Research Database

Dr. Sittampalam is determining whether circulating tumor cells can be a useful blood-based tumor marker in untreated patients with extensive-stage small cell lung cancer who are planning to receive chemotherapy. He is also exploring the feasibility of genomic profiling using circulating tumor cells.

Dr. Tryggestad is developing magnetic resonance imaging (MRI)-based methods to characterize breathing motion. This information can then be used for radiotherapy planning, delivery, and optimization for the treatment of lung cancer patients.

HSP90, a heat shock protein, protects cancer cells from chemotherapy. Dr. Vielhauer’s laboratory is developing novel targeted therapy that selectively blocks HSP90 and kills lung cancer cells.

Dr. Wigle is investigating the effectiveness of stereotactic radiation therapy (SBRT) versus surgery in patients with compromised pulmonary function. This project is a phase II clinical trial whose results will set the stage for more-definitive phase III trials.

A region in chromosome 7 has more copies than normal in patients with adenocarcinomas. Dr. Wilgus is determining whether these extra copies contribute to the development of lung cancer and how it can be targeted to lessen its effects.

Dr. Yendamuri is conducting a clinical trial among stage-1 non-small cell lung cancer patients to confirm a microRNA signature for the prediction of the recurrence of lung cancer after surgery. He then will develop a blood-based microRNA profile for the detection of lung cancer recurrence.

Dr. Yendamuri is conducting a clinical trial among stage-1 non-small cell lung cancer patients to confirm a microRNA signature for the prediction of the recurrence of lung cancer after surgery.  He then will develop a blood-based microRNA profile for the detection of lung cancer recurrence.

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.

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.