026
PERIOD OF PERFORMANCE END DATE: 06/30/2029

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Mechanisms of epigenetic disruption due to DNA damage and replication stress - ABSTRACT: Epigenetic memory of gene expression programs is critical for the development and maintenance of cellular identity. Epigenetic dysregulation is a hallmark of human cancers, as widespread alterations in gene expression can lead to misexpression of oncogenes or inappropriate repression of tumor suppressor genes. Different cell types have different epigenetic signatures which may require different epigenetic targets as cancer therapies. Additionally, treatment resistance is a common problem in current cancer therapies. Understanding how epigenetic fidelity is initially lost may provide critical insights for the future development of cancer therapies. Prior work has shown that DNA damage causes widespread epigenetic dysregulation. Additionally, there is strong evidence that replication stress disrupts the inheritance of heterochromatin, which then leads to derepression of cell type-specific genes and loss of cell identity. The precise mechanisms of this epigenetic loss are unknown. Cells face genomic threats such as endogenous DNA damage and replication fork stalling in each cell division. It is important to understand how these challenges contribute to epigenetic disruptions. In the proposed work, I seek to define how two threats to epigenetic stability, DNA repair of double stranded breaks and replication stress, affect heterochromatin maintenance. Using fission yeast, a powerful model for heterochromatin inheritance, I will seek to identify the steps in DNA repair and fork stalling which lead to heterochromatin loss. In aim 1, I propose to induce double strand breaks at a targeted, inducible heterochromatin locus using CRISPR- Cas9 to first define the effects of double strand breaks on heterochromatin maintenance and second, determine whether distinct repair pathways differentially affect heterochromatin maintenance. In aim 2, I propose to determine how sequences predicted to stall the replisome affect heterochromatin maintenance. In aim 3, I will seek to identify novel pathways which have roles in maintaining epigenetic fidelity in the face of replication stress and DNA repair by performing a genetic screen.


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 = $36,458 )
2026	2026	PRESIDENT AND FELLOWS OF HARVARD COLLEGE	25 SHATTUCK ST	BOSTON	MA	02115	SUFFOLK	USA	Cancer Research Manpower	000	1	4/27/2026	NEW	$36,458
2026	2026	PRESIDENT AND FELLOWS OF HARVARD COLLEGE	25 SHATTUCK ST	BOSTON	MA	02115	SUFFOLK	USA	Cancer Research Manpower	001	1	4/27/2026	NEW	$0
														Subtotal = $36,458

Grand Total All Awards = $36,458

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Mechanisms of epigenetic disruption due to DNA damage and replication stress

Award Number: F31CA310572

ORGANIZATION: NATIONAL CANCER INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 07/01/2026

PERIOD OF PERFORMANCE END DATE: 06/30/2029

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