utilizing Stuart Scott Memorial Cancer Fund matching funds
Lung cancer is more common and deadly in African American patients compared to other racial groups. One reason for this difference may depend on the genetics of the tumor and how genes are expressed. We plan to study lung cancer samples to find differences in genes between African American and Caucasian tumors. We will also use a ‘Just Ask’ cultural training program to improve the engagement of African‐American lung cancer patients in research and tissue banking. Our hope is that this work will improve the understanding of reasons for racial differences in lung cancer. We hope that by studying the gene expression of tumors we will find new ways to treat patients with lung cancer in the future.
The purpose of our study is to test psychosocial interventions to improve quality of life (QOL) (psychological, physical, social and spiritual well-being) for Latinas with breast cancer and their informal caregivers who are helping them during their cancer journey. Latinas and their caregivers often experience severe psychological distress during cancer treatment and this distress can negatively affect health and well-being. Participants in our study are assigned to either an 8-week supportive health education intervention or an 8-week telephone interpersonal counseling intervention. Both the health education and the counseling are provided over the telephone, and each person is called separately. Our trained health care workers call the women and their caregivers at times that are convenient for them. Sessions are about 30 minutes on the phone each week for 8 weeks. Using the telephone to deliver this service removes many of the access barriers normally associated with counseling or health education. In addition to participating in the 8 education or counseling sessions, we will gather biomarkers using saliva at each measurement period to determine if the intervention was effective at the physiological level. We ask the women and their caregivers to complete some questionnaires 4 times over the next 6 months to determine if the intervention was helpful to them. All study related materials, assessments and sessions are conducted in English or Spanish, depending on the person’s preference. At the end of our study, we also tell them about any other clinical trials that may be of interest.
Neuroblastoma is the third most common childhood cancer. Unfortunately, despite intensive treatment, two-thirds of children with advanced neuroblastoma succumb to their disease. New treatment options must be developed to improve outcomes in this devastating disease. This requires a better understanding of how neuroblastoma cells survive in the face of these intensive therapies. N-Myc is a member of a family of proto-oncogenes (genes capable of leading to cancer development) implicated as a cause of several cancers. N-Myc plays a central role in the aggressiveness of neuroblastoma tumors. Children whose neuroblastoma tumors have extra copies of the N-Myc gene (N-Myc amplification) fare worse than children whose tumors have the normal number of N-Myc genes. However, it is unknown why extra N-Myc leads to poor outcomes. Mxi1 is a protein related to the Myc family, however, it counteracts the ability of N-Myc to cause cell growth. Mxi0 is a similar protein, but it does not inhibit N-Myc like Mxi1. In this proposal, we will test the hypothesis that the balance of Mxi1 and Mxi0 expression is important for maintaining normal growth, and that N-Myc alters this balance, leading to treatment resistance. To accomplish this, we developed a new kind of mouse which has its Mxi1 or Mxi0 genes removed. In this project, we will examine the impact of decreasing Mxi1 or Mxi0 expression on neuroblastoma tumor formation and response to treatment, with the overall goal of finding a mechanism to bypass the effects of N-Myc and improve the outcomes of children with neuroblastoma.
V Scholar Plus Award- extended funding for exceptional V Scholars
Aggressive lymphomas are cancers of white blood cells. The most common type is called diffuse large B cell lymphoma (DLBCL). Most patients with DLBCL can be cured by chemotherapy, but some patients either do not respond to treatment or the disease comes back after a certain time (‘relapse’). If we can identify those patients likely to relapse earlier, we hope to improve their chance of survival. Circulating tumor DNA (‘ctDNA’) is DNA that comes from tumor cells and gets in the blood stream. CtDNA in the patient’s blood can be analyzed to get more information about the tumor. In this study, we developed a blood test to profile ctDNA at different stages of the disease and to identify patients at risk for relapse. We found that ctDNA in the patient’s blood contains information that can be used to tell how well the patients will do with chemotherapy. We also observed that analysis of ctDNA over the course of treatment could show how their lymphomas change over time. For example, we detected new mistakes (‘mutations’) in ctDNA that could be used as an early signal to predict that certain treatments would no longer work in these patients. Also, we found that ctDNA in the blood after treatment predicts disease relapse months earlier than any other clinical method. Our test can also give physicians early warning that the tumor is changing from a slow growing to a fast growing lymphoma type. All this information in ctDNA can be used to learn more about lymphoma biology and to find patient groups with high risk for relapse.
V Scholar Plus Award- extended funding for exceptional V Scholars
Gene regulation is vital for our health and abnormal regulations lead to many diseases, including cancer. There are two mechanisms that control genes: Genetic info and epigenetic. Genetic alterations are stable and we cannot target them. However, epigenetic is dynamic as it changes over time. Epigenetic can control gene expression in tissues. It is the loss of this control that causes cancer. In cancer, only select genes are abnormal while the rest are normal. We need to target only abnormal genes. Current therapy is based on chemicals that target all of the genes in the cell. Thus they have side effects. This proposal develops a novel tool that can target a specific gene. Thus, it can correct an aberrant gene only. The tool also has strong therapeutic potential. This will be very valuable for basic research.
“Precision medicine” aims to develop better treatments by understanding the molecular causes of disease. This is essential in cancer because each type (breast, brain, or blood cancer, for example) represents dozens of different kinds of cancer at the molecular level. And each of these different molecular sub-types requires different treatments.
Based on research of the past twenty years, we understand a great deal about what drives cancers. Many drugs have been devised that specifically target these causes – molecular “smart bombs.” However, the cancer cells rapidly adapt and find escape routes. Drugs that seem to work ultimately fail. We get many hopeful responses but few cures.
Our research seeks to identify and block these escape routes. We look at the molecular changes inside cancer cells after drugs are applied, and we then use other drugs to “slam the door” so the cancer cannot escape treatment. Our approach is already proving successful: We are testing one of these combinations in people to treat Mantle Cell Lymphoma. We propose to look at similar cancers that might benefit from this approach. We also want to better understand ways that cancer cells might escape from our combination treatments. Our goal is to improve responses to therapy and turn temporary responses into real cures.
Pancreatic cancer is one of the deadliest cancers, largely because most therapies are poorly active in patients or are too toxic when administered. Indeed, pancreatic cancer patients become ill very quickly, and cannot withstand the side effects of chemotherapy that patients with other types of cancer can tolerate. Therefore, we need to identify new therapies that kill pancreatic cancer cells effectively and are well tolerated by patients. To accomplish this goal, we have developed a new model system from pancreatic tumors, called organoids. Organoids are 3D cultures grown in an extracellular material rich matrix, called Matrigel, and can faithfully mimic the patient’s tumor, from which it was derived. Organoids can be used to sequence for mutations in the cancer cells and to test for therapies that could kill the cells. Using organoids, we have identified a number of compounds that can surprisingly kill the different cell types present in pancreatic tumors, including several drugs that are given to millions of people daily and are well tolerated but not previously considered to be cancer medicines. Importantly, we also find that certain combinations of these new drugs can shrink human pancreatic tumors engrafted in mice. Here, we propose to extend these exciting preliminary findings to a broader collection of drugs and a larger collection of organoids, and develop the most promising candidates as new strategies for an early phase clinical trial. Our goal is to test at least one novel combination of non-traditional drugs in pancreatic cancer patients within three years.
Funded by the Stuart Scott Memorial Cancer Research Fund
PSA is a blood test used to check men for harmful prostate cancer (PCa). A man with high levels of PSA may have harmful PCa, but if we catch it early, it is almost 100% curable. Men with high PSA may also have harmless PCa or they may not have cancer at all. To diagnose harmful PCa, doctors take biopsies of the prostate using painful needles. Fortunately, most of the men end up having large prostates or harmless forms of PCa. This causes many men to suffer through the biopsy and then worry about potentially having a harmful cancer. Some men with harmless PCa will have surgery or radiation from fear, but can have bad side effects.
Prostate Health Index (PHI) is an improved version of PSA that better predicts which men have harmful, PCa. Doctors use PHI to help men avoid prostate biopsies. Unfortunately, PHI was never tested for accuracy in African American men (AAM). AAM have the highest chance of dying from harmful PCa. We need to prove that the test works in AAM like it does in White men. We will compare how well the test works for predicting harmful PCa in 300 African American men in comparison to 100 White men that are having a prostate biopsy. If PHI works, we will be able to detect harmful PCa earlier for African American men. This test will reduce their chances of dying from the disease.
In this project, we aim to develop a safe and effective treatment for a childhood cancer called neuroblastoma. Recently, there has been some success harnessing the human immune system to fight cancer. We have developed an immune-based strategy to target one specific cancer-promoting gene that is known to cause an aggressive form of neuroblastoma. This gene is present in about half of all cases with poor disease outcomes in our patient population. We developed a new cancer vaccine for this gene that causes immune cells in the body to fight cancer cells directly. A mouse version of this vaccine proved safe and potent in mice, so we think we can use the same strategy to create a clinical-grade vaccine that will be safe and effective in humans, too. In this study, we first will test each part of this vaccine separately and then will re-assemble them in a very clean laboratory room. Indeed, this vaccine will be produced under such strict conditions that it will be ready for clinical testing in children with neuroblastoma after this grant is completed. Because we are targeting a gene that is expressed on cancer cells but not on cells of healthy tissues, our vaccine is unlikely to be as toxic as others treatments that are available now in the clinic. This vaccine is easy to deliver, as it can be swallowed and so does not involve a shot, making it easier for pediatric patients.
Rhabdomyosarcoma is a connective tissue cancer with features of skeletal muscle, and the most common soft tissue cancer of childhood and adolescence. While most children with the embryonal variant of rhabdomyosarcoma are cured, there is a sub-group of children with high-risk features, making their chance of survival less than one in three. One hypothesis underlying these high-risk features is that there are rhabdomyosarcoma stem cells that can persist in the body despite current standard therapy. A goal of our research laboratory is to identify the cellular pathways that contribute to this persistence of rhabdomyosarcoma stem cells. Over the past several years we have observed that some cellular pathways active during normal skeletal muscle development have been hijacked by embryonal rhabdomyosarcoma cells. We even think that these development pathways communicate with one another to support and reinforce rhabdomyosarcoma stem cells. Our aim in this project is to understand how these cellular pathways communicate with one another, whether they can be inhibited by gene manipulations or pharmacologic agents, then test combinations of these treatments in rhabdomyosarcoma cells in culture and in laboratory mice. We hope to someday translate these findings to clinical trials, opening the door to new treatments for children with this disease.
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