New concepts in follicular lymphoma biology: From BCL2 to
epigenetic regulators and non-coding RNAs

J 2018

New concepts in follicular lymphoma biology: From BCL2 to epigenetic regulators and non-coding RNAs

DEVÁN, Ján, Andrea JANÍKOVÁ a Marek MRÁZ

Základní údaje

Originální název

New concepts in follicular lymphoma biology: From BCL2 to epigenetic regulators and non-coding RNAs

Autoři

DEVÁN, Ján (703 Slovensko, domácí), Andrea JANÍKOVÁ (203 Česká republika, domácí) a Marek MRÁZ (203 Česká republika, garant, domácí)

Vydání

SEMINARS IN ONCOLOGY, PHILADELPHIA, W B SAUNDERS CO-ELSEVIER INC, 2018, 0093-7754

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

30204 Oncology

Stát vydavatele

Spojené státy

Utajení

není předmětem státního či obchodního tajemství

Odkazy

URL

Impakt faktor

Impact factor: 3.606

Kód RIV

RIV/00216224:14740/18:00105658

Organizační jednotka

Středoevropský technologický institut

DOI

http://dx.doi.org/10.1053/j.seminoncol.2018.07.005

UT WoS

000454187700005

Klíčová slova anglicky

Follicular lymphoma; Epigenetics; BCR signaling; Tumor microenvironment; Transformation; miRNA

Štítky

14110212, podil, rivok

Příznaky

Mezinárodní význam, Recenzováno

Změněno: 18. 3. 2019 14:21, Mgr. Pavla Foltynová, Ph.D.

Anotace

V originále

The molecular pathogenesis of follicular lymphoma (FL) was partially revealed 3 decades ago, with the discovery of the translocation that brings BCL2 under the influence of immunoglobulin heavy chain enhancers in a vast majority of cases. Despite the importance of this seminal observation, it has become increasingly clear that additional genetic alterations need to occur to trigger neoplastic transformation and disease progression. The evolution of FL involves developmental arrest and disruption of the normal function of one or more of epigenetic regulators including KMT2D/MLL2, EZH2, CBP/CREBBP, p300/EP300, and HIST1H1 in >95% of cases. B-cells "arrested" in germinal centers acquire dozens of additional genetic aberrations that influence key pathways controlling their physiological development including B Cell Receptor (BCR) signaling, PI3K/AKT, TLR, mTOR, NF-kappa B, JAK/STAT, MAPK, CD40/CD4OL, chemokine, and interleukin signaling. Additionally, most cases of FL do not result from linear accumulation of genomic aberrations, but rather evolve from a common progenitor cell population by diverse evolution, creating multiple FL subclones in one patient. Moreover, one of the subclones might acquire a combination of aberrations involving genes controlling cell survival and proliferation including MDM2, CDKN2A/B, BCL6, MYC, TP53, beta 2M, FOXO1, MYD88, STAT3, or miR-17-92, and this can lead to the transformation of an initially indolent FL to an aggressive lymphoma (2%-3% risk per year). The complexity of the disease is also underscored by the importance of its interactions with the microenvironment that can substantially influence disease development and prognosis. Interpreting individual aberrations in relation to their impact on normal processes, their frequency, position in the disease evolution, and the consequences of their (co)occurrence, are the basis for understanding FL pathogenesis. This is necessary for the identification of patients with risk of early progression or transformation, for the development of novel targeted therapies, and for personalized treatment approaches. In this review, we summarize recent knowledge of molecular pathways and microenvironmental components involved in FL biology, and discuss them in the context of physiological B-cell development, FL evolution, and targeted therapies. (C) 2018 Elsevier Inc. All rights reserved.

Návaznosti

NV18-03-00054, projekt VaV

Název: ÚLOHA MICRORNA A JEJICH CÍLOVÝCH MOLEKUL V TRANSFORMACI FOLIKULÁRNÍHO LYMFOMU A AGRESIVITĚ CHRONICKÉ LYMFOCYTÁRNÍ LEUKÉMIE

Investor: Ministerstvo zdravotnictví ČR, ÚLOHA MICRORNA A JEJICH CÍLOVÝCH MOLEKUL V TRANSFORMACI FOLIKULÁRNÍHO LYMFOMU A AGRESIVITĚ CHRONICKÉ LYMFOCYTÁRNÍ LEUKÉMIE

Citovat

DEVÁN, Ján, Andrea JANÍKOVÁ a Marek MRÁZ. New concepts in follicular lymphoma biology: From BCL2 to epigenetic regulators and non-coding RNAs. SEMINARS IN ONCOLOGY. PHILADELPHIA: W B SAUNDERS CO-ELSEVIER INC, 2018, roč. 45, 5-6, s. 291-302. ISSN 0093-7754. Dostupné z: https://dx.doi.org/10.1053/j.seminoncol.2018.07.005.

@article{1488078,
   author = {Deván, Ján and Janíková, Andrea and Mráz, Marek},
   article_location = {PHILADELPHIA},
   article_number = {5-6},
   doi = {http://dx.doi.org/10.1053/j.seminoncol.2018.07.005},
   keywords = {Follicular lymphoma; Epigenetics; BCR signaling; Tumor microenvironment; Transformation; miRNA},
   language = {eng},
   issn = {0093-7754},
   journal = {SEMINARS IN ONCOLOGY},
   title = {New concepts in follicular lymphoma biology: From BCL2 to epigenetic regulators and non-coding RNAs},
   url = {https://linkinghub.elsevier.com/retrieve/pii/S0093775417301288},
   volume = {45},
   year = {2018}
}

TY  - JOUR
ID  - 1488078
AU  - Deván, Ján - Janíková, Andrea - Mráz, Marek
PY  - 2018
TI  - New concepts in follicular lymphoma biology: From BCL2 to epigenetic regulators and non-coding RNAs
JF  - SEMINARS IN ONCOLOGY
VL  - 45
IS  - 5-6
SP  - 291-302
EP  - 291-302
PB  - W B SAUNDERS CO-ELSEVIER INC
SN  - 00937754
KW  - Follicular lymphoma
KW  - Epigenetics
KW  - BCR signaling
KW  - Tumor microenvironment
KW  - Transformation
KW  - miRNA
UR  - https://linkinghub.elsevier.com/retrieve/pii/S0093775417301288
N2  - The molecular pathogenesis of follicular lymphoma (FL) was partially revealed 3 decades ago, with the discovery of the translocation that brings BCL2 under the influence of immunoglobulin heavy chain enhancers in a vast majority of cases. Despite the importance of this seminal observation, it has become increasingly clear that additional genetic alterations need to occur to trigger neoplastic transformation and disease progression. The evolution of FL involves developmental arrest and disruption of the normal function of one or more of epigenetic regulators including KMT2D/MLL2, EZH2, CBP/CREBBP, p300/EP300, and HIST1H1 in >95% of cases. B-cells "arrested" in germinal centers acquire dozens of additional genetic aberrations that influence key pathways controlling their physiological development including B Cell Receptor (BCR) signaling, PI3K/AKT, TLR, mTOR, NF-kappa B, JAK/STAT, MAPK, CD40/CD4OL, chemokine, and interleukin signaling. Additionally, most cases of FL do not result from linear accumulation of genomic aberrations, but rather evolve from a common progenitor cell population by diverse evolution, creating multiple FL subclones in one patient. Moreover, one of the subclones might acquire a combination of aberrations involving genes controlling cell survival and proliferation including MDM2, CDKN2A/B, BCL6, MYC, TP53, beta 2M, FOXO1, MYD88, STAT3, or miR-17-92, and this can lead to the transformation of an initially indolent FL to an aggressive lymphoma (2%-3% risk per year). The complexity of the disease is also underscored by the importance of its interactions with the microenvironment that can substantially influence disease development and prognosis. Interpreting individual aberrations in relation to their impact on normal processes, their frequency, position in the disease evolution, and the consequences of their (co)occurrence, are the basis for understanding FL pathogenesis. This is necessary for the identification of patients with risk of early progression or transformation, for the development of novel targeted therapies, and for personalized treatment approaches. In this review, we summarize recent knowledge of molecular pathways and microenvironmental components involved in FL biology, and discuss them in the context of physiological B-cell development, FL evolution, and targeted therapies. (C) 2018 Elsevier Inc. All rights reserved.
ER  -

DEVÁN, Ján, Andrea JANÍKOVÁ a Marek MRÁZ. New concepts in follicular lymphoma biology: From BCL2 to epigenetic regulators and non-coding RNAs. \textit{SEMINARS IN ONCOLOGY}. PHILADELPHIA: W B SAUNDERS CO-ELSEVIER INC, 2018, roč.~45, 5-6, s.~291-302. ISSN~0093-7754. Dostupné z: https://dx.doi.org/10.1053/j.seminoncol.2018.07.005.

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