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Start Over Author "Sharat Damodar" Journal cell death and disease
2 results on '"Sharat Damodar"'

1. Exovesicular-Shh confers Imatinib resistance by upregulating Bcl2 expression in chronic myeloid leukemia with variant chromosomes

Author

Anusha, Hamza Dalal, Sitalakshmi Subramanian, Snijesh V. P., Divya A. Gowda, Krishnamurthy H., Sharat Damodar, and Neha Vyas

Subjects
Cytology, QH573-671
Abstract

Abstract Chronic myeloid leukemia (CML) patients with complex chromosomal translocations as well as non-compliant CML patients often demonstrate short-lived responses and poor outcomes on the current therapeutic regimes using Imatinib and its variants. It has been derived so far that leukemic stem cells (LSCs) are responsible for Imatinib resistance and CML progression. Sonic hedgehog (Shh) signaling has been implicated in proliferation of this Imatinib-resistant CD34(+) LSCs. Our work here identifies the molecular mechanism of Shh-mediated mutation-independent Imatinib resistance that is most relevant for treating CML-variants and non-compliant patients. Our results elucidate that while Shh can impart stemness, it also upregulates expression of anti-apoptotic protein—Bcl2. It is the upregulation of Bcl2 that is involved in conferring Imatinib resistance to the CD34(+) LSCs. Sub-toxic doses of Bcl2 inhibitor or Shh inhibitor (<

Published
2021
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2. Exovesicular-Shh confers Imatinib resistance by upregulating Bcl2 expression in chronic myeloid leukemia with variant chromosomes

Author

Hamza Yusuf Dalal, Divya A. Gowda, Anusha, Sharat Damodar, Neha Vyas, Sitalakshmi Subramanian, H Krishnamurthy, and V. P. Snijesh

Subjects
Cancer Research, Immunology, CD34, Antineoplastic Agents, Chromosomal translocation, Article, Cellular and Molecular Neuroscience, Downregulation and upregulation, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, hemic and lymphatic diseases, Antineoplastic Combined Chemotherapy Protocols, Chromosomes, Human, Humans, Medicine, Hedgehog Proteins, Sonic hedgehog, lcsh:QH573-671, Protein Kinase Inhibitors, neoplasms, Chronic myeloid leukaemia, biology, Imatinib resistance, business.industry, lcsh:Cytology, Veratrum Alkaloids, Myeloid leukemia, Imatinib, Cell Biology, Up-Regulation, Gene Expression Regulation, Neoplastic, Thiazoles, Cancer therapeutic resistance, Proto-Oncogene Proteins c-bcl-2, Drug Resistance, Neoplasm, Imatinib Mesylate, Neoplastic Stem Cells, Cancer research, biology.protein, Stem cell, K562 Cells, business, medicine.drug
Abstract

Chronic myeloid leukemia (CML) patients with complex chromosomal translocations as well as non-compliant CML patients often demonstrate short-lived responses and poor outcomes on the current therapeutic regimes using Imatinib and its variants. It has been derived so far that leukemic stem cells (LSCs) are responsible for Imatinib resistance and CML progression. Sonic hedgehog (Shh) signaling has been implicated in proliferation of this Imatinib-resistant CD34(+) LSCs. Our work here identifies the molecular mechanism of Shh-mediated mutation-independent Imatinib resistance that is most relevant for treating CML-variants and non-compliant patients. Our results elucidate that while Shh can impart stemness, it also upregulates expression of anti-apoptotic protein—Bcl2. It is the upregulation of Bcl2 that is involved in conferring Imatinib resistance to the CD34(+) LSCs. Sub-toxic doses of Bcl2 inhibitor or Shh inhibitor (<

Published
2021

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