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

J 2018

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

LOBELLO, Cosimo, Vasileios BIKOS, A. JANIKOVA a Šárka POSPÍŠILOVÁ

Základní údaje

Originální název

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

Autoři

LOBELLO, Cosimo (380 Itálie, domácí), Vasileios BIKOS (300 Řecko, domácí), A. JANIKOVA (203 Česká republika) a Šárka POSPÍŠILOVÁ (203 Česká republika, garant, domácí)

Vydání

Cancers, BASEL, MDPI, 2018, 2072-6694

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

30204 Oncology

Stát vydavatele

Švýcarsko

Utajení

není předmětem státního či obchodního tajemství

Impakt faktor

Impact factor: 6.162

Kód RIV

RIV/00216224:14740/18:00102938

Organizační jednotka

Středoevropský technologický institut

DOI

http://dx.doi.org/10.3390/cancers10030064

UT WoS

000428776200006

Klíčová slova anglicky

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)

Štítky

rivok

Příznaky

Mezinárodní význam, Recenzováno

Změněno: 13. 3. 2019 17:14, Mgr. Pavla Foltynová, Ph.D.

Anotace

V originále

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.

Návaznosti

LQ1601, projekt VaV

Název: CEITEC 2020 (Akronym: CEITEC2020)

Investor: Ministerstvo školství, mládeže a tělovýchovy ČR, CEITEC 2020

675712, interní kód MU

Název: ALK Activation as a target of TRAanslational Science (ALKATRAS): Break free from cancer (Akronym: ALKATRAS)

Investor: Evropská unie, ALK Activation as a target of TRAanslational Science (ALKATRAS): Break free from cancer, MSCA Marie Skłodowska-Curie Actions (Excellent Science)

Citovat

LOBELLO, Cosimo, Vasileios BIKOS, A. JANIKOVA a Šárka POSPÍŠILOVÁ. The Role of Oncogenic Tyrosine Kinase NPM-ALK in Genomic Instability. Cancers. BASEL: MDPI, 2018, roč. 10, č. 3, s. 64-75. ISSN 2072-6694. Dostupné z: https://dx.doi.org/10.3390/cancers10030064.

@article{1419885,
   author = {Lobello, Cosimo and Bikos, Vasileios and Janikova, A. and Pospíšilová, Šárka},
   article_location = {BASEL},
   article_number = {3},
   doi = {http://dx.doi.org/10.3390/cancers10030064},
   keywords = {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)},
   language = {eng},
   issn = {2072-6694},
   journal = {Cancers},
   title = {The Role of Oncogenic Tyrosine Kinase NPM-ALK in Genomic Instability},
   volume = {10},
   year = {2018}
}

TY  - JOUR
ID  - 1419885
AU  - Lobello, Cosimo - Bikos, Vasileios - Janikova, A. - Pospíšilová, Šárka
PY  - 2018
TI  - The Role of Oncogenic Tyrosine Kinase NPM-ALK in Genomic Instability
JF  - Cancers
VL  - 10
IS  - 3
SP  - 64
EP  - 64
PB  - MDPI
SN  - 20726694
KW  - NPM-ALK (nucleophosmin-anaplastic lymphoma kinase)
KW  - ALK
KW  - anaplastic large cell lymphoma (ALCL)
KW  - DNA damage response
KW  - genomic instability
KW  - DNA repair
KW  - p53
KW  - MutS protein homolog 2 (MSH2)
N2  - 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.
ER  -

LOBELLO, Cosimo, Vasileios BIKOS, A. JANIKOVA a Šárka POSPÍŠILOVÁ. The Role of Oncogenic Tyrosine Kinase NPM-ALK in Genomic Instability. \textit{Cancers}. BASEL: MDPI, 2018, roč.~10, č.~3, s.~64-75. ISSN~2072-6694. Dostupné z: https://dx.doi.org/10.3390/cancers10030064.

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