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Mohd Askandar Iqbal

Researcher at Jawaharlal Nehru University

Publications -  6
Citations -  372

Mohd Askandar Iqbal is an academic researcher from Jawaharlal Nehru University. The author has contributed to research in topics: PKM2 & Glycolysis. The author has an hindex of 5, co-authored 6 publications receiving 327 citations. Previous affiliations of Mohd Askandar Iqbal include University of Texas MD Anderson Cancer Center.

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Pyruvate kinase M2 and cancer: An updated assessment

TL;DR: Constant evidence suggests a critical role played by the low‐activity‐dimeric PKM2 in tumor progression, supported by the identification of mutations which result in the down‐regulation of its activity and tumorigenesis in a nude mouse model.
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Insulin enhances metabolic capacities of cancer cells by dual regulation of glycolytic enzyme pyruvate kinase M2

TL;DR: The study identifies new PKM2-mediated effects of insulin on cancer metabolism, thus, advancing the understanding of insulin’s role in cancer.
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Resveratrol inhibits cancer cell metabolism by down regulating pyruvate kinase M2 via inhibition of mammalian target of rapamycin.

TL;DR: It is observed that resveratrol down-regulated PKM2 expression by inhibiting mTOR signaling and suppressed cancer metabolism, adjudged by decreased glucose uptake, lactate production and reduced anabolism (macromolecule synthesis) in various cancer cell lines.
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Missense Mutations in Pyruvate Kinase M2 Promote Cancer Metabolism, Oxidative Endurance, Anchorage Independence, and Tumor Growth in a Dominant Negative Manner

TL;DR: This study provides the first evidence linking natural mutations in PKM2 with cancer, and demonstrates for the first time the possible predisposition of Bloom syndrome patients with impaired PKM1 activity to cancer and the importance of studying genetic variations inPKM2 in the future to understand their relevance in cancer in general.
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Interplay between epigenetics & cancer metabolism.

TL;DR: The role of cellular metabolism in regulation of the epigenome is discussed and how epigenetic changes may contribute to establish cancer-specific metabolic features are discussed.