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We fund translational research to move knowledge as quickly as possible from basic discovery to treatment of patients.
Since 2002, LUNGevity has invested in 183 research projects at 69 institutions in 24 states and the District of Columbia focusing on early detection as well as more effective treatments of lung cancer.
Dr. Tainsky has developed a technology that takes advantage of the responses of the human immune system to identify cancer-associated proteins that bind to antibodies present in the blood of cancer patients but not in the blood of healthy subjects or those with benign diseases. Dr. Tainsky is working to develop a non-invasive screening test for the early detection of lung cancer by using cancer-associated antigens as biomarkers.
Dr. Baldwin is identifying and testing new therapeutic targets for KRAS-positive lung cancer. KRAS activates the factor NF-κβ, which, when abnormally active, can contribute to the growth of lung tumors. This activation involves two kinases, and well-validated inhibitors of these pathways exist. This project is determining whether these inhibitors will block the initiation and/or progression of lung tumors.
The protein osteopontin plays a significant role in the malignant potential of numerous types of cancer, including lung cancer. There are three distinct forms of this protein in humans. Dr. Donington is studying how the individual forms play significantly different roles in determining the invasive metastatic potential in lung cancer.
The p53 gene can stop cells from becoming cancerous. It is mutated in non-small cell lung cancer, allowing cancer cells to grow in an uncontrolled manner. Dr. Duan is evaluating whether a new type of targeted therapy called PRIMA-1, used alone or in combination with other chemotherapies such as cisplatin, can stop the growth of non-small cell lung cancer cells.
The rationale behind Dr. Goodglick’s research is that the hormone estrogen and estrogen-pathway activation are important for lung cancer progression. Aromatase is an enzyme that makes estrogen in the body. Dr. Goodglick is conducting extensive pre-clinical evaluations of three aromatase inhibitors to understand steps in the estrogen stimulation pathway that affect tumor progression.
Dr. Krupnick’s laboratory has shown that non-small cell lung cancer may develop resistance to immune-mediated destruction due to IFN gamma insensitivity. Dr. Krupnick is now investigating his hypothesis that lung cancer cells develop the ability to escape the immune system by stopping the production of IFN gamma.
Genes that can suppress the development of tumors are often lost or silenced during the development of human lung tumors. Because they function as a “brake” that normally prevents the onset of lung tumors, they provide new targets for the development of replacement therapies for the effective treatment of lung cancers. Dr. Lisanti is testing the effectiveness of the replacement of a novel tumor suppressor gene, caveolin-1.
The IDO protein stops immune cells from recognizing cancer cells and mounting an attack against the cancer. Dr. Prendergast is determining how the IDO protein works in non-small cell lung cancer cells that have mutations in the KRAS gene. He is also testing new compounds that can inhibit IDO in non-small cell lung cancer.
Cancer-causing proteins called heat shock proteins (HSPs) protect cancer cells from the effects of chemotherapy. Dr. Regan is testing how inhibiting the protein chaperon HSP90 affects the growth of different lung cancer cells.
NNK is a powerful nicotine-derived carcinogen. Dr. Schuller is determining the exact role of estrogen in tumors caused by NNK. This understanding will provide new targets for the early diagnosis, prevention, and therapy of lung cancer in women.
Patients with EGFR mutations are treated with EGFR drugs such as gefitinib (Iressa) and erlotinib (Tarceva). However, the cancer cells eventually develop resistance to these drugs. Dr. Sharma is aiming to understand the processes by which non-small cell lung cancer cells develop resistance to gefitinib and erlotinib as well as how these processes can be targeted to develop new therapeutic strategies for patients in whom gefitinib and erlotinib have failed.
When cancer cells start spreading to other parts of the body, their shape changes through a process called EMT (epithelial-to-mesenchymal transition). The process of EMT in non-small cell lung cancer cells is mediated by the Snail protein. Dr. Yanagawa is studying how the Snail protein controls the EMT process through a protein called MMP2.
Lung cancer screening is not established as a public health practice, yet the results of a large randomized controlled trial among a high-risk population showed that screening with low-dose spiral computed tomography reduces lung cancer mortality. Milliman Consulting Company is conducting a cost-benefit analysis to demonstrate whether improved health outcomes (by catching the lung cancer early so that it can be treated) correlate with increased cost savings among this population.
Dr. Nana-Sinkam is delineating the role of microRNA expression profiling in the diagnosis, management, and prognosis of lung cancer. He is testing whether microRNA expression profiles are detectable in the blood of lung cancer patients. He will compare individuals with lung cancer with current and former smokers without lung cancer.
Dr. Hastings is establishing how parathyroid hormone-related protein (PTHrP) slows lung cancer growth, evaluating why lung cancers in men are less sensitive to PTHrP, and testing whether changes in hormone levels can affect the growth of lung cancer cells. His research may also determine whether changing the levels of male hormones makes it possible to improve the response to PTHrP.