Funded by the Coopers Catch fundraiser, Tampa Bay Lightning Foundation and Dick Vitale
Melanoma arising in young patients (under age 21) has becoming an increasingly major problem in the US. Very little is known about the specific causes of melanoma in younger individuals, and the prognosis is very difficult to determine. In many cases, even whether a mole is benign or malignant is in question, adding to the stress of a difficult situation for patients and families. Newer molecular tests, developed for analyzing other forms of cancer, could potentially help establish the diagnosis, prognosis and treatment for patients, but these tests have not been validated in young patients and are usually not covered by insurance – forcing families to pay out-of-pocket when and if they can. Moffitt Cancer Center is one of the world’s leading centers for diagnosis, treatment and research in melanoma in children, adolescents and young adults. This project will involve molecular testing of the tumor specimens from patients under 21 who have known or suspected melanoma, avoiding out-of-pocket expenses for unproven technology, and the results of these tests will be correlated with standard pathology analysis and the results of medically necessary surgery (such as wide excision and sentinel node biopsy) and/or medical treatments (such as immunotherapy). The results will set the stage for larger efforts to discover why melanoma occurs in such young individuals, and for the validation of clinical tests to determine how patients should be treated – which could then be used to support insurance coverage for those tests that are most helpful.
Funded by the Coopers Catch fundraiser, Tampa Bay Lightning Foundation and Dick Vitale
In the 1970’s, cancer in children and young adults was almost always fatal. To address this, pediatric cancer doctors across the United States joined forces to do research as a group so they could figure out the best way to treat the cancers in this population. Through over 40 years, these research studies (also called clinical trials) have enabled pediatric cancer doctors to raise the cure rates to nearly 90%. That still means 1 of 10 children with cancer will unfortunately die. Over the years research has shown that children that enroll on clinical trials may have better survival than those that do not, and only around 40% of children enroll on treatment studies. A major reason some families do not enroll their children is that they are not properly educated by the medical team. In addition, African-Americans and Hispanic patients enroll at lower rates than Caucasian patients for several reasons, an important one being education about what clinical trials are all about. This project will create bilingual educational materials to teach families and patients about research protocols and their purpose. They will be less intimidated and more willing to allow their children to have access to the most cutting edge therapies and other studies available. We hope that these materials will lead to increased clinical trial participation and consequently greater cure rates.
V Scholar Plus Award – extended funding for exceptional V Scholars
Ewing sarcoma is the second most common bone cancer in children and is a very aggressive cancer with a rate of survival of only 60-70%. One important path to finding new treatments for this disease comes from the fact that all Ewing sarcoma cases have an abnormal fusion protein known as EWS-FLI1 which activates genes that drive the formation of tumors. In a prior study we characterized the genes that are activated by EWS-FLI1 in Ewing sarcoma and identified the kinase VRK1 as a promising new therapeutic target. We have also demonstrated that inactivation of VRK1 results in a strong reduction of Ewing sarcoma growth. In this proposal our goal is to characterize the role of VRK1 in Ewing sarcoma and to better understand the mechanisms that regulate its expression in these tumors. These experiments will validate the potential of VRK1 as a therapeutic target and will point to molecular pathways that account for its importance in this disease.
Queen of the Valley Medical Center (QVMC) in collaboration with OLE Health and St. Helena Hospital (SHH) will develop and launch a countywide colon cancer screening initiative. This integrated effort will ensure timely diagnosis and access to treatment and care for patients regardless of health insurance status. OLE Health will provide the outreach to patients, administer the FIT test and refer patients to Queen or the Valley Medical Center or SHH as indicated for further testing and treatment. Queen of the Valley will collaborate with OLE Health to identify patients that may also be candidates for clinical trials or research. The three organizations will work together on shared messaging to the community to raise awareness about the collaboration and opportunity for cancer screening.
This V Foundation grant will stimulate an innovative countywide “new” system of care between OLE Health, Queen of the Valley and SHH utilizing cancer nurse navigators to ensure a warm hand off and a solid continuum of care. Queen of the Valley Medical Center Patient Navigator role will support and link the continuum of care for patients referred from OLE Health for further cancer diagnostics and care as appropriate. This grant will be used to hire staff and support other components of patient navigation. Queen of the Valley Medical Center believes that our cancer patients deserve the very best in treatment – more cures, and better quality of life.
V Scholar Plus Award – extended funding for exceptional V Scholars
Cervical cancer is responsible for 15% of cancer-related deaths in women worldwide, with highest frequency occurring in resource-limited settings. In addition, incidence and mortality rates are disproportionately higher in African-American and Hispanic populations within the United States, compared with other ethnic/racial groups. Many patients die of cancer either because it spreads to other body organs (metastasis), or because the cancer grows again in the same organ (recurrence). In cervical cancer, 90% of recurrence cases occur within 3 years of diagnosis, and less than 5% of these patients survive beyond 5 years. It is therefore essential to find ways to predict the likelihood of tumor recurrence in order to improve the management and prognosis of cancer patients. We hypothesize that the biological events that lead to tumor recurrence are already at play, even at the time of treatment. In particular, we believe that several biological molecules (human, viral and bacterial) play role in this complex process. We therefore seek to identify and compare these factors in surgically removed cervical tumors and their adjacent normal tissues between 2 groups of women: those with tumor recurrence within 3 years of surgery, and those without recurrence despite longer follow-up. We hope to identify differences in the relative abundance of these biological molecules that will serve as sentinels (we call them biomarkers) to warn us of the likelihood of tumor recurrence. This work has the potential to lead to the development of diagnostic tools for predicting and preventing recurrence in and beyond cervical cancer.
OLE Health will focus on increasing the number of patients successfully completing fecal immunochemical test (FIT) tests for colorectal cancer screening, and providing referrals for the patients determined to need follow-up tests and treatment. Cancer screening is the crucial life-saving step needed to ensure early detection and treatment. It is particularly important to OLE Health patients because screening rates are generally lower in Hispanic/Latino populations, and Latinos represent 62% of OLE’s patients. In addition, 88% of OLE patients are uninsured, on Medi-Cal, or Medicare. According to the American Cancer Society’s Cancer Facts & Figures 2015, “Uninsured patients and those from ethnic minorities are substantially more likely to be diagnosed with cancer at a later stage, when treatment can be more extensive, more costly, and less successful.
Cancer therapy has undergone a revolution in recent years as a result of the success of several immunotherapies, providing hope to patients with once-thought incurable cancers. One of the most powerful technologies is engineered T cell therapy. By reprogramming a T cell, a type of immune cell, to recognize and kill a cancerous cell, we have seen remissions in over 90% of children and young adults with very resistant acute lymphoblastic leukemia (ALL). Because T cells are living cells, they have the potential to last in the body for months or years and may provide long-term disease control. While most of these remissions are long-lasting, with 60% of responding patients still in remission at 1 year, relapse remains the key mode of treatment failure. One of the reasons for relapse is short lifespan of the engineered T cells in some patients. In this study, we will ask why T cells live many months to years in some patients while they live only weeks to a few months in others. We will use this information to open a clinical trial to test the combination of engineered T cells with a medication to augment T cell function. As we improve on the percentage of long-term remissions, we hope to not only increase the chance of cure but also reduce the number of patients who require intensive therapies, including bone marrow transplant.
Funded in partnership with the Kansas City Chiefs Football Club
Recent successes demonstrate the power of using the immune system clinically to destroy cancer. One such therapy involves the infusion of cells called natural killer (NK) cells. This therapy works well for blood cancers. However, there has been limited success with this therapy against solid cancers. The ultimate goal of our research is to increase this efficacy. NK cell killing occurs when receptors expressed on the NK cells are bound. One of these receptors, Natural killer group 2 member D (NKG2D), plays a critical role in the killing of cancers in both mice and humans. My lab has recently generated data that indicate there is a role for NKG2D-binding partners expressed on NK cells in cancer destruction. We demonstrate that upon activation, human and mouse NK cells express these binding partners on the cell surface. We further show that this alters the secretion of factors that play critical roles in cancer destruction. We propose to test the hypothesis that expression of these NKG2D binding partners alters the ability of NK cells to kill cancer cells and that manipulation of this expression can be used to increase the efficacy of NK cell therapy. We will use mouse models to test this hypothesis with both mouse and human NK cells and cancers. At the completion of these studies we will know 1) whether expression of NKG2D binding partners by NK cells affects NK cancer therapy and 2) whether manipulation of this expression is likely to increase the efficacy of clinical NK therapy.
Funded in partnership with St. Baldrick’s Foundation
Alveolar rhabdomyosarcoma is one of the most common children tumors. Traditional dogma is that a particular molecular event is unique to the tumor, like a “signature”. We recently found the same event in normal cells, with a physiological function. This discovery raises the possibility that the tumors initiated from the same cells that harbor this “signature” fusion during normal development. Like fingerprints at a crime scene, this molecular event is giving us clues about the process of tumorigenesis. We will figure out the meaning of this signature molecular in normal development and how its’ going awry will drive rhabdomyosarcoma. In addition, cells at the same development stages harbor several other fusions that are also present in alveolar rhabdomyosarcoma. One of the newly identified fusions led us to uncover a potential new oncogene, which drives the tumor. Our finding will not only lead to better understanding of the tumor, but also have the potential for uncovering new treatment for the disease.
Although childhood cancer survival rates have improved over the past 40 years, pediatric acute myeloid leukemia (AML) is still very difficult to treat successfully. This is partially because the immune system has a hard time recognizing and killing AML cells. Though white blood cells usually fight infections or cancer, certain types of “tumor-permissive” white blood cells (APCs) make it easier for cancer to escape being recognized by the immune system. These tumor-permissive APCs send out signals to other immune cells telling them to relax and not kill leukemia cells. Our research goal is to find ways to make these APCs stop sending tumor-permissive signals, so that the immune system can recognize AML cells better and get rid of the leukemia. Specifically, we found that APCs use a protein called MerTK to send tumor-permissive signals to other immune cells. When we block MerTK using a new orally-active drug, APCs stop sending tumor-permissive signals and instead, start sending new signals that tell other immune cells to fight leukemia. MerTK drugs are headed to clinical trials for their anti-cancer effects; our research demonstrates that these drugs could also be used to boost the immune system against cancer. With this grant, we will investigate the cellular steps involved in blocking MerTK, so that we can determine how to use MerTK inhibitors most effectively to treat pediatric patients with AML. We hope to show that this novel therapy will help improve pediatric AML survival rates and patient’s quality of life.
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