Genitourinary Cancers Symposium

GU 2017 Daily News - Saturday

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Dr. W. Marston Linehan to Discuss Genetic Conditions With Predisposition to Renal Cell Carcinoma W . Marston Linehan, MD, chief of the Urologic On- cology Branch at the National Cancer Institute (NCI) Center for Cancer Research, National Insti- tutes of Health, will provide an overview of genetic conditions with predisposition to renal cell carcinoma (RCC) during his keynote lecture on February 18. He will also dis- cuss the latest insights from clinical trials involving patients with genetically defi ned forms of familial RCC, including von Hippel-Lindau (VHL) syndrome, hereditary papillary renal cell car- cinoma (HPRCC), Birt-Hogg-Dubé (BHD) syndrome, and hereditary leiomyomatosis and renal cell carcinoma (HLRCC). Understanding the Genetic Basis of RCC Since 1982, Dr. Linehan's clinical research career has been focused on the identifi cation of tumor suppressor genes and oncogenes in familial and sporadic genitourinary malignancies. His greatest con- tribution to the fi eld so far is the discovery of the genetic basis of RCC, specifi cally the genes and gene pathways involved in the de- velopment of this disease. In an interview with the Genitourinary Cancers Symposium Daily News, Dr. Linehan debunked some of the common misconceptions about RCC. "When we started studying kidney cancer in the early 1980s, it was considered to be a single disease," he said. This view resulted in uniform treatment strategies for all patients with RCC and, consequently, with some poor outcomes. "We performed the same operation for all types of kidney cancer, and we gave the same drugs, none of which were effective, to all patients with metastatic disease," Dr. Linehan explained. Largely owing to the continued research efforts of Dr. Linehan and his team, we now know that RCC is not a single disease. "It is made up of a number of different types of cancer, each with a distinct histology, each with a different clinical course, each responding differently to therapy, and each caused by a different gene," he said. At least 15 different genes have been identifi ed as RCC-causing genes. Dr. Linehan said that most insights about the genetic basis of RCC stem from studies of families with the disease. "There are a number of different types of genetically defi ned Treatment of Oligometastatic Prostate Cancer: Systemic Therapy, Primary Local Prostate Therapy, Metastasectomy, and Beyond Jeanny B. Aragon-Ching, MD, FACP T he last decade has heralded advances in the treatment of pros- tate cancer that have resulted in paradigm shifts in the treat- ment of metastatic castration-sensitive disease. Androgen deprivation therapy (ADT) had been the cornerstone of treat- ment for high-risk, locally advanced metastatic disease for decades, but the addition of chemotherapy with docetaxel has changed the standard of care in patients with metastatic hormone-sensitive or castration-sensitive disease. 1 Although de novo metastatic prostate cancer has a relatively low incidence of 4% per year according to the Surveillance, Epidemiology, and End Results (SEER) Program database, recent studies have shown an increase in metastatic dis- ease diagnoses. This could be because of the changes in the PSA screening guidelines 2 or because better and more frequent imaging detects metastatic disease more readily. It is also clear that patients with a higher volume of metastatic disease benefi t substantially from early chemotherapy. But what about those patients with low-volume disease? The term "oligometastatic disease" hails from the Greek word "oligos," mean- ing few or little. How many lesions defi ne oligometastatic disease: one, two, three, or less than fi ve? There is no uniform description, although there are data to suggest that patients with oligometastatic disease fare better than those with more widespread disease. 3 Does having one solitary lesion herald a seminal event versus pre- senting with multiple lesions? One can contemplate whether maxi- mally treating the patient using systemic therapy alone with ADT and chemotherapy would be a suffi cient optimal approach for con- trolling their cancer and addressing the tumor microenvironment. Attendee Tip of the Day Listen to the ASCO Daily News Podcast series. Podcasts feature renowned oncologists discussing the research in their areas of expertise. Download the podcasts to your device for listening anywhere. ➤ Listen: am.asco.org/asco-daily-news-podcast See Dr. Linehan, Page 10 See Oligometastatic Prostate Cancer, Page 3 2016 SUO Annual Meeting Highlights 8 Young Investigator Awards Advance Research 10 Symposium Essentials: Networking 12 The Evolving Role of Active Surveillance in Small Renal Tumors 12 Noninvasive Imaging in Muscle-Invasive and Metastatic Bladder Cancer 16 Symposium Essentials: Before Heading Home 16 Big Data Comes to Radiation Oncology Research 20 My Meeting Experience: An Early-Career Oncologist's Perspective 24 CCF-Funded Study Examines Attitudes Toward Active Surveillance 24 Symposium Essentials: Stay Connected 24 Symposium Essentials: Audience Participation 25 INSIDE T A R G E T I N G C A N C E R C A R E Safety and Effi cacy of Anti–PD-1/–PD-L1 Agents in Urothelial Carcinoma R obert Dreicer, MD, MS, FACP, FASCO, answers a question posed by an at- tendee during a Best of ASCO ® Meeting. Dr. Dreicer is the medical oncology section head and deputy director of the University of Virginia Cancer Center. Question: In urothelial car- cinoma, is there a difference in effi cacy or safety among agents that target PD-1 versus agents that target PD-L1? Answer: Given the astonishing speed in which anti–PD-1/–PD- L1 agents have become an inte- gral part of our therapeutic arma- mentarium in an ever-growing number of neoplasms, includ- ing advanced urothelial cancer, it should come as little surprise See Anti–PD-1/–PD-L1 Agents, Page 16 2017 S A T U R D A Y, F E B R U A R Y 1 8 O R L A N D O , F L Dr. W. Marston Linehan Clinical Corner

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