10 GSBS students awarded American Legion Auxiliary fellowshipsNovember 02, 2012
2012 ALA awardees (from left to right): Howard Rosoff, Sarah Klein, Nathan Ihle, Christa Manton, Drew Deniger, Connie Larsson and Adam Yock. Not pictured are Kaitlin Gutierrez, Tamara Laskowski and Jacquelyn Reuther.
Ten students from The University of Texas Graduate School of Biomedical Sciences at Houston were awarded American Legion Auxiliary fellowships at a luncheon at Trevisio Restaurant and Conference Center in the Texas Medical Center on November 2. Each awardee received $5,000 for their work on a cancer-related project which supplements their graduate research assistantship. The fellowships may be competitively renewed for up to three years.
The awards are funded by the American Legion Auxiliary, the world’s largest women’s patriotic service organization. Founded in 1919, ALA currently has a membership of nearly 800,000 (more than 38,000 in Texas); with local units having a strong presence in more than 9,500 communities nationwide. The American Legion Auxiliary’s mission is to support The American Legion and to honor the sacrifice of those who serve by enhancing the lives of our veterans, military and their families, both at home and abroad.
This year's recipients are:
1st Year Recipients:
Kaitlin Gutierrez (Advisor: Ellen Richie, Ph.D.): Molecular Mechanisms Regulating Thymus Organogenesis: The thymus is an organ that produces a type of white blood cell that can recognize and eliminate cancer cells and other infections, while avoiding self-reactivity, however aging, chemotherapy, or treatments to prepare cancer patients for bone marrow transplants cause the thymus to shrink. This shrinkage decreases the production of these white blood cells which have the ability to mount effective immune responses against cancer and new challenges to our immune system. My research investigates how to prevent or reverse this issue and ways to develop therapeutic strategies to counteract thymus shrinking.
Sarah Klein (Advisor: Juan Fueyo, M.D.): A Novel Immunotherapeutic Strategy for the Treatment of Gliomas: The Role of JNK-dependent Autophagy in Immune Presentation of Antigens: Immunotherapy using viruses has shown promising results for suppressing tumors such as glioblastoma multiforme – the most common and lethal brain tumor in adults. My research is developing and optimizing virus-based therapies that can be utilized in the treatment of this devastating disease.
Christa Manton (Advisor: Joya Chandra, Ph.D.): Targeting beta Subunits of the Proteasome for Glioblastoma Therapy: My research investigates whether a class of anti-cancer drugs called proteasome inhibitors can be used to treat glioblastoma brain tumors. My research will determine factors important for the effectiveness of these inhibitors in brain tumors so that the most effective treatment strategies can be developed using the most powerful therapeutic agents for patients.
Adam Yock (Advisor: Laurence Court, Ph.D.): Consideration of Target Morphology During Image-guided Radiation Therapy: Radiation Therapy is often administered in a series of treatment sessions to take advantage of the differential radiobiological response of healthy and diseased tissue. However, certain factors can compromise the precision of the radiation treatment and a geometric margin around the tumor is added to ensure the diseased tissue receives the prescribed dose. However, such margins result in radiation also being delivered to non-diseased tissues. My work will attempt to improve current methods of determining margins in order to decrease the dose of radiation delivered to healthy tissue while maintaining the full dose to the tumor.
2nd Year Recipients:
Drew Deniger (Advisor: Laurence Cooper, M.D., Ph.D.): Targeting Ovarian Cancer with Hypoxia Sensitive T-cells: Ovarian cancer is a lethal disease and women who initially respond to therapy often relapse to a more progressive disease status. My project has made four major advances in creating novel cell-based ovarian cancer treatments.
Nathan Ihle (Advisor: Garth Powis, D.Phil.): Redefining KRAS Signaling and Treatment of Tumors Driven by this Oncogene: When DNA is damaged in a particular way, it instructs a protein to be made that cannot be turned off and tells cells to continuously grow; leading to cancer. This damaged DNA code is known as an oncogene. One of the earliest discovered oncogenes was KRAS, but despite numerous attempts to make a drug to inhibit the KRAS protein and stop the inappropriate growth: all have failed. This year, I have found a new way to suppress KRAS activity by stopping it from communicating with other proteins in a cell.
Connie Larsson (Advisor: Guillermina Lozano, Ph.D.): Restoration of p53 Activity in Tumors with p53 Missense Mutations: One of the most important tumor suppressors mutated in more than 50 percent of all human cancers is p53 and mutations to this gene result in de-regulated p53 activity. I am investigating the effects of combining chemotherapy with reactivation of p53 function in cancer, since many cancer therapies now use a combination of treatments in order to achieve a greater tumor response.
Jacquelyn Reuther (Advisor: Ann Killary, Ph.D.): Discovery and Functional Characterization of Somatic Mutations in the Novel Tumor Suppressor DEAR1: My research centers on the function of a gene, DEAR1, and how loss of its function, a common occurrence in breast cancer, is involved in tumor development. I will try to determine if DEAR1 can negatively regulate a survival mechanism that breast cancer cells often activate.
Howard Rosoff (Advisor: Dean Lee, M.D., Ph.D.): Predictive Models of Autologous NK Cell Re-education in Altered Self Environments: My research focuses on testing combinations of immune cells and cancer cells to identify which of malignant cell killers will exhibit the highest degree of toxicity against a given tumor.
3rd Year Recipient:
Tamara Laskowski (Advisor: Brian Davis, Ph.D.): Genome Editing in Hematopoietic Stem Cells as a Therapy for Wiskott-Aldrich Syndrome: My work focuses on the development of a new form of therapy to target and correct cells that carry disease-causing genetic defects. The disease I worked with in this project is called Wiskott-Aldrich Syndrome (WAS), and it results from a genetic defect on the DNA of blood cells, making these cells weak and not capable of fighting infections.