Avid Bioservices Inc (CDMO)

[biopharm]

2-9-17/AACR Article: R.Birge+PPHM, “PS Sensing by TAM Receptors Regulates AKT-dependent Chemoresistance & PD-L1 Expression”. Lead author, Rutgers' Dr. Raymond Birge. Also, 2 co-authors from Advanced Proteome Therapeutics, in addition to PPHM scientists.

2-9-17/AACR: “Phosphatidylserine Sensing by TAM Receptors Regulates AKT-dependent Chemoresistance and PD-L1 Expression”
Rec. 10-27-16, rev. 12-30-16, Acc 1-13-17, PUB. 2-9-17
*RUTGERS: Canan Kasikara, Sushil Kumar, Stanley Kimani, Wen-I Tsou, Ke Geng, Viralkumar Davra, Ganapathy Sriram, Connor Devoe, Khanh-Quynh Nguyen, Anita Antes, Sergei V Kotenko, Raymond B. Birge [Lead Author http://birgelab.org ]
*ADVANCED PROTEOME THERAPEUTICS: Allen Krantz, Andrzej Wilczynski http://advancedproteome.com
*BOSTON UNIV: Grzegorz Rymarczyk
*PEREGRINE: Cyril Empig, Bruce D Freimark, Michael Gray, Kyle Schlunegger, Jeff Hutchins
http://mcr.aacrjournals.org/content/early/2017/02/09/1541-7786.MCR-16-0350
https://www.ncbi.nlm.nih.gov/pubmed/28184013

Good thing PS Targeting reduces MDSCs

?Np63-driven recruitment of myeloid-derived suppressor cells promotes metastasis in triple-negative breast cancer

Sushil Kumar,1
David W. Wilkes,1
Nina Samuel,1
Mario Andres Blanco,1
Anupma Nayak,2
Kevin Alicea-Torres,3
Christian Gluck,4
Satrajit Sinha,4
Dmitry Gabrilovich,3 and
Rumela Chakrabarti1

First published October 8, 2018 - More info

J Clin Invest. https://doi.org/10.1172/JCI99673.
Copyright © 2018, American Society for Clinical Investigation

First published October 8, 2018 - Version history
Received: January 5, 2018; Accepted: August 28, 2018
Abstract
Triple-negative breast cancer (TNBC) is particularly aggressive, with enhanced incidence of tumor relapse, resistance to chemotherapy, and metastases. As the mechanistic basis for this aggressive phenotype is unclear, treatment options are limited. Here, we showed an increased population of myeloid-derived immunosuppressor cells (MDSCs) in TNBC patients compared with non-TNBC patients. We found that high levels of the transcription factor ?Np63 correlate with an increased number of MDSCs in basal TNBC patients, and that ?Np63 promotes tumor growth, progression, and metastasis in human and mouse TNBC cells. Furthermore, we showed that MDSC recruitment to the primary tumor and metastatic sites occurs via direct ?Np63-dependent activation of the chemokines CXCL2 and CCL22. CXCR2/CCR4 inhibitors reduced MDSC recruitment, angiogenesis, and metastasis, highlighting a novel treatment option for this subset of TNBC patients. Finally, we found that MDSCs secrete prometastatic factors such as MMP9 and chitinase 3–like 1 to promote TNBC cancer stem cell function, thereby identifying a nonimmunologic role for MDSCs in promoting TNBC progression. These findings identify a unique crosstalk between ?Np63+ TNBC cells and MDSCs that promotes tumor progression and metastasis, which could be exploited in future combined immunotherapy/chemotherapy strategies for TNBC patients.

https://www.jci.org/articles/view/99673