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Investigating the influence of phospholipases onimmune evasion

Award Number: F31CA301546
ORGANIZATION: NATIONAL CANCER INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 12/01/2026
PERIOD OF PERFORMANCE END DATE: 11/30/2027

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Investigating the influence of phospholipases onimmune evasion - PROJECT SUMMARY/ABSTRACT Cancer development and progression relies on genetic and epigenetic perturbations that disrupt normal tumor suppressive mechanisms. One such mechanism is immune surveillance, in which the immune system can detect and destroy malignant cells. Studies characterizing how certain tumors bypass immune surveillance have led to advances in immunotherapy, including immune checkpoint blockade (ICB) and chimeric antigen receptor (CAR) T cell therapy. However, only a subset of patients qualify for these therapies, and a number of those who undergo treatment fail to respond, suggesting that a complete understanding of immune evasion mechanisms remains elusive. Study of this phenomenon is further complicated by the genetic heterogeneity of cancer; each tumor contains a unique combination of germline and somatic variants that may have the potential to influence tumor-immune interactions. The central hypothesis of this proposal is that context- dependent somatic variation observed within cancer patients contributes to immune evasion and immunotherapy failure. An in vitro co-culture system amenable to high-throughput screening of thousands of patient-derived missense mutations engineered with base editing was developed to test this hypothesis. The screen and subsequent validation experiments identified genetic paralogs Plcg1 and Plcg2 as a putative immunomodulatory genes in pancreatic cancer. Now, two aims will be tested to elucidate how these mutations contribute to immune evasion across different contexts. Aim 1 will determine the mechanism of Plcg1/2- mediated immune evasion within different cell types through cellular, molecular, and biochemical experiments. Meanwhile, Aim 2 will test how tumor microenvironment and immunotherapy impact growth of Plcg1/2-mutant cancer. This research proposal is innovative because it uses precision genome editing to screen thousands of endogenously expressed, patient-derived missense mutations and identify genetic mediators of immune evasion. It is significant because it will provide mechanistic insight into how somatic variation influences tumor- immune interactions and could guide the development of new immunotherapies. The work proposed in this training plan will be conducted within the Koch Institute at MIT, a highly collaborative cancer research center with access to all of the necessary equipment, facilities, and collaborators needed to perform experimental work.


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 = $50,114 )
2026	2026	MASSACHUSETTS INSTITUTE OF TECHNOLOGY	77 MASSACHUSETTS AVE	CAMBRIDGE	MA	02139	MIDDLESEX	USA	Cancer Research Manpower	000	1	4/13/2026	NEW	$50,114
														Subtotal = $50,114

Grand Total All Awards = $50,114

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Investigating the influence of phospholipases onimmune evasion

Award Number: F31CA301546

ORGANIZATION: NATIONAL CANCER INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 12/01/2026

PERIOD OF PERFORMANCE END DATE: 11/30/2027

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