Researchers develop new nanoparticle to boost immune system
Vanderbilt researchers have developed a new nanoparticle that can more effectively get drugs inside of cells to boost the immune system and fight diseases like cancer.
Featured Speakers:
Alan Ashworth, PhD, FRS
(UCSF Helen Diller Family Comprehensive Cancer Center)
is the President of the Helen Diller Family Comprehensive Cancer Center at University of California, San Francisco and Senior Vice President for clinical services, UCSF Health. Dr. Ashworth was a key member of the team that discovered the BRCA2 gene in 1995, which is linked to an increased risk of breast, ovarian and other cancers. In 2005, his lab identified a way to exploit genetic weaknesses (using synthetic lethality) in cancer cells with mutated BRCA1 or 2 genes, leading to a new approach to cancer treatment, PARP inhibition. Four different PARP inhibitors have now been approved by the FDA for the treatment of ovarian, breast, pancreatic and prostate cancer based on this observation, which was named by Nature in the top 20 discoveries in cancer in the 21st century. He continues to develop new treatments for cancer using genetic principles.
Judy E. Garber, MD, MPH
(Dana Farber Cancer Institute)
is the Susan F. Smith Chair and Chief of the Division of Cancer Genetics and Prevention at Dana-Farber Cancer Institute and a Professor of Medicine at Harvard Medical School. She conducts research in clinical cancer genetics, with a special focus in the genetics of breast cancer. Dr. Garber is also a leader in research into the characteristics and treatment of triple negative breast cancer, the most common form in women with BRCA1 mutations and an expert in Li-Fraumeni Syndrome. Her translational research focuses on the evaluation of novel agents targeting DNA repair defects in breast cancer, including PARP inhibitors for treatment and prevention of breast cancer and other BRCA-associated cancers, and the study of other agents for reduction of breast cancer risk.
Padma Sheila Rajagopal
(National Institute of Health, Cancer Data Science Laboratory)
is a recipient of the Ruth L. Kirschstein F32 Postdoctoral Fellowship and the American Society of Clinical Oncology / Breast Cancer Research Foundation Conquer Cancer Young Investigator Award for her research on integrating germline variants through a predicted transcriptome model of the breast and comparing prognostication of outcomes in breast cancer to the tumor transcriptome. She joined the Cancer Data Science Laboratory as an Assistant Clinical Investigator in 2021. Dr. Rajagopal’s laboratory currently investigates how genomic and transcriptomic interactions between germline variants / inherited cancer syndromes and somatic development in tumors can improve clinical prediction and prognostication in patients with cancer.
Bert Vogelstein, MD
(Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins)
is the Clayton Professor of Oncology and Pathology, An Investigator of the Howard Hughes Medical Institute, and a Director of the Ludwig Institute and Lustgarten Dedicated Laboratory for Pancreatic Cancer Research at the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins. Dr. Vogelstein and his colleagues discovered the genetic basis of human colorectal tumors. In the process, they discovered many of the genes, pathways, and concepts that are the foundation of modern cancer research. His group's basic scientific studies have been distinguished by a focus on practical applications of the knowledge gained from their work. For example, Vogelstein and his colleagues not only participated in the discovery of the genetic bases for hereditary colorectal cancer predisposition syndromes in the 90's, but a more recently developed an effective form of therapy for one such syndrome that is based on understanding of its genetic defect. From a broader perspective, his group initiated a new chapter in diagnostics in 1992 when they demonstrated that somatically acquired driver gene mutations can be used as biomarkers for cancer. This approach is now often referred to as "liquid biopsies". His group currently focuses on developing new approaches to detect cancers earlier as well as developing novel immunotherapeutic agents that can combat cancer if it is not detected early enough.
This phase III trial studies how well inguinal lymph node dissection (ILND) surgery alone or after chemotherapy with or without intensity-modulated radiation therapy works in treating patients with penile cancer that has spread to other places in the body. Surgery is used to remove the lymph nodes and may be able to cure the cancer. Drugs used in chemotherapy, such as paclitaxel, ifosfamide, and cisplatin, work in different ways to stop the growth of tumor cells, either by killing the cells, by stopping them from dividing, or by stopping them from spreading. Intensity-modulated radiation therapy uses high-energy x-rays to kill tumor cells and shrink tumors. It is not known whether having surgery after chemotherapy with or without radiation therapy is better than having surgery alone.
This phase IV trial evaluates how well giving standard of care (SOC) peptide receptor radionuclide therapy (PRRT) after SOC surgical removal of as much tumor as possible (debulking surgery) works in treating patients with grade 1 or 2, somatostatin receptor (SSTR) positive, gastroenteropancreatic neuroendocrine tumors (GEP-NETs) that have spread from where they first started (primary site) to the liver (hepatic metastasis). Lutetium Lu 177 dotatate is a radioactive drug that uses targeted radiation to kill tumor cells. Lutetium Lu 177 dotatate includes a radioactive form (an isotope) of the element called lutetium. This radioactive isotope (Lu-177) is attached to a molecule called dotatate. On the surface of GEP-NET tumor cells, a receptor called a somatostatin receptor binds to dotatate. When this binding occurs, the lutetium Lu 177 dotatate drug then enters somatostatin receptor-positive tumor cells, and radiation emitted by Lu-177 helps kill the cells. Giving lutetium Lu 177 dotatate after surgical debulking may better treat patients with grade 1/2 GEP-NETs.
This phase III trial uses the Decipher risk score to guide therapy selection. Decipher score is based on the activity of 22 genes in prostate tumor and may predict how likely it is for recurrent prostate cancer to spread (metastasize) to other parts of the body. Decipher score in this study is used for patient selection and the two variations of treatment to be studied: intensification for higher Decipher score or de-intensification for low Decipher score. Patients with higher Decipher risk score will be assigned to the part of the study that compares the use of 6 months of the usual treatment (hormone therapy and radiation treatment) to the use of darolutamide plus the usual treatment (intensification). The purpose of this section of the study is to determine whether the additional drug can reduce the chance of cancer coming back and spreading in patients with higher Decipher score. The addition of darolutamide to the usual treatment may better control the cancer and prevent it from spreading. Alternatively, patients with low Decipher risk score will be assigned to the part of the study that compares the use of radiation treatment alone (de-intensification) to the usual approach (6 months of hormone therapy plus radiation). The purpose of this part of the study is to determine if radiation treatment alone is as effective compared to the usual treatment without affecting the chance of tumor coming back in patients with low Decipher score prostate cancer. Radiation therapy uses high energy to kill tumor cells and reduce the tumor size. Hormone therapy drugs such as darolutamide suppress or block the production or action of male hormones that play role in prostate cancer development. Effect of radiation treatment alone in patients with low Decipher score prostate cancer could be the same as the usual approach in stabilizing prostate cancer and preventing it from spreading, while avoiding the side effects associated with hormonal therapy.
