Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Mass cytometry data revealed that BCL2 protein is enriched in leukemia stem/progenitor cells, primarily in venetoclax-sensitive samples and that cobimetinib suppressed cytokine-induced pERK and pS6 signaling pathways.
|
31123034 |
2020 |
Childhood Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Compound 7a notably inhibited the expression and activity of PIM kinases, as evidenced by reduced B‑cell lymphoma‑2 (Bcl‑2)‑associated death promoter phosphorylation at Ser112.
|
31789392 |
2020 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Tet methylcytosine dioxygenase (Tet2), B-cell lymphoma 2 (Bcl2), and solute carrier family 23 member 2 (Slc23a2) are the major target genes in the treatment of leukemia and are relevant to vitamin C.
|
31467227 |
2020 |
Childhood Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The characteristic high-level expression of BCL2 in CLL that can enhance leukemia-cell survival has now become an Achilles heel targeted by clinically effective drugs such as venetoclax.
|
31764118 |
2020 |
Childhood Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The compound decreased the antiapoptotic Bcl-2 levels and increased proapoptotic Bax proteins in leukemia and myeloma cell lines.
|
31046873 |
2019 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Venetoclax (ABT-199/GDC-0199) is a highly selective bioavailable inhibitor of BCL-2 protein, which is more effective and less valid against BCL-xL in BCL2-dependent leukemia and lymphoma cell.
|
31293422 |
2019 |
Childhood Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
BCL2 is also overexpressed in CLL, the most common human leukemia.
|
28653191 |
2019 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Abbreviations: APC/C: Anaphase-Promoting Complex/Cyclosome; BAD: BCL2-Associated agonist of cell Death; BAK1: BCL2 Antagonist Kinase1; BAX: BCL2-Associated X; BCL2: B-cell Chronic Lymphocytic Leukaemia (CLL)/Lymphoma 2; BH: BCL2 Homology Domain; BID: BH3-Interacting domain Death agonist; BIM: BCL2-Interacting Mediator of cell death; BUB: Budding Uninhibited by Benzimidazoles; CDC: Cell Division Cycle; CDH1: Cadherin-1; CDK1: Cyclin-Dependent Kinase 1; CEP55: Centrosomal Protein (55 KDa): CIN: Chromosomal Instability; CTA: Cancer Testis Antigen; EGR1: Early Growth Response protein 1; ERK: Extracellular Signal-Regulated Kinase; ESCRT: Endosomal Sorting Complexes Required for Transport; GIN: Genomic Instability; MAD2: Mitotic Arrest Deficient 2; MCL1: Myeloid Cell Leukemia sequence 1; MPS1: Monopolar Spindle 1 Kinase; MYT1: MYelin Transcription factor 1; PLK1: Polo Like Kinase 1; PUMA: p53-Upregulated Mediator of Apoptosis; SAC: Spindle Assembly Checkpoint; TAA: Tumor-Associated Antigen.
|
30601084 |
2019 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
New targeted therapies for hematological malignancy include chimeric antigen receptor T cells (CAR T cells), Bi-specific T-cell Engager (BiTE) blinatumomab, and the antibody-drug conjugate (ADC) of calicheamicin inotuzumab ozogamicin for acute lymphoblasic leukemia (ALL) and lymphoma; the Bruton's tyrosine kinase (BTK) inhibitor ibrutinib and phosphatidylinositol 3-kinase (PI3Kδ) inhibitor idelalisib for lymphoma and graft-versus-host disease (GVHD); FMS-like tyrosine kinase 3 (FLT3) inhibitors, such as midostaurin, sorafenib and gilteritinib for acute myeloid leukemia (AML); and the BCL-2 inhibitor venetoclax for a range of hematological malignancies including lymphoma and leukemia.
|
31688198 |
2019 |
Childhood Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The anti-apoptotic factors Mcl-1, Bcl-2, and Bcl-xL were also found to be over-expressed in acute myeloid leukemia (AML) (Kaufmann et al., 2016) and acute lymphocytic leukemia (ALL) (Findley, Gu, Yeager, & Zhou, 1997), suggesting that dis-regulated apoptotic processes could be a factor in the instigation of leukemia and/or its relapse.
|
30347215 |
2019 |
Childhood Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
These results shed new light on the oncogenic function of ribosomal mutations in cancer, provide a novel mechanism for BCL-2 upregulation in leukemia, and highlight BCL-2 inhibition as a novel therapeutic opportunity in RPL10 R98S defective T-ALL.
|
29930300 |
2019 |
Childhood Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The protein expression levels of B‑cell lymphoma 2 (BCL2) and myeloid cell leukemia sequence 1 (MCL1) were also compared between transfected and wild‑type HLE‑B3 cells by western blot analysis.
|
30569090 |
2019 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
We previously developed cell-penetrating VDAC1-derived peptides that interact with hexokinase (HK), Bcl-2, and Bcl-xL to prevent the anti-apoptotic activities of these proteins and induce cancer cell death, with a focus on leukemia and glioblastoma.
|
29698587 |
2018 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
They could markedly down-regulate the expressions of the c-Myc, Bcl-2 and CDK6 oncogenes in MV4-11 in the qRT-PCR and western blot studies, which further demonstrated that compound 1 and its derivatives could serve as a promising therapeutic strategy for MLL leukemia by targeting BRD4_BD1 protein.
|
29730189 |
2018 |
Childhood Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Sorafenib-related IL-15 production caused an increase in CD8<sup>+</sup>CD107a<sup>+</sup>IFN-γ<sup>+</sup> T cells with features of longevity (high levels of Bcl-2 and reduced PD-1 levels), which eradicated leukemia in secondary recipients.
|
29431743 |
2018 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
We found statistically significant increase in mRNA expression of all investigated proteins (p53, BAX, Bcl-2 and Bcl-XL) between the leukemia samples and leukocytes from healthy volunteers.
|
29515335 |
2018 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Together, these studies indicate that targeting STAT5 or STAT5-regulated pathways may provide a new approach for therapy development in Ph+ ALL, especially the relapsed/TKI-resistant disease.<b>Significance:</b> Suppression of STAT5 by BCL2 and PIM kinase inhibitors reduces leukemia burden in mice and constitutes a new potential therapeutic approach against Ph+ ALL, especially in tyrosine kinase inhibitor-resistant disease.<i></i>.
|
30154155 |
2018 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Thus, inhibition of anti-apoptotic BCL-2 family proteins has been proposed as a possible antineoplastic strategy, and BCL-2 inhibitors are currently being clinically trailed in patients with leukemia, lymphoma or non-small cell lung cancer.
|
29496539 |
2018 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Targeting the B-cell lymphoma 2 (BCL-2) family of proteins is an attractive option to combat chemoresistance in leukemia.
|
28751770 |
2018 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Overexpression of the pro-survival member BCL-2 is a well-established mechanism contributing to oncogenesis and chemoresistance in several cancers, including lymphoma and leukemia.
|
29732004 |
2018 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Surprisingly, STAT5 inhibition does not significantly affect IL-7-mediated Bcl-2 upregulation, suggesting that, contrary to normal T-cells, STAT5 promotes leukemia cell survival through a Bcl-2-independent mechanism.
|
30185437 |
2018 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
We report that inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) using statins enhances the proapoptotic activity of the B cell lymphoma-2 (BCL2) inhibitor venetoclax (ABT-199) in primary leukemia and lymphoma cells but not in normal human peripheral blood mononuclear cells.
|
29899021 |
2018 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Dysregulation of BCL-2 family proteins by leukemia fusion genes.
|
28717011 |
2017 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Small molecules that target Bcl-2 are used in the clinic to treat leukemia, but tight and selective inhibitors are not available for Bcl-2 paralog Bfl-1.
|
28594323 |
2017 |
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
BLI and PB were subsequently used to evaluate efficacy of the Bcl-2 inhibitor venetoclax.<b>Results:</b> BLI considerably accelerated and enhanced detection of leukemia burden compared with PB and identified sites of residual disease during treatment in a quantitative manner, highlighting limitations in current PB-based scoring criteria.
|
28119366 |
2017 |