Research Database

Dr. Borgia is working to develop new biomarkers to strengthen the capabilities of the existing blood test for identifying the presence of metastatic progress in non-small cell lung cancer that he has developed. He plans to adapt the blood test to a diagnostic card format so that high-risk individuals can put blood droplets on diagnostic cards at home and mail them to a test facility where the blood will be extracted and tested for the biomarkers in the panel.

Dr. Borgia has developed a blood test for identifying the presence of metastatic progression in non-small cell lung cancer. His current project allows for revision of the test to improve its accuracy and potentially reach an accuracy rate that will allow it to be useful as a stand-alone staging test.

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.

Dr. Shofer’s research builds on work of earlier investigators who developed a lung cancer risk signature based on genetic changes in lung cells in smokers. Dr. Shofer hypothesizes that the lung cancer risk signature model is an indicator of how lung cells change during the process of cancer development. Should his hypothesis be correct, the lung cancer risk signature could be established as a sensitive biomarker capable of diagnosing patients with lung cancer by checking cells taken from the throat using a swab.

Previously conducted clinical trials have suggested an increased risk of lung cancer from hormone replacement therapy (HRT). Dr. Slatore is studying women who have both undergone HRT and smoked  to determine whether there is a relationship between HRT, tobacco use, and 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.

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.

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.