Jump to Main Content


Special Scientific Symposia

Friend or Foe: The Microbiome, Antibiotics and Death After Transplant

The importance of the intestinal microbiome for graft-versus-host disease (GvHD) after allogeneic hematopoietic cell transplantation (allo-HCT) was initially demonstrated both in preclinical and clinical studies several decades ago. Since then major advances in microbiome research have resulted in a better understanding of the interplay between microbiome and host in health and disease.  This session will address various aspects of the role of the intestinal microbiome in patients with hematological malignancies (especially allo-HCT recipients), including novel methodologies to study interactions between microbiome and host, preclinical and clinical studies regarding the intestinal microbiome and GvHD and the clinical potential of fecal microbiota transplant in allo-HCT patients.

Dr. Ami Bhatt will discuss how alterations in the human gut microbiome are correlated with disease prognosis, treatment response, and complications of therapy in patients with hematologic disorders. Recently developed technologies and bioinformatic approaches have enabled us to understand the mechanisms that might underlie these interactions. By understanding microbes at the strain level and defining the macromolecules that microbes use to communicate with one another and the host, her lab hopes to characterize the rich signaling interface between microbes in humans. In so doing, it is anticipated that modifying and eventually controlling this type of signaling could help improve patient outcomes.

Dr. Marcel van den Brink will discuss preclinical and clinical studies demonstrating the role of changes in the intestinal microbiota of recipients of allo-HCT and its effects on GvHD, as well as infections, relapse and engraftment.

Dr. Mette Hazenburg will discuss how disruption of the intestinal microbiome is a key element of GvHD pathophysiology. This has led to the hypothesis that with fecal microbiota transplantation (FMT) the damaged microbiome can be repaired by FMT, and that reparation of the microbiome may cure GvHD. By inference, it can be hypothesized that reconstitution of a healthy microbiome before or shortly after allogeneic HCT by FMT could prevent severe GvHD. In this presentation, both hypotheses will be addressed, based on the literature available and also including Dr. Hazenburg’s own data on FMT in steroid-refractory patients.


Marcel R.M. van den Brink, MD, PhD
Memorial Sloan- Kettering Cancer Center
New York, NY


Ami S. Bhatt, MD, PhD
Stanford University
Stanford, CA
Basic Biology of the Microbiome Universe

Marcel R.M. van den Brink, MD, PhD
Memorial Sloan- Kettering Cancer Center
New York, NY
The Microbiome and Graft Versus Host Disease

Mette D. Hazenberg, MD, PhD
Amsterdam UMC
Amsterdam, Netherlands
Fecal Microbiota Transplants

back to top

Special Joint Education-Scientific Symposium: Hormones and Hematology


Lydia H. Pecker, MD
Johns Hopkins University
Baltimore, MD


Jean M. Connors, MD
Brigham & Women's Hospital, Dana Farber Cancer Institute
Boston, MA
Coagulation Issues in Transgender Individuals

E. Dale Abel, MD, PhD
University of Iowa
Iowa City, IA
OPA1 A Novel Regulator of Sex-Dependent Differences in Thrombosis

Robert Richard, MD, PhD
Veterans Affairs Puget Sound Health Care System
Seattle, WA
Steroids and Erythropoeisis: We're Going to Pump You Up

back to top

Special Symposium on the Basic Science of Hemostasis and Thrombosis

It has become increasingly evident that inflammatory processes are intimately linked with the hemostatic system. In this joint session, these interactions are highlighted in three talks focusing on recent progress in the field of coagulation, vascular biology and platelet research. Coagulation activation is a driving force for vascular dysfunction in sickle cell disease. Conversely, genetic predisposition leading to vascular dysfunction in cerebral cavernous malformations promotes hemorrhage by overactivation of the anticoagulant pathway. The autoimmune pathology of heparin-induced thrombocytopenia is moreover critically dependent on the activation of the humoral complement defense pathway. The session will discuss implications of these links for therapies of thrombotic and vascular disorders.

Dr. Rafal Pawlinski will discuss the interplay between coagulation and inflammation in sickle cell disease (SCD). Contribution of vascular inflammation and hypercoagulable state to the pathology of SCD has been recently recognized. Chronic activation of coagulation not only leads to the increased incidence of pro-thrombotic complications, but it is also an important mediator of vascular inflammation and end-organ damage observed in SCD. Preliminary data from Dr. Pawlinski’s lab indicates that inhibiting the activation of the intrinsic coagulation and/or contact pathways by targeting factor XIIa could provide benefits associated with reduced thrombosis, vascular inflammation and end-organ damage in SCD without increasing risk of bleeding complications.

Dr. Mark Ginsberg will discuss vascular signaling in the pathology of cerebral cavernous malformations (CCM). CCM are common brain vascular malformations prone to acute and chronic hemorrhage with significant clinical sequelae. Endothelial cell specific deletion of CCM susceptibility genes (Krit1, Pdcd10) in mice identified upregulation of transcription factors KLF2 and KLF4 as the cause for elevated expression of anticoagulant endothelial receptors. The resulting excessive generation of activated protein C(APC) contributes to CCM hemorrhage and blocking antibodies to anticoagulant endothelial receptors reduce CCM hemorrhage. Plasma levels of soluble thrombomodulin may represent a biomarker for hemorrhagic risk in CCMs and regulators of the Protein C pathway are potential targets for reducing hemorrhage in CCM. 

Dr. Gowthami Arepally will discuss the role of complement activation in the pathogenesis of heparin induced thrombocytopenia (HIT). HIT is an aggressive thrombotic disorder initiated by ultra-large immune complexes (ULICs) containing IgG antibodies to a multivalent antigen composed of platelet factor 4 (PF4) and heparin (H). Patients with HIT remain at risk of death and major morbidity despite optimum anticoagulation. The mechanisms underlying thrombosis in HIT are only partially understood. HIT ULICs activate cellular FcgRIIA to initiate diverse cellular effector functions that engender a prothrombotic environment. However, ULICs also exert other biologic effects. HIT serum and IgG robustly activate complement leading to its deposition on endothelial cells and circulating platelets. To what extent these disparate activities of HIT ULICs contribute to the hypercoagulable state in HIT is not known. In this session, Dr. Arepally will review recent data showing that the complement activating effects of HIT antibodies essentially mediate FcgR-dependent cellular activation. Using in vitro and in vivo models, they demonstrate that HIT ULICs activate complement via the classical pathway, mediate cellular activation via FcgRIIA and support the procoagulant effects of HIT antibodies. These studies provide a rationale for developing non-anticoagulant interventions in HIT and insights into the contribution of complement to other immune-complex mediated thrombotic disorders.


Shannon L. Meeks, MD
Emory University
Atlanta, GA

Wolfram Ruf, MD
Johannes Gutenberg University Medical Center
Mainz, CA, Germany

Angara Koneti Rao, MBBS
Temple University
Philadelphia, PA


Rafal Pawlinski, PhD
University of North Carolina
Chapel Hill, NC
Hemostasis: Coagulation and Inflammation

Mark H Ginsberg, MD
University of California - San Diego
La Jolla, CA
Thrombosis/Vascular Biology: Cavernous Malformations and Thrombosis

Gowthami M. Arepally, MD
Duke University Medical Center
Durham, NC
Complement Activation in Heparin Induced Thrombocytopenia