The Happy Lungs Project, Inc., a 501c3 non-profit, was awarded a $2 million matching grant for research to fight RET positive non-small cell lung cancer.
The Happy Lungs Project has been instrumental in building a research consortium of the leading cancer centers, identifying critical NSCLC research, raising funds and creating research milestones.”— Dr. Steve Artandi, M.D., Ph.D.
AUSTIN, TEXAS, USA, May 24, 2022 /EINPresswire.com/ -- The Happy Lungs Project, Inc., a 501c3 non-profit, was awarded a $2 million matching grant for research to fight RET positive non-small cell lung cancer (NSCLC). RET positive lung cancer is caused by a mutation that allows cancer cells to grow out of control. This “driver mutation” occurs in 1-2% of NSCLC patients, and is more common among young, never-smokers, often the mothers of school-age children. J Clin Oncol. 2020;38(11):1209-1221. doi:10.1200/JCO.19.02551. With 2 million new lung cancers worldwide in 2020, about 1.6 million are NSCLC, and of these, 60%–70% are in advanced stage IV at the time of diagnosis. Oncol., 21 December 2021. doi.org/10.3389/fonc.2021.761042.
The Happy Lungs Project’s scientific advisory board — composed of leading researchers and clinicians at MD Anderson, Memorial Sloan Kettering, Massachusetts General Hospital and Stanford Cancer Institute — identified the most important research needed to find new treatments and a cure for RET-driven lung cancer. This research includes:
1. Develop a RET NSCLC registry to collect clinical data and patient specimens.
This project will develop a multi-center registry of patient information and tumor samples for research at major cancer centers (Stanford, Mass General, Sloak Kettering, UCLA, MD Anderson).
2.Characterize the molecular landscape of RET-fusion and resistance mechanisms from patients.
RET registry material will be used to generate structural information about RET-mutated proteins and the changes that lead to resistance to inhibitor medications.
3. Generate RET-mutation cell lines and animal models, including models resistant to RET-inhibitors.