American Society of Hematology

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General Sessions

Following is a schedule of General Sessions at the 2011 ASH annual meeting:

Ham-Wasserman Lecture
Plenary Scientific Session
Announcement of Awards
E. Donnall Thomas Lecture
Ernest Beutler Lecture and Prize
Presidential Symposium
Best of ASH
Announcement of the Dameshek Prize and the Stratton Medal

Ham-Wasserman Lecture

December 10, 2011 12:30 PM-1:30 PM
San Diego Convention Center (Hall AB)

Understanding the molecular basis of the formation of blood vessels (angiogenesis) is of great medical relevance. Indeed, insufficient angiogenesis leads to tissue ischemia, while an excess of angiogenesis promotes cancer, inflammation, and other disorders. Research over the last decades has focused primarily on promoting or blocking blood vessel branching. To date, hundreds of thousands of patients have benefited from vascular endothelial growth factor (VEGF) blockers, but limited efficacy and resistance remain problematic. More recent insights show also that vessels in pathological disorders, especially in cancer, are abnormal in structure and function. Emerging mechanisms of resistance against anti-angiogenic therapy and novel strategies and molecular drug targets to overcome these challenges will be discussed. In addition, the emerging paradigm of vessel normalization as a novel therapeutic approach will be put into perspective as it relates to current anti-angiogenic therapies.

Chair(s):

Peter Carmeliet, MD, PhD
VIB - Katholieke Universiteit Leuven, Vesalius Research Center
Leuven, Belgium

Plenary Scientific Session

December 11, 2011 2:00 PM-4:00 PM
San Diego Convention Center (Hall AB)

During this prestigious session and highlight of the annual meeting, attendees will hear the presentations of the highest caliber scientific abstracts selected by the Program Committee from among the thousands submitted from around the world. Plenary Scientific Session speakers will be announced on the ASH website (www.hematology.org) when the abstracts are posted online in early November.

Announcement of Awards

December 11, 2011 1:30 PM-2:00 PM
San Diego Convention Center (Hall AB)

E. Donnall Thomas Lecture

December 12, 2011 9:00 AM-10:00 AM
San Diego Convention Center (Hall AB)

Hematology research is critically dependent on disease models. Genetically engineered murine strains, as well as marrow transplant models, have provided important insights into disease mechanisms across the spectrum from leukemia to non-malignant genetic disorders. Murine model systems proved the culpability of the BCR/ABL oncoprotein in chronic myeloid leukemia and established the principle that autologous, rejection-proof pluripotent stem cells can be harnessed to treat genetic blood disease by combining gene repair with cell therapy. Where murine models prove limited, genetically modified human embryonic stem cells and personalized induced pluripotent stem (iPS) cells derived from patients by somatic cell reprogramming are emerging as powerful platforms for illuminating disease mechanisms and developing novel therapeutics. Although promising, the path to date has been fraught with obstacles - political, scientific, and clinical - and critical challenges lie ahead.

Chair(s):

George Q. Daley, MD, PhD
Children's Hospital Boston and Howard Hughes Medical Institute
Boston, MA, USA

Ernest Beutler Lecture and Prize

December 12, 2011 1:30 PM-2:30 PM
San Diego Convention Center (Hall AB)

Chronic myeloid leukemia (CML) was virtually uniformly fatal before the late 1990s with a median survival of about three years. In 1960, a unique small marker chromosome called the Philadelphia (Ph1) chromosome was identified. In 1973, it was determined to be a translocation that led to a fusion of the involved genes on chromosomes 9 and 22; the gene on 9 was the Abelson (ABL) oncogene, a known tyrosine kinase. This knowledge led to the development of an inhibitor of the ABL tyrosine kinase that specifically killed cultured CML cells. Clinical trials confirmed these pre-clinical observations and this oral drug, imatinib (Gleevec or STI571), has revolutionized treatment with five-year survival rates of almost 90 percent. Thus, although it took 40 years, CML is a story of success, from the identification of a unique genetic change to the development of a remarkably effective genetically targeted therapy. Dr. Janet Rowley will discuss the discovery of the chromosome translocations and cloning of the translocation breakpoint. Dr. Brian Druker will discuss the pre-clinical and clinical development of ABL inhibitors, including the problem of resistance.

Chair(s):

Janet D. Rowley, MD
Univ. of Chicago Med. Ctr.
Chicago, IL, USA

Brian J. Druker, MD
Oregon Health and Science University
Portland, OR, USA

Presidential Symposium

December 13, 2011 9:45 AM-11:15 AM
San Diego Convention Center (Hall AB)

This session will focus on recent advances in understanding the molecular basis of inherited and acquired bone marrow failure syndromes. Surprisingly, the damaged genes that cause marrow failure are not necessarily specific to blood cell development but, instead, are involved in essential functions for most cells, including telomere maintenance, ribosome biogenesis, and DNA damage repair. Recent studies have identified several mechanisms by which defects in these housekeeping pathways can lead to various diseases that share an inability to sustain normal blood production. Dr. Monica Bessler will discuss the role of telomerase defects in the pathogenesis of bone marrow failure in a range of congenital and more common disorders originally thought to be acquired. Conditions caused by telomerase dysfunction may vary in clinical expression, severity, and age group affected. The combination of telomerase mutations with other environmental, genetic, and epigenetic factors is responsible for dyskeratosis congenita, Hoyeraal Hreidarsson syndrome, aplastic anemia, pulmonary fibrosis, osteoporosis, liver cirrhosis, and cancer. Many of these conditions show genetic anticipation due to the inheritance of short telomeres and also mimic idiopathic conditions because of variable penetrance. Dr. Bessler will discuss several ways by which the impairment of a pathway that is important for every dividing cell may lead to these variable disease phenotypes. Dr. Benjamin Ebert will discuss defects in ribosome biogenesis that are associated with Diamond-Blackfan anemia, as well as other pediatric bone marrow failure states that may link to ribosome dysfunction, such as Schwachman-Diamond syndrome. He will present recent discoveries that link ribosome dysfunction to acquired myelodysplastic syndrome in adults, particularly the 5q- syndrome. Ribosome dysfunction leads to activation of p53, which promotes cell death, and Dr. Ebert will present the results from experimental models in zebrafish and mice that support this pathophysiologic mechanism. The activation of p53 may represent a common pathway that links several different types of bone marrow failure. Dr. Alan D'Andrea will discuss the causal relationship between defects in the response to DNA damage and the occurrence of bone marrow failure, leukemia, and cancer. Many discoveries in this field arose from studies of Fanconi anemia, an autosomal recessive cancer susceptibility disorder that is characterized by bone marrow failure, developmental defects, and hypersensitivity to ionizing radiation and DNA crosslinking agents. Fanconi anemia is caused by mutations in at least 15 distinct genes that function in a common signaling pathway to detect DNA crosslinks or double-strand breaks and repair them, and one of these genes is the breast cancer susceptibility gene BRCA2. Dr. D'Andrea will present several aspects of this novel signaling pathway, including the pathogenesis of marrow failure in Fanconi anemia and the role of somatic mutations and epigenetic silencing of Fanconi anemia genes, in a variety of cancers.

Chair(s):

J. Evan Sadler, MD, PhD
Washington University Medical School
St. Louis, MO, USA

Speaker(s):

Monica Bessler MD, PhD
The Children's Hospital of Philadelphia
Philadelphia, PA, USA
Telomere Maintenance In the Pathogenesis of Bone Marrow Failure

Benjamin Ebert MD, PhD
Brigham and Women's Hospital
Boston, MA, USA
Ribosome Dysfunction As a Cause of Bone Marrow Failure

Alan D'Andrea MD
Dana-Farber Cancer Institute
Boston, MA, USA
Fanconi Anemia: Pathogenesis and Novel Drug Targets

Best of ASH

December 13, 2011 12:00 PM-1:00 PM
San Diego Convention Center (Room 20ABC)

Before heading home on Tuesday, make time to attend "Best of ASH" for a review of some of the key themes from this year's meeting. Don't miss this one-hour session, led by the 2011 Annual Meeting Scientific Program Co-Chairs, to hear about the biggest breakthroughs from the meeting's more than 4,000 abstract presentations.