|
Chronic Lymphocytic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Arguably the MYC activity gain is the most constantly observed phenomenon (>70% of cases) in transformed FL/MALT/CLL (Richter's transformation) and co-occurs with specific aberrations such as the loss of p53, CDKN2A/B, or gain of BCL2/BCL6.
|
31631728 |
2020 |
|
Chronic Lymphocytic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Here, we identify B cell leukemia/lymphoma 6 (BCL6) as a critical regulator of dormancy in brown adipocytes but not for their commitment, differentiation, or cold-induced activation.
|
31375635 |
2019 |
|
Chronic Lymphocytic Leukemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
IgM signaling induced prolonged activation of ERK kinases and promoted CLL cell survival, CCL3 and CCL4 chemokine secretion, and downregulation of BCL6, the transcriptional repressor of CCL3 In contrast, IgD signaling induced activation of the cytoskeletal protein HS1, along with F-actin polymerization, which resulted in rapid receptor internalization and failure to support downstream responses, including CLL cell survival and chemokine secretion.
|
27534555 |
2016 |
|
Chronic Lymphocytic Leukemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Although there are conflicting data regarding prognostic implications of isolated MYC aberrancy in these non-BLs, the co-occurrence of MYC rearrangements and either the antiapoptotic gene B-cell chronic lymphocytic leukemia/lymphoma 2 (BCL2) or the transcriptional repressor BCL6 leads to an entity termed double-hit B-cell lymphoma (DHL) (or triple-hit if all 3 abnormalities are observed) with a particularly poor prognosis and no established treatment paradigms.
|
25060588 |
2014 |
|
Chronic Lymphocytic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Genetic aberrations of B-cell leukemia/lymphoma 2 (BCL2), BCL6, v-myc avian myelocytomatosis viral oncogene homolog (MYC), mouse double minute 2 oncogene E3 ubiquitin protein ligase (MDM2), MDM4, and tumor protein 53 (TP53) were rare or absent.
|
24648050 |
2014 |
|
Chronic Lymphocytic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
The mechanism whereby BCOR functions during eye development to prevent colobomata is not known, but in other contexts it serves as a transcriptional corepressor that potentiates transcriptional repression by B cell leukemia/lymphoma 6 (BCL6).
|
23669349 |
2013 |
|
Chronic Lymphocytic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
The expressions of the 4 antigens were B-cell leukemia/lymphoma (BCL)-2(88.8%), BCL-6(80.6%), CD10(62.2%), and Ki67(50.0%), respectively.
|
22968395 |
2012 |
|
Chronic Lymphocytic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
In this study, expression of the p53, Human homolog of murine Double Minute 2 (HDM2), p14Alternating Reading Frame (ARF), Zinc Finger and BTB domain containing 7A (ZBTB7A), and B-Cell Lymphoma 6 (BCL6) genes was quantitatively investigated by real-time polymerase chain reaction (PCR) in the peripheral blood of patients with chronic lymphocytic leukemia (CLL) and healthy controls.
|
22047081 |
2012 |
|
Chronic Lymphocytic Leukemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
CLL cases expressing high levels of BCL6 have significantly shorter treatment-free interval.
|
19367498 |
2009 |
|
Chronic Lymphocytic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Btz is a promising pharmacologic agent for the treatment of B-CLL, but its efficacy seems to be related to IgVH and BCL-6 mutational status, therefore, it could be interesting to further investigate the mechanisms involved in the different behavior of the cells in response to apoptosis induction by this drug.
|
17134969 |
2006 |
|
Chronic Lymphocytic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
We examined the distribution of IgVH and BCL-6 gene mutations in 95 well-characterized patients with Binet stage A B-CLL, and correlated them with clinical, laboratory, cytogenetic findings and disease progression.
|
14961033 |
2004 |
|
Chronic Lymphocytic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
These data indicate that somatic mutation of the V(H) and bcl-6 loci may not necessarily occur in tandem in CLL, suggesting diverse pathways operating on the 2 genes.
|
10828040 |
2000 |
|
Chronic Lymphocytic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Overall, the distribution of BCL-6 and IgV mutations in B-CLL reinforce the notion that this leukemia is histogenetically heterogeneous and that a substantial subgroup of these lymphoproliferations derives from post-germinal center B cells.
|
10803511 |
2000 |
|
Chronic Lymphocytic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
These results indicate that a subset of B-CLL derives from a cell that has been exposed to the somatic hypermutation mechanism and support the hypothesis that BCL-6 mutations result from the same process that targets immunoglobulin genes.
|
11059755 |
2000 |
|
Chronic Lymphocytic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
The B cell transcriptional coactivator BOB1/OBF1 gene fuses to the LAZ3/BCL6 gene by t(3;11)(q27;q23.1) chromosomal translocation in a B cell leukemia line (Karpas 231).
|
8618432 |
1996 |
|
Chronic Lymphocytic Leukemia
|
0.400 |
CausalMutation
|
disease |
CGI |
|
|
|