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Fazlul H. Sarkar

Researcher at Wayne State University

Publications -  626
Citations -  48133

Fazlul H. Sarkar is an academic researcher from Wayne State University. The author has contributed to research in topics: Cancer & Pancreatic cancer. The author has an hindex of 114, co-authored 625 publications receiving 44744 citations.

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Book ChapterDOI

The Biological Significance of Zinc in Inflammation and Aging

TL;DR: This chapter discusses the role of chronic inflammation, oxidative stress, and DNA damage in the aging process, especially in age-related degenerative diseases including cancer, and the detailed mechanisms of the protective action of zinc as a potential anti-aging agent inAge-related cellular signaling involving the NF-κB, A20, Nrf2, and p53 pathways.
Journal ArticleDOI

Bryostatin 1 induces differentiation and potentiates the antitumor effect of Auristatin PE in a human pancreatic tumor (PANC-1) xenograft model.

TL;DR: It is demonstrated that bryo1 induces differentiation and potentiates the antitumor effect of AuriPE in a human pancreatic tumor (PANC-1) xenograft model in severe combined immune deficient (SCID) mice, the first report where this effect is demonstrated in pancreatic tumors.
Journal ArticleDOI

Protein kinases C isozymes are differentially expressed in human breast carcinomas.

TL;DR: Investigation of the expression of certain PKC isoforms in human breast cancer specimens relative to adjacent uninvolved tissue and in the normal breast tissue obtained from patients undergoing reduction mammoplasty found them to be specific targets for the development of new therapies and for the prevention and treatment of this disease.
Journal Article

EGF-receptor related protein causes cell cycle arrest and induces apoptosis of colon cancer cells in vitro and in vivo.

TL;DR: It is proposed that ERRP functions by inhibiting the activation of the EGF-receptor signaling and its downstream effectors such as ERK and Akt kinases, underscoring the potential of ERRP for the treatment of colorectal cancer where the E GF pathway is known to be activated.
Journal ArticleDOI

Systems analysis reveals a transcriptional reversal of the mesenchymal phenotype induced by SNAIL-inhibitor GN-25

TL;DR: It is shown that GN-25 could cause reversal of EMT leading to mesenchymal-to-epithelial transition (MET) in a well-recognized HMLE-SNAIL and Kras-HMLE- SNAIL models and thereby reducing cancer cell aggressiveness.