The Role of Oncogenic Tyrosine Kinase NPM-ALK in Genomic Instability

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Publikace nespadá pod Fakultu sportovních studií, ale pod Středoevropský technologický institut. Oficiální stránka publikace je na webu muni.cz.
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LOBELLO Cosimo BIKOS Vasileios JANIKOVA A. POSPÍŠILOVÁ Šárka

Rok publikování 2018
Druh Článek v odborném periodiku
Časopis / Zdroj Cancers
Fakulta / Pracoviště MU

Středoevropský technologický institut

Citace
Doi http://dx.doi.org/10.3390/cancers10030064
Klíčová slova NPM-ALK (nucleophosmin-anaplastic lymphoma kinase); ALK; anaplastic large cell lymphoma (ALCL); DNA damage response; genomic instability; DNA repair; p53; MutS protein homolog 2 (MSH2)
Popis Genomic stability is crucial for cell life and transmitting genetic material is one of the primary tasks of the cell. The cell needs to be able to recognize any possible error and quickly repair it, and thus, cells have developed several mechanisms to detect DNA damage and promote repair during evolution. The DNA damage response (DDR) and DNA repair pathways ensure the control of possible errors that could impair the duplication of genetic information and introduce variants in the DNA. Endogenous and exogenous factors compromise genomic stability and cause dysregulation in the DDR and DNA repair pathways. Cancer cells often impair these mechanisms to overcome cellular barriers (cellular senescence and/or apoptosis), leading to malignancy. NPM (nucleophosmin)-ALK (anaplastic lymphoma kinase) is an oncogenic tyrosine kinase that is involved in the development of anaplastic large cell lymphoma (ALCL). NPM-ALK is known to be involved in the activation of proliferative and anti-apoptotic signaling pathways. New evidence reveals that NPM-ALK translocation also impairs the ability of cells to maintain the genomic stability through both DDR and DNA repair pathways. This review aims to highlight the role of the oncogenic tyrosine kinase NPM-ALK in the cell, and pointing to new possible therapeutic strategies.
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