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Exploiting Necroptosis for Therapy of Acute Lymphoblastic Leukemia


Mezzatesta, Caterina; Bornhauser, Beat C (2019). Exploiting Necroptosis for Therapy of Acute Lymphoblastic Leukemia. Frontiers in Cell and Developmental Biology, 7:40.

Abstract

Escape from chemotherapy-induced apoptosis is a hallmark of drug resistance in cancer. The recent identification of alternative programmed cell death pathways opens up for possibilities to circumvent the apoptotic blockade in drug resistant cancer and eliminate malignant cells. Indeed, we have recently shown that programmed necrosis, termed necroptosis, could be triggered to induce cell death in a subgroup of primary acute lymphoblastic leukemia (ALL) including highly refractory relapsed cases. In this review we focus on molecular mechanisms that drive drug resistance in ALL of childhood and discuss the potential of necroptosis activation to eradicate resistant disease.

Abstract

Escape from chemotherapy-induced apoptosis is a hallmark of drug resistance in cancer. The recent identification of alternative programmed cell death pathways opens up for possibilities to circumvent the apoptotic blockade in drug resistant cancer and eliminate malignant cells. Indeed, we have recently shown that programmed necrosis, termed necroptosis, could be triggered to induce cell death in a subgroup of primary acute lymphoblastic leukemia (ALL) including highly refractory relapsed cases. In this review we focus on molecular mechanisms that drive drug resistance in ALL of childhood and discuss the potential of necroptosis activation to eradicate resistant disease.

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Item Type:Journal Article, not_refereed, original work
Communities & Collections:04 Faculty of Medicine > University Children's Hospital Zurich > Medical Clinic
Dewey Decimal Classification:610 Medicine & health
Scopus Subject Areas:Life Sciences > Developmental Biology
Life Sciences > Cell Biology
Language:English
Date:2019
Deposited On:13 Jan 2020 09:12
Last Modified:29 Jul 2020 12:22
Publisher:Frontiers Research Foundation
ISSN:2296-634X
OA Status:Gold
Free access at:PubMed ID. An embargo period may apply.
Publisher DOI:https://doi.org/10.3389/fcell.2019.00040
PubMed ID:30941349

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