scispace - formally typeset
T

Thomas Force

Researcher at Temple University

Publications -  143
Citations -  20770

Thomas Force is an academic researcher from Temple University. The author has contributed to research in topics: Kinase & Signal transduction. The author has an hindex of 66, co-authored 141 publications receiving 19102 citations. Previous affiliations of Thomas Force include Tufts Medical Center & Thomas Jefferson University.

Papers
More filters
Journal ArticleDOI

Expert Consensus for Multimodality Imaging Evaluation of Adult Patients during and after Cancer Therapy: A Report from the American Society of Echocardiography and the European Association of Cardiovascular Imaging.

TL;DR: The noninvasive evaluation of LVEF has gained importance, and notwithstanding the limitations of the techniques used for its calculation, has emerged as the most widely used strategy for monitoring the changes in cardiac function, both during and after the administration of potentially car- diotoxic cancer treatment.
Journal ArticleDOI

Cardiotoxicity of the cancer therapeutic agent imatinib mesylate

TL;DR: Cardiotoxicity is an unanticipated side effect of inhibition of c-Abl by imatinib, where cardiomyocytes in culture show activation of the endoplasmic reticulum (ER) stress response, collapse of the mitochondrial membrane potential, release of cytochrome c into the cytosol, reduction in cellular ATP content and cell death.
Journal ArticleDOI

Expression cloning of a common receptor for parathyroid hormone and parathyroid hormone-related peptide from rat osteoblast-like cells: a single receptor stimulates intracellular accumulation of both cAMP and inositol trisphosphates and increases intracellular free calcium

TL;DR: Using expression cloning, a cDNA clone is isolated encoding rat bone PTH/PTHrP receptor from rat osteosarcoma cells that is 78% identical to the opossum kidney receptor and indicates striking conservation of this receptor across distant mammalian species.
Journal ArticleDOI

Cardiotoxicity associated with tyrosine kinase inhibitor sunitinib

TL;DR: Left ventricular dysfunction might be due, in part, to direct cardiomyocyte toxicity, exacerbated by hypertension, and patients treated with sunitinib should be closely monitored for hypertension and LVEF reduction, especially those with a history of coronary artery disease or cardiac risk factors.