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Clock Disruption Accelerates Colorectal Cancer and Promotes Immunosuppression

Award Number: F31CA287992
ORGANIZATION: NATIONAL CANCER INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 03/02/2024
PERIOD OF PERFORMANCE END DATE: 09/13/2024

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Clock Disruption Accelerates Colorectal Cancer and Promotes Immunosuppression - ABSTRACT Colorectal cancer (CRC) is the third most diagnosed cancer in the United States. With increasing public knowledge of cancer risk factors and screening, the incidence of CRC has steadily decreased in individuals over the age of 50 over the last several decades. However, the incidence of CRC in younger populations has been on the rise. Individuals under the age of 50 are increasingly afflicted by light-at-night exposure, night-shift work, and erratic eating patterns, which are known to disrupt the circadian clock. Importantly, disruption of circadian rhythms is a known risk factor for CRC. Therefore, it is likely that disruption of the circadian clock is a contributing factor for the alarming increase in early-onset CRC cases. This emerging link between the circadian clock and cancer has enormous potential for cancer prevention strategies. While causal links are clear, the underlying mechanism of how the circadian clock impinges on antitumor immunity to create a permissive environment for tumorigenesis is unknown. The goal of this project is to understand how both genetic and environmental circadian clock disruption alter the immune landscape to promote tumorigenesis. Our preliminary findings suggest that disruption of the circadian clock promotes inflammation and alters host immunity. Based on these findings, we hypothesize that clock disruption promotes inflammation to create an immunosuppressive microenvironment suitable for cancer initiation and progression. This central hypothesis will be addressed with the following Specific Aims. Aim 1 will determine how clock disruption alters the in vivo immune landscape through the activation of MDSCs and the suppression of cytotoxic CD8+ T cells. Aim 2 will define the molecular mechanism for how clock disruption impacts host immunity to accelerate tumorigenesis through the Wnt signaling pathway and MYC. The outcome of our findings will define the mechanistic underpinning linking disruption of the circadian clock to altered host anti-tumor immunity. The long-term goal of this study is to improve cancer prevention and treatment through lifestyle and pharmacological manipulation of the link between the circadian clock and the immune system.


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 = -$27,188 )
2025	2024	UNIVERSITY OF CALIFORNIA IRVINE	160 ALDRICH HALL	IRVINE	CA	92697	ORANGE	USA	Cancer Research Manpower	000	1	11/19/2024	NEW	-$13,521
2025	2024	UNIVERSITY OF CALIFORNIA IRVINE	160 ALDRICH HALL	IRVINE	CA	92697	ORANGE	USA	Cancer Research Manpower	001	1	7/25/2025	NEW	-$13,667
														Subtotal = -$27,188

Issue Date FY: 2024 ( Subtotal = $44,850 )
2024	2024	UNIVERSITY OF CALIFORNIA IRVINE	160 ALDRICH HALL	IRVINE	CA	92697	ORANGE	USA	Cancer Research Manpower	001	1	3/1/2024	NEW	$0
2024	2024	UNIVERSITY OF CALIFORNIA IRVINE	160 ALDRICH HALL	IRVINE	CA	92697	ORANGE	USA	Cancer Research Manpower	000	1	3/1/2024	NEW	$43,570
2024	2024	UNIVERSITY OF CALIFORNIA IRVINE	160 ALDRICH HALL	IRVINE	CA	92697	ORANGE	USA	Cancer Research Manpower	002	1	5/7/2024	NEW	$1,280
														Subtotal = $44,850

Grand Total All Awards = $17,662

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Clock Disruption Accelerates Colorectal Cancer and Promotes Immunosuppression

Award Number: F31CA287992

ORGANIZATION: NATIONAL CANCER INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 03/02/2024

PERIOD OF PERFORMANCE END DATE: 09/13/2024

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