Funded Projects

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.

The role of the hormone estrogen in the development of lung cancer has been established. Dr. Heymach is studying how estrogen affects signaling by the EGFR gene and secretion of proteins that fuel the development of new blood vessels necessary to sustain the growth of the cancer.

Dr. Kim’s hypothesis is that bronchioloalveolar carcinomas, a subtype of non-small cell lung cancer, are maintained by a small population of cells often referred to as cancer stem cells. Dr. Kim is identifying these stem cells and drugs that inhibit them.

The landscape of lung cancer treatment has changed with the initial discovery of an EGFR mutation in 2004. Now, drugs that block specific driver mutations are being considered for the treatment of non-small cell lung cancer (NSCLC). The LOGIC group (Lung Oncology Group in Chicago) is studying the correlative effects of agents used in conjunction with targeted therapies in the treatment of lung cancer.

Two commonly mutated genes in non-small cell lung cancer are KRAS and BRAF. Dr. McDaid is studying how these two genes control the synthesis of proteins in lung cancer cells. She is also testing how targeting the LKB1 mutation that often co-occurs with KRAS mutations can neutralize the effects of the KRAS mutation.

The Hedgehog (Hh) signaling pathway is active in both small cell and non-small cell lung cancer and provides a “don’t stop growing” signal to cancer cells. Dr. Robbins is working to identify and validate a panel of biomarkers that can be used to determine whether the lung cancer is sensitive to drugs that stop Hh signaling.

Dr. Seferos is developing new nanoparticle-based agents that are 13 nanometers in diameter to treat lung cancer. Unlike traditional chemotherapy, these particles can target the cancer cells directly and so reduce the side effects that are commonly associated with chemotherapy.

In order to identify mutated genes that cause lung cancer, Dr. Starr has developed a system that is capable of randomly mutating genes within cells, resulting in tumor formation. The genes mutated by this method can easily be identified using standard molecular biology techniques. He can then test their role in lung cancer formation.