Scott Armstrong, MD, PhD [Chair] ('13)
Oliver W. Press, MD, PhD [Vice Chair] ('13)
Angela Dispenzieri, MD ('14)
Michael J. Hallek, MD (’13)
Sami Malek, MD ('16)
Kerry Joanne Savage, MD ('13)
Velizar S. Shivarov, MD ('14)
Wendy Stock, MD ('15)
J.J.M. Van Dongen, MD, PhD ('14)
Meir Wetzler, MD ('15)
The Lymphoid Neoplasia Scientific Committee is focused on the biology and treatment of lymphoid malignancies. It differentiates itself from the committee on Lymphocyte Biology in its focus on the pathobiology of lymphoid malignancies. While there are obviously areas of biological overlap between the committees, such as sessions on pathways, our committee emphasizes their role in pathogenesis and therapeutic targeting. Malignancies of lymphoid origin (B and T cell) will be covered. Overlap entities such as NK/T cell malignancies may be included in a general discussion of T cell processes. “Pre-malignant” lymphoid diseases such as lymphomatoid granulomatosis, polymorphic EBV+ PTLD and chronic EBV lymphoproliferative disorders are relevant to our committee and would be considered. We would consider multi-lineage diseases of myeloid and lymphoid origin to be covered by the committee on myeloid neoplasia as they are typically treated as myeloid diseases. There is also potential overlap between the Scientific Committee on Lymphoid Neoplasia and the ad hoc Scientific Committee on Plasma Cell Neoplasia. Topics related to multiple myeloma and plasma cell disease and biology will be covered by the Plasma Cell Neoplasia Committee. To avoid overlapping biological topics of interest, the Chair of the two committees will review their topics with one another.
This appropriate sessions may include:
- Biology: (relevant to disease pathogenesis and targeting): genetic mutations; differentiation; cellular metabolism; signaling pathways; microenvironment; epigenetics; stem cells.
- Technology: spectral karyotyping; cytogenetics; microsatellite analysis; DNA fingerprinting; sequencing.
- Epidemiology: single nucleotide polymorphisms; familial cancer genes; environmental causation
Therapeutics: Phase I/II and III studies:
Systemic treatments include: cytotoxics; small targeted molecules; monoclonal antibodies (naked, conjugated-toxins and isotopes, bifunctional); immunotherapy (cellular (T-cells; CAR); cytokine (interferon; interleukins; chemokines); immunomodulatory (ImIDs))
External treatments include: external radiotherapy; brachytherapy; radiofrequencying PET (novel tracers like flt); MRI, CT.
Biomarkers including pharmacodynamics; target (binding, inhibition); pharmacokinetics; pharmacogenomics.