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Asish Mallick

Researcher at Indian Institute of Chemical Biology

Publications -  11
Citations -  421

Asish Mallick is an academic researcher from Indian Institute of Chemical Biology. The author has contributed to research in topics: Lymphoblast & Apoptosis. The author has an hindex of 9, co-authored 11 publications receiving 396 citations. Previous affiliations of Asish Mallick include Council of Scientific and Industrial Research.

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Withaferin A induces apoptosis by activating p38 mitogen-activated protein kinase signaling cascade in leukemic cells of lymphoid and myeloid origin through mitochondrial death cascade.

TL;DR: Findings suggest that p38MAPK in leukemic cells promotes WA-induced apoptosis, and therefore WA holds promise as a new, alternative, inexpensive chemotherapeutic agent for the treatment of patients with leukemia of both lymphoid and myeloid origin.
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Apoptotic effects of mahanine on human leukemic cells are mediated through crosstalk between Apo-1/Fas signaling and the Bid protein and via mitochondrial pathways.

TL;DR: Results provide evidence for involvement of the death receptor-mediated extrinsic pathway of apoptosis in the mahanine-induced anticancer activity in MOLT-3 cells, but not in K562 cells, which are deficient in Fas/FasL.
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O -acetylation of sialic acids is required for the survival of lymphoblasts in childhood acute lymphoblastic leukemia (ALL)

TL;DR: It is hypothesized that Neu5,9Ac2-GPs and their antibodies play a prominent role in promoting the survival of lymphoblasts in ALL and hint toward a disbalanced homeostasis, thereby enabling the cancer cells to escape host defense.
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Bak Compensated for Bax in p53-null Cells to Release Cytochrome c for the Initiation of Mitochondrial Signaling during Withanolide D-Induced Apoptosis

TL;DR: Withanolide D (WithaD), a steroidal lactone isolated from Withania somnifera, induced cellular apoptosis in which mitochondria and p53 were intricately involved in p53-wild type cells.
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Interferon gamma promotes survival of lymphoblasts overexpressing 9‐O‐acetylated sialoglycoconjugates in childhood acute lymphoblastic leukaemia (ALL)

TL;DR: It is reasonable to hypothesise that O‐acetylation of sialic acids on PBMCALL may be an additional mechanism that promotes the survival of lymphoblasts by avoiding apoptosis via IFN‐γ‐induced NO production.