NIH-funded research R01 grant

How loss of SETD2 drives lung adenocarcinoma growth

Official title: Identifying the Impact of SETD2 Inactivation in Lung Adenocarcinoma

Funded at University of Pennsylvania · NIH-11240268 · Data updated 2026-11-12

This project looks at whether cutting dietary methionine or using drugs that change methionine-related metabolism can slow lung cancers that have lost the SETD2 gene.

More Adenocarcinoma research and trials

Quick facts

Grant typeR01 grant
Study typeNIH-funded research
Funding institutionUniversity of Pennsylvania
NIH-funded
Lab location1 site (Philadelphia, United States)
Project startDecember 10, 2021
Project endNovember 30, 2026
Funding year2026
Award (this year)$436,693
NIH project number5R01CA262619-05
Project IDNIH-11240268 on NIH RePORTER

Who could benefit from this research

Could help

Ideal candidates would be people with lung adenocarcinoma whose tumors have SETD2 loss-of-function mutations, especially those with KRAS-driven disease.

Less likely to help

Patients without SETD2-deficient tumors or those with other lung cancer types (for example, squamous cell carcinoma) are less likely to benefit from these specific approaches.

What this research studies

From my perspective as a patient, the team studies lung tumors that lack the gene SETD2 using lab-grown tumor cells and mouse models. They found that losing SETD2 raises levels of S-adenosyl methionine (SAM) and turns on mTORC1, which helps tumors grow. The researchers showed that lowering dietary methionine slowed KRAS-driven lung tumors in mice and now plan to test drugs that target the methionine/one-carbon cycle. The goal is to find drug or dietary approaches that selectively hurt SETD2-deficient tumors and could move toward patient testing.

Why it matters

Potential benefit: If successful, this work could point to new metabolic or dietary-based treatments for patients whose lung tumors have SETD2 loss.

How similar studies have gone: Preclinical mouse work by the team showed methionine restriction can slow KRAS-driven tumors, but targeting SAM/one-carbon metabolism in SETD2-deficient human tumors is a relatively new and translational step.

Where this research is happening

  • University of Pennsylvania
    Philadelphia, United States
    Active

Researchers

  • Principal investigator: Feldser, David — University of Pennsylvania
  • Study coordinator: Feldser, David

Related research

Other NIH-funded projects on the same topics.

About this research

  1. This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
  2. Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
  3. For full project details, budget, and progress reports, visit the official NIH RePORTER page.
Last reviewed 2026-11-14 by the Find a Trial editorial team. Information on this page is for educational purposes and is not medical advice. Always consult qualified healthcare professionals about clinical trial participation.