scispace - formally typeset
A

Amit Maity

Researcher at University of Pennsylvania

Publications -  136
Citations -  10821

Amit Maity is an academic researcher from University of Pennsylvania. The author has contributed to research in topics: Cancer & Radiation therapy. The author has an hindex of 44, co-authored 121 publications receiving 9115 citations. Previous affiliations of Amit Maity include Johns Hopkins University School of Medicine & Hospital of the University of Pennsylvania.

Papers
More filters
Journal ArticleDOI

Radiation and dual checkpoint blockade activate non-redundant immune mechanisms in cancer

TL;DR: Major tumour regressions are reported in a subset of patients with metastatic melanoma treated with an anti-CTLA4 antibody and radiation and reproduced this effect in mouse models, showing that PD-L1 on melanoma cells allows tumours to escape anti- NCTLA4-based therapy, and the combination of radiation, anti- CTLA4 and anti-PD-L 1 promotes response and immunity through distinct mechanisms.
Journal ArticleDOI

PI3K/AKT/mTOR Pathway in Angiogenesis

TL;DR: The PI3K pathway plays an important role in regulating angiogenesis both in normal tissues and in cancers, and numerous inhibitors targeting the PI3k/AKT/mTOR pathway have been developed, and these agents have been shown to decrease VEGF secretion and angiynthesis.
Journal ArticleDOI

Tumor Interferon Signaling Regulates a Multigenic Resistance Program to Immune Checkpoint Blockade.

TL;DR: It is demonstrated that prolonged interferon signaling orchestrates PDL1-dependent and PDL 1-independent resistance to immune checkpoint blockade (ICB) and to combinations such as radiation plus anti-CTLA4, and biomarkers for interferons-driven resistance associate with clinical progression after anti-PD1 therapy.
Journal ArticleDOI

Regulation of glut1 mRNA by Hypoxia-inducible Factor-1 INTERACTION BETWEEN H-ras AND HYPOXIA

TL;DR: Results indicate that H-Ras up-regulates theglut1 promoter, at least in part, by increasing HIF-1α protein levels leading to transactivation of promoter through the HIF1 binding site.