Gareth J. Morgan, BSc, MRCP, PhD [Chair] ('14)
Rafat Abonour, MD [Vice Chair] ('14)
Wee-Joo Chng, MBBS, PhD, FRCPath, FRCP ('15)
Madhav Dhodapkar, MBBS ('15)
Rafael Fonseca, MD ('16)
Jonathan Keats, PhD ('14)
Edward Libby, MD ('17)
Jan Moreb, MD ('17)
Flavia Pichiorri, PhD ('16)
Saad Usmani, MD ('16)
Ares of biological/mechanistic interest:
The Scientific Committee on Plasma Cell Neoplasia was formed in 2008 to specifically address the very rapid scientific developments in our understanding of biology of normal plasma cells, but importantly the perturbation in molecular events leading to development of multiple myeloma and other plasma cell neoplasms. The observed genomic correlates and clear difference in pathogenesis from other B cell malignancies provides an important clue to improving our understanding of B cell maturation and malignant transformation.
The clinical areas:
Myeloma has been a model disease with well established in vitro and in vivo models that are utilized to identify and validate novel targets and therapies. With 5 new drugs approved in last 10 years the clinical landscape has entirely changed. Focused on the developments, our ad hoc committee covers a broader area that includes premalignant conditions MGUS/SMM, as well as Multiple Myeloma, Extramedullary Plasmacytomas, Plasma Cell Leukemia, Amyloidosis and Waldenstrom’s macroglobulinemia. Clinical use of molecularly-defined new agent combinations and their correlative science data highlight the rapid progress in further development.
The methodological aspects:
The methodological aspects covered are also broader than plasma cells, and include bone and marrow stem/stromal cells/niches/signaling, bone biology, protein chemistry and genomic, transcriptomic and proteamic changes.
The emerging areas of interest are a) Genomic changes and genome evolution and their functional impact; b) novel molecular pathways determining sensitivity and resistance; c) novel targeted therapies and their incorporation into management, d) protein chemistry and catabolism in cellular homeostasis; e) the cytokine networks and cellular interaction of bone formation and disease; f) understanding the mechanism involved in the transformation of a "benign" into a "malingnant" PC clone.
Potential overlap and resolution with other scientific committees:
The Plasma Cell Neoplasia Committee differs from Committees on Lymphoid Neoplasia (which previously took plasma cell topics under its umbrella) because lymphocyte disciplines do not cover bone, proteins, or the very different nature of myeloma biology and targets.
Thus, appropriate sessions at the ASH annual meeting may include:
- Role of protein catabolism in plasma cell disorders
- Genomic evolution and plasma cell dysfunction
- Cellular targets of therapy
- Mechanisms involved in the Transformation of MGUS &SMM into symptomatic MM.
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