scispace - formally typeset
A

Aamir Ahmad

Researcher at University of Alabama at Birmingham

Publications -  257
Citations -  15418

Aamir Ahmad is an academic researcher from University of Alabama at Birmingham. The author has contributed to research in topics: Cancer & Cancer stem cell. The author has an hindex of 63, co-authored 251 publications receiving 13404 citations. Previous affiliations of Aamir Ahmad include Aligarh Muslim University & Hamad Medical Corporation.

Papers
More filters
Journal ArticleDOI

Acquisition of Epithelial-Mesenchymal Transition Phenotype of Gemcitabine-Resistant Pancreatic Cancer Cells Is Linked with Activation of the Notch Signaling Pathway

TL;DR: Molecular evidence is provided showing that the activation of Notch signaling is mechanistically linked with chemoresistance phenotype (EMT phenotype) of PC cells, suggesting that the inactivation of notch signaling by novel strategies could be a potential targeted therapeutic approach for overcoming chemores resistance toward the prevention of tumor progression and/or treatment of metastatic PC.
Journal ArticleDOI

Gemcitabine sensitivity can be induced in pancreatic cancer cells through modulation of miR-200 and miR-21 expression by curcumin or its analogue CDF.

TL;DR: A significant reduction in cell viability was revealed in CDF-treated cells compared with curcumin- treated cells, which were also associated with the induction of apoptosis, and these results were consistent with the downregulation of Akt, cyclooxygenase-2, prostaglandin E(2), vascular endothelial growth factor, and NF-kappaB DNA binding activity.
Journal ArticleDOI

Evolving role of uPA/uPAR system in human cancers

TL;DR: An overview of emerging data is provided, from basic research as well as clinical studies, highlighting the evolving role of uPA/uPAR system in tumor progression, which represents a highly attractive target that warrants further in-depth studies.
Journal ArticleDOI

Epithelial to mesenchymal transition is mechanistically linked with stem cell signatures in prostate cancer cells.

TL;DR: In this article, a mechanistic understanding of prostate cancer recurrence and metastasis is proposed, which is closely linked with the biology of prostate stem cells or cancer-initiating cells that is reminiscent of the acquisition of Epithelial to Mesenchymal Transition (EMT) phenotype.
Journal ArticleDOI

Metformin inhibits cell proliferation, migration and invasion by attenuating CSC function mediated by deregulating miRNAs in pancreatic cancer cells

TL;DR: It is found that metformin significantly decreased cell survival, clonogenicity, wound-healing capacity, sphere-forming capacity (pancreatospheres), and increased disintegration of pancreatospheres in both gemcitabine-sensitive and gemcitABine-resistant pancreatic cancer cells.