ASH News Daily 2013 - Day 1 - (Page A1)

Read this issue online at Follow us on Twitter using #ASH13 SCHEDULE 11:15 a.m. - 12:15 p.m. Grassroots Network Lunch (ticketed session) Riverbend Ballroom, New Orleans Downtown Marriott at the Convention Center 11:15 a.m. - 12:15 p.m. How I Treat: Bringing Science to Clinical Dilemmas (ticketed sessions) 11:15 a.m. - 12:15 p.m. Continuing Conversations (ticketed sessions) Meet the Scientist (ticketed sessions) 12:30 - 1:30 p.m. Ham-Wasserman Lecture Speaker: Clara Camaschella, MD Topic: Iron and Hepcidin Hall F 2:00 - 3:00 p.m. Special Symposium: Clinical Practice Guidelines Room 393-396, Convention Center 4:00 - 5:30 p.m. Special Scientific Symposium: Approaches for Inhibiting "Undruggable" Targets in Cancer New Orleans Theater C, Convention Center 5:30 - 7:30 p.m. Welcome Reception Poster Halls E and G Dr. Janis Abkowitz, ASH President, welcomes attendees and highlights special programming and new meeting offerings. Who Puts the Quality in Quality? BY JULIE KANTER, MD " Q uality improvement" has become a commonplace term in medicine today. New Medicare programs and private insurance companies have tied measurements of quality to monetary and professional reimbursement. Quality improvement projects are required as part of maintenance of certification (licensure) in many disciplines. Thus, with all of this discussion, it would seem that "quality" should be easily defined, implemented, and measured. However, this is not necessarily the case. This afternoon from 2:00 to 3:30 p.m., the issues surrounding quality-of-care implementation will be discussed during the Special Symposium on Quality: Clinical Practice Guidelines. This session, which will take place in Room 393-396 in the Ernest N. Morial Convention Center, will review how clinical practice guidelines can be developed for blood disorders to both optimize quality of care for patients and satisfy ACO. The committee chairs, Dr. Adam Cuker of the University of Pennsylvania, and Dr. Mary Cushman of the University of Vermont, have assembled a program in which speakers will define the current challenges facing the field of guideline development in a manner that is both methodologically rigorous and user friendly. Dr. Holger Schünemann of McMaster University, Hamilton, ON, will begin the symposium with an explanation of the history of the development of clinical practice guidelines and on the evolution of guideline methodology. Having served »» QUALITY Page A-16 The 2013 Ham-Wasserman Lecture - BY MARK M. UDDEN, MD IN THIS SECTION Speaker Updates A-4 Obstetric Consultation A-4 Venus Thromboembolism A-7 Crossword Puzzle A-8 T-Cell Tolerance A-13 ASH Outreach A-17 -"Iron, cold Iron ... is ruler of them all." Iron is critical to mitochondrial function and heme iron is necessary to transport oxygen; however, iron can be a loose cannon generating unwanted oxidation. It is a ruler that requires protective custody by chaperones such as transferrin and the storage protein ferritin and careful regulation of its entrance and exit from the circulating iron pool. This year, Dr. Clara Camaschella R will offer us a vision of the brave new world of iron metabolism in her lecture Iron and Hepcidin: A Story of Recycling and Balance. The lecture will be held today in Hall F in the Ernest N. Morial Convention Center Iron in the Balance from 12:30 to 1:30 p.m. As Dr. Camaschella will show us, it turns out that iron has its own master since it is ruled by the hepcidin ferroportin axis that regulates flux of iron from enterocytes and macrophages to the circulating iron pool. Iron availability must be closely regulated to avoid excess or deficiency. To achieve this, there is a delicate balance between hepcidin degradation and upregulation. Hepcidin degrades the iron exporter ferroportin thereby inhibiting iron flux to the plasma, and hepcidin upregulation is linked to an important signaling cascade in which bone morphogenic protein receptor (BMPR) complex activates SMAD, which then upregulates hepcidin. When BMP is diminished, as it is in hemochromatosis types 1, 2, and 3, hepcidin is reduced and iron accumulates because ferroportin is un- udyard Kipling famously observed that of the metals gold, silver, and copper checked. For effective erythropoiesis, an adequate amount of iron must be provided, and hepcidin must be suppressed when there is a call for more red cells. A desirable increase in iron availability occurs in iron deficiency and during hypoxia, and an unwanted iron overload occurs in thalassemia because hepcidin is typically suppressed in these states. Another area of interest that Dr. Camaschalla will discuss is her lab's investigation of the role of TMPRSS6, a serum protease that inhibits hepcidin. Matriptase-2, a serine protease encoded by TMPRSS6, is mutated in the Mask mouse, which suffers from a microcytic anemia, high hepcidin, and inability to absorb oral iron. Thus, TMPRSS6 is the key to understanding how hypoxia »» HAM-WASSERMAN Page A-16

Table of Contents for the Digital Edition of ASH News Daily 2013 - Day 1

Table of Contents

ASH News Daily 2013 - Day 1