scispace - formally typeset
B

Benjamin Boyerinas

Researcher at National Institutes of Health

Publications -  16
Citations -  2360

Benjamin Boyerinas is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Immune system & Cytotoxic T cell. The author has an hindex of 9, co-authored 15 publications receiving 2114 citations. Previous affiliations of Benjamin Boyerinas include University of Chicago.

Papers
More filters
Journal ArticleDOI

MicroRNAs: key players in the immune system, differentiation, tumorigenesis and cell death

TL;DR: The role of miRNAs and their targets in contributing to human cancers and their function as regulators of apoptotic pathways and the immune system are summarized.
Journal ArticleDOI

The role of let-7 in cell differentiation and cancer

TL;DR: The role of let-7 in normal development and differentiation is discussed, the regulation oflet-7 expression, cancer-relevantLet-7 targets, and the relationship between let-8 and drug sensitivity are highlighted, and an overview of the relationships between deregulated let- 7 expression and tumorigenesis is provided.
Journal ArticleDOI

Antibody-Dependent Cellular Cytotoxicity Activity of a Novel Anti-PD-L1 Antibody Avelumab (MSB0010718C) on Human Tumor Cells.

TL;DR: The ability of avelumab to lyse a range of human tumor cells in the presence of PBMC or NK effectors is demonstrated and IFNγ can enhance tumor cell PD-L1 expression and, in some cases, enhance ADCC tumor cell lysis.
Journal ArticleDOI

Identification of Let-7–Regulated Oncofetal Genes

TL;DR: The data suggest that a substantial part of the growth inhibitory activities of let-7 comes from suppressing the expression of IMP-1, which could be novel therapeutic targets and potential biomarkers for cancer treatment.
Journal ArticleDOI

Adhesion to osteopontin in the bone marrow niche regulates lymphoblastic leukemia cell dormancy

TL;DR: It is shown that osteopontin (OPN), an extracellular matrix molecule secreted by osteoblasts, can function to anchor leukemic blasts in anatomic locations supporting tumor dormancy, and that this interaction induces cell cycle exit in leukedmic blasts, protecting them from cytotoxic chemotherapy.