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, roč. 45, 5-6, s. 291-302. ISSN 0093-7754. doi:10.1053/j.seminoncol.2018.07.005. 2018.
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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
Originální jazyk angličtina
Typ výsledku Článek v odborném periodiku
Obor 30204 Oncology
Stát vydavatele Spojené státy
Utajení není předmětem státního či obchodního tajemství
WWW 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
Změnil Změnila: Mgr. Pavla Foltynová, Ph.D., učo 106624. Změněno: 18. 3. 2019 14:21.
Anotace
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 VaVNázev: 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
VytisknoutZobrazeno: 29. 3. 2024 12:59