Survival control of malignant lymphocytes by anti-apoptotic MCL-1.

Fernandez Marrero, Yuniel; Spinner, S; Jost, P J; Kaufmann, Thomas (2016). Survival control of malignant lymphocytes by anti-apoptotic MCL-1. Leukemia, 30(11), pp. 2152-2159. Nature Publishing Group 10.1038/leu.2016.213

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Programmed apoptotic cell death is critical to maintain tissue homeostasis and cellular integrity in the lymphatic system. Accordingly, the evasion of apoptosis is a critical milestone for the transformation of lymphocytes on their way to becoming overt lymphomas. The anti-apoptotic BCL-2 family proteins are pivotal regulators of the mitochondrial apoptotic pathway and genetic aberrations in these genes are associated with lymphomagenesis and chemotherapeutic resistance. Pharmacological targeting of BCL-2 is highly effective in certain indolent B-cell lymphomas; however, recent evidence highlights a critical role for the BCL-2 family member MCL-1 in several lymphoma subtypes. MCL-1 is recurrently highly expressed in various kinds of cancer including non-Hodgkin's lymphoma of B- and T-cell origin. Moreover, both indolent and aggressive forms of lymphoma require MCL-1 for lymphomagenesis and for their continued survival. This review summarizes the role of MCL-1 in B- and T-cell lymphoma and discusses its potential as a therapeutic target.Leukemia advance online publication, 2 September 2016; doi:10.1038/leu.2016.213.

Item Type:

Journal Article (Review Article)

Division/Institute:

04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Pharmacology

Graduate School:

Graduate School for Cellular and Biomedical Sciences (GCB)

UniBE Contributor:

Fernández Marrero, Yuniel, Kaufmann, Thomas (B)

Subjects:

600 Technology > 610 Medicine & health

ISSN:

0887-6924

Publisher:

Nature Publishing Group

Language:

English

Submitter:

Debora Scherrer

Date Deposited:

09 Nov 2016 12:39

Last Modified:

29 Mar 2023 23:35

Publisher DOI:

10.1038/leu.2016.213

PubMed ID:

27479182

BORIS DOI:

10.7892/boris.89239

URI:

https://boris.unibe.ch/id/eprint/89239

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