8:21 PM
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Nov 29, 2018
 |  BC Innovations  |  Targets & Mechanisms

Adhesion targets emerge at ASH 2018

Emerging science on adhesion molecules, RNA-binding proteins and more at ASH 2018

Editor's Note: This article was updated on Dec 14, 2018 at 12:15 PM PST

The next wave of targets in blood cancers and hematology will come from adhesion molecules, innate immune cells and regulators of gene expression, according to BioCentury’s analysis of emerging targets at ASH 2018.

BioCentury’s analysis of abstracts released ahead of this year’s meeting of the American Society of Hematology (ASH) identifies 19 new and 58 emerging targets (see “Table: New Targets at ASH 2018” and “Figure: Emerging Functions”).


Figure: Emerging functions

BioCentury identified 58 emerging targets in abstracts at the 2018 meeting of the American Society of Hematology (ASH) 2018 meeting, where “emerging” is defined as a target whose mentions increased at least threefold over last year. Specifically, at ASH 2017, each emerging target was featured in zero, one or two abstracts, whereas in 2018, each target was featured in four or more. Of these, 52 clustered into eight functional categories with at least three members each. The adhesion category includes mechanosensors and extracellular matrix regulators; it also includes one target family, lectins, which appeared in seven abstracts this year vs. two in 2017. The other emerging target classes consist of gene expression regulators such as epigenetic modifiers, transcription factors and RNA-binding proteins; innate immune regulators of phagocytosis, antigen presentation and NK cell activity; post-translational modifiers such as kinases, phosphatases, sugar-modifying enzymes, ubiquitin-like molecules and endoplasmic reticulum-targeting proteins; and targets involved in growth factor and hormone signaling, metabolism, oxidative damage and hypoxia, and apoptosis. Full target names can be found in BioCentury’s BCIQ database. Source: ASH 2018 abstracts as of Nov. 1

Table: New targets at ASH 2018

Select new cancer targets presented at the 2018 American Society of Hematology (ASH) meeting. The list includes proteins with proposed therapeutic or biomarker potential based on preclinical studies highlighted in the abstracts. New targets were defined as targets with translational potential not included in BioCentury’s BCIQ database. Source: ASH abstracts as of Nov. 1

TargetIndicationStudy type(s)DescriptionLead company or institutionAbstract No.
Junctional adhesion molecule-A (JAM-A; F11R)Multiple myeloma (MM) Patient sampleExpression levels of JAM-A could help predict survival.University Hospital Würzburg4455
Poly(ADP-ribose) polymerase-14 (PARP-14)LymphomaCell-basedInhibiting PARP-14 could help treat signal transducer and activator of transcription 6 (STAT6)-mutant follicular lymphoma (FL).Ludwig Maximilians University of Munich2842
Polypyrimidine tract binding protein 3 (PTBP3; ROD1)Acute myelogenous leukemia (AML)Patient sample; mouse; cell-basedPTBP3 overexpression promotes aberrant RNA splicing and tumor progression in AML.Dana-Farber Cancer Institute3895
Protein S (PROS1)MMMouse; cell-basedOverexpression of PROS1 promotes destructive myeloma bone disease.University Medical Center Hamburg-Eppendorf1922
Autophagy related 12 (ATG12)MMMouse; cell-basedExpression levels of ATG12 could predict dexamethasone resistance in MM.Huazhong University of Science and Technology4469
MicroRNA-185 (miR-185)Acute lymphoblastic leukemia (ALL); chronic myelogenous leukemia (CML)Patient sample; mouse; cell-basedOverexpression of miR-185 or inhibition of miR-185 target p21 protein (Cdc42 Rac)-activated kinase 6 (PAK6) could help treat BCR-ABL tyrosine kinase (BCR-ABL)-positive, tyrosine kinase inhibitor-resistant ALL and CML.University of British Columbia931
Unc-51 like autophagy activating kinase 2 (ULK2; ATG1B) AMLCell-basedAn inhibitor of unc-51 like autophagy...

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