Two main genetic pathways lead to the transformation of chronic lymphocytic leukemia to Richter syndrome

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023736%3A_____%2F13%3A00011024" target="_blank" >RIV/00023736:_____/13:00011024 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1182/blood-2013-03-489518" target="_blank" >http://dx.doi.org/10.1182/blood-2013-03-489518</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1182/blood-2013-03-489518" target="_blank" >10.1182/blood-2013-03-489518</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Two main genetic pathways lead to the transformation of chronic lymphocytic leukemia to Richter syndrome

Popis výsledku v původním jazyce

To better understand the pathogenesis of RS, we analyzed a series of cases including 59 RS, 28 CLL phase of RS, 315 CLL, and 127 de novo DLBCL. RS demonstrated a genomic complexity intermediate between CLL and DLBCL. Cell-cycle deregulation via inactivation of TP53 and of CDKN2A was a main mechanism in the histologic transformation from CLL phase, being present in approximately one half of the cases, and affected the outcome of the RS patients. A second major subgroup was characterized by the presence of trisomy 12 and comprised one third of the cases. Although RS shared some of the lesions seen in de novo DLBCL, its genomic profile was clearly separate. The CLL phase preceding RS had not a generalized increase in genomic complexity compared with untransformed CLL, but it presented clear differences in the frequency of specific genetic lesions.

Název v anglickém jazyce

Two main genetic pathways lead to the transformation of chronic lymphocytic leukemia to Richter syndrome

Popis výsledku anglicky

To better understand the pathogenesis of RS, we analyzed a series of cases including 59 RS, 28 CLL phase of RS, 315 CLL, and 127 de novo DLBCL. RS demonstrated a genomic complexity intermediate between CLL and DLBCL. Cell-cycle deregulation via inactivation of TP53 and of CDKN2A was a main mechanism in the histologic transformation from CLL phase, being present in approximately one half of the cases, and affected the outcome of the RS patients. A second major subgroup was characterized by the presence of trisomy 12 and comprised one third of the cases. Although RS shared some of the lesions seen in de novo DLBCL, its genomic profile was clearly separate. The CLL phase preceding RS had not a generalized increase in genomic complexity compared with untransformed CLL, but it presented clear differences in the frequency of specific genetic lesions.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

FD - Onkologie a hematologie

OECD FORD obor

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Projekt

—

Návaznosti

N - Vyzkumna aktivita podporovana z neverejnych zdroju

Rok uplatnění

2013

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Blood

ISSN

0006-4971

e-ISSN

—

Svazek periodika

122

Číslo periodika v rámci svazku

15

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

10

Strana od-do

2673-2682

Kód UT WoS článku

000326079400026

EID výsledku v databázi Scopus

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