July 2017 — Medicaid Cuts Linked to Later-Stage Cancer Diagnoses
Medicaid is the largest insurance program in the United States and provides health care coverage for many low-income individuals. Medicaid is administered at the state level, and therefore, the structure and extent of coverage provided in each state varies across the country and is subject to economic policy changes.
Lindsay Sabik, PhD, Associate Professor of Health Policy and Management and member of the Hillman Biobehavioral Oncology Program, studies the impact of government policies on health care. In particular, she is interested in the role of health insurance in facilitating access to care and the impact of changes in insurance on cancer outcomes.
In a study recently published in the journal Cancer, Dr. Sabik and colleagues examined the effects of a Medicaid policy change in Tennessee in 2005. Due to financial difficulties, the Tennessee Medicaid program terminated coverage for nonelderly adults who failed to meet traditional requirements, resulting in the disenrollment of 170,000 patients. Using cancer registry data, the researchers determined that women who were diagnosed with breast cancer after the Medicaid cuts had later-stage disease at diagnosis than those who were diagnosed before the cuts. Furthermore, women living in low-income zip codes were found to have the largest increase in late stage of disease at the time of diagnosis after the disenrollment, suggesting that these women were not able to access screening services that could have facilitated an earlier diagnosis.
Watch Dr. Sabik discuss these findings in the video below.
June 2017 — Targeting Regulatory T Cells Could Improve Cancer Immunotherapy
Immunotherapy drugs that utilize the immune system to detect and kill cancer cells have been successful against several cancers, yet they are still only effective in approximately 10 to 30 percent of patients with certain tumor types. UPMC Hillman Cancer Center researchers have recently discovered that selectively targeting a group of immune cells called regulatory T cells (Tregs) within a tumor may be a way to boost the immune system’s anti-cancer response.
Dario Vignali, PhD, Leader of the Hillman Cancer Immunology Program, Frank Dixon Chair in Cancer Immunology, and Professor and Vice Chair of Immunology at the University of Pittsburgh School of Medicine, and his colleagues discovered a few years ago that a surface protein called neuropilin-1 (Nrp1), which is expressed on almost all Tregs that infiltrated mouse tumors, was required to maintain the function, integrity and survival of Tregs within the harsh tumor microenvironment. Thus, Nrp1 on Tregs helps suppress the body’s natural anti-tumor immune response thereby helping the tumor survive. Importantly, blocking or deleting Nrp1 in Tregs in mice only impacted their function in tumors and not in the rest of the body, resulting in tumor eradication without inducing autoimmune or inflammatory disease.
More recent studies led by graduate student Abby Overacre-Delgoffe in Dr. Vignali’s lab, and published in Cell, demonstrated that tumor growth in a genetically modified mouse model in which the Nrp1 gene was deleted in only half the Treg cell population, but not the other half, was dramatically reduced when compared to a normal mouse in which Nrp1 was present in all Tregs. Genomic and cellular analyses revealed that a secreted immune molecule called interferon-gamma (IFNy) prevented the suppressive function of Tregs in the mice, particularly and selectively in the tumor microenvironment.
Using another genetically modified mouse model, they found that the role of IFNy in diminishing Treg function was crucial to the success of immunotherapies targeting the PD1 protein that have been proven to be very effective in patients.
Watch Abby and Dr. Vignali discuss this research further in the video below, and read more here.
May 2017 — Novel Gene Editing Approach to Cancer Treatment Shows Promise in Mice
A novel gene therapy using CRISPR genome editing technology effectively targets cancer-causing “fusion genes” and improves survival in mouse models of aggressive liver and prostate cancers, UPCI researchers reported in a study published this month in Nature Biotechnology.
Fusion genes, which are often associated with cancer, form when two previously separate genes become joined together and produce an abnormal protein.The UPCI research team, led by Jian-Hua Luo, MD, PhD, Professor of Pathology and Director of the University of Pittsburgh High Throughput Genome Center, used viruses to deliver gene editing tools that cut out the mutated DNA of the fusion gene and replaced it with a gene that leads to death of the cancer cells.
Watch Dr. Luo discuss this research further in the video below, and read more here.