3:02 PM
 | 
Nov 17, 2016
 |  BC Innovations  |  Product R&D

Hemorrhaging targets

An ASH abstract preview by target, indication, modality and more

An analysis of the almost 5,000 abstracts set to be presented at the 2016 American Society of Hematology (ASH) meeting next month indicates this year’s hot topics in preclinical research include a spattering of new targets to watch, a growing role for nucleic acid based therapies, and a continued expansion of cell type subsets beyond the commonly used B cells and Tregs.

This year’s meeting, which takes place December 3-6 in San Diego, has a heavy emphasis on hematological malignancies, which account for more than 75% of the preclinical abstracts.

Indeed, BioCentury identified eight new therapeutic targets which all fall in oncology, two of which are new chimeric antigen receptor (CAR) T cell targets in the continually growing cancer immunology space (see “Novel targets at ASH”).

Table: Novel targets at ASH

Select new targets for hematological malignancies and other cancers presented at the 2016 American Society of Hematology (ASH) conference. Source: ASH Abstracts

TargetStandard IndicationResearch summaryInstitution(s)Abstract
Ankyrin repeat and sterile α motif domain containing 1B (ANKS1B)Acute lymphoblastic leukemia (ALL) ANKS1B was confirmed as a target upregulated by the transcription factor 3 (TCF3; E2A)-PBX homeobox 1 (PBX1) fusion found in a subset of B cell ALL patients.Tampere University Hospital; University of California San Francisco; University of Eastern Finland; University of Helsinki; University of Tampere4077
B-cell receptor-associated protein 31 (BCAP31; BAP31)LeukemiaBCAP31 was discovered as an additional target of the protein disulfide isomerase (PDI) inhibitor PS89, and its engagement is required for the inhibitor's pro-apoptotic effect when combined with a cell growth inhibitor.Helmholtz Center Munich; Ludwig Maximilian University of Munich; Saarland University; Technical University of Munich2319
C-type lectin domain family 11 member A (CLEC11A)Multiple myeloma (MM)In MM cell lines, CLEC11A knockdown increased apoptosis.Icahn School of Medicine at Mount Sinai; Multiple Myeloma Research Foundation (MMRF)802
CDC42 binding protein kinase α (CDC42BPA)MMIn MM cell lines, CDC42BPA knockdown increased apoptosis.Icahn School of Medicine at Mount Sinai; Multiple Myeloma Research Foundation (MMRF)802
CD7 molecule (CD7)ALL; acute myelogenous leukemia (AML)In AML and T cell ALL cell lines, T cells designed to express chimeric antigen receptors (CARs) targeting CD7 decreased the number of leukemia colonies.Baylor College of Medicine4555
Early B-cell factor 3 (EBF3)ALLEBF3 was identified as a tumor suppressor gene regulated by the TCF3-PBX1 fusion in B cell ALL patientsTampere University Hospital; University of California San Francisco; University of Eastern Finland; University of Helsinki; University of Tampere4077
Lysosomal associated membrane protein family member 5 (LAMP5)

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