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Blockade of cMYC oncogenic function by pregnancy-induced alterations and remodeling of the mammary gland

Award Number: R01CA284630
ORGANIZATION: NATIONAL CANCER INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 09/01/2023
PERIOD OF PERFORMANCE END DATE: 08/31/2028

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Blockade of cMYC oncogenic function by pregnancy-induced alterations and remodeling of the mammary gland - Abstract/Project Summary The goal of this proposal is to understand how transitions through pregnancy influence the molecular and cellular state of mammary epithelial cells and oncogenesis. Numerous epidemiological studies have found that pregnancy alters the risk of breast cancer. These studies have shown consistently that a full-term pregnancy prior to the age of 25 is associated with a one-third decrease in the life-time incidence of breast cancer. While a protective effect of pregnancy has been validated in rodent models of cancer, the underlying molecular basis for this effect remains unclear. We have found that pregnancy leads to persistent changes in the epigenome and enhancer landscape of MECs. Using an inducible c-MYC mouse model, we also find that oncogenesis and the transcriptional output downstream of this oncogene are reduced in post-pregnancy MECs. In this proposal we will investigate the molecular basis underlying these robust phenotypes. We will use epigenomics, ex vivo, in vivo and biochemical methods to define how the transcriptional function of c-MYC is modulated by pregnancy. We hypothesize that c- MYC interactions with cofactors and with specific cis-regulatory elements are altered in this system. We will also study how specific chromatin regulators contribute to pregnancy-mediated epigenomic rewiring. These efforts will build upon our recent data suggesting that EZH2 supports the post-pregnancy epigenome in wild-type mice. Collectively, this research will provide fundamental insights into the cell biology of the mammary gland and carry the potential for discoveries that could be harnessed to develop preventative treatments that modulate breast cancer risk in humans.


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 = $482,133 )
2025	2025	COLD SPRING HARBOR LABORATORY	1 BUNGTOWN RD	COLD SPG HBR	NY	11724	SUFFOLK	USA	Cancer Cause and Prevention Research	000	3	8/7/2025	NON-COMPETING CONTINUATION	$482,133
														Subtotal = $482,133

Issue Date FY: 2024 ( Subtotal = $443,162 )
2024	2024	COLD SPRING HARBOR LABORATORY	1 BUNGTOWN RD	COLD SPG HBR	NY	11724	SUFFOLK	USA	Cancer Cause and Prevention Research	000	2	8/15/2024	NON-COMPETING CONTINUATION	$443,162
														Subtotal = $443,162

Issue Date FY: 2023 ( Subtotal = $509,988 )
2023	2023	COLD SPRING HARBOR LABORATORY	1 BUNGTOWN RD	COLD SPRING HARBOR	NY	11724	SUFFOLK	USA	Cancer Cause and Prevention Research	000	1	8/29/2023	NEW	$509,988
														Subtotal = $509,988

Grand Total All Awards = $1,435,283

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Blockade of cMYC oncogenic function by pregnancy-induced alterations and remodeling of the mammary gland

Award Number: R01CA284630

ORGANIZATION: NATIONAL CANCER INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

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

PERIOD OF PERFORMANCE START DATE: 09/01/2023

PERIOD OF PERFORMANCE END DATE: 08/31/2028

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