|
Chronic Lymphocytic Leukemia
|
0.420 |
GeneticVariation
|
disease |
GWASCAT |
Genome-wide association analysis of chronic lymphocytic leukaemia, Hodgkin lymphoma and multiple myeloma identifies pleiotropic risk loci.
|
28112199 |
2017 |
|
Chronic Lymphocytic Leukemia
|
0.420 |
GeneticVariation
|
disease |
BEFREE |
These findings are consistent with rs539846 influencing CLL susceptibility through differential RELA binding, with direct modulation of BMF expression impacting on anti-apoptotic BCL2, a hallmark of oncogenic dependency in CLL.
|
27524613 |
2016 |
|
Chronic Lymphocytic Leukemia
|
0.420 |
Biomarker
|
disease |
CTD_human |
Genome-wide association study identifies multiple risk loci for chronic lymphocytic leukemia.
|
23770605 |
2013 |
|
Chronic Lymphocytic Leukemia
|
0.420 |
Biomarker
|
disease |
BEFREE |
Resistance was associated with a partial reactivation of extracellular signal-regulated kinase 1/2 (ERK1/2) signaling, recovery of G1/S cell-cycle events, and suppression of the pro-apoptotic B-cell leukemia/lymphoma 2 (Bcl-2) homology domain 3 (BH3)-only proteins, Bcl-2-interacting mediator of cell death-extra large (Bim-EL) and Bcl-2 modifying factor (Bmf).
|
22858545 |
2012 |
|
Liver Cirrhosis, Experimental
|
0.300 |
Biomarker
|
disease |
CTD_human |
Systems level analysis and identification of pathways and networks associated with liver fibrosis.
|
25380136 |
2014 |
|
Body Height
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
|
Vital capacity
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
New genetic signals for lung function highlight pathways and chronic obstructive pulmonary disease associations across multiple ancestries.
|
30804560 |
2019 |
|
Vital capacity
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
|
Hodgkin Disease
|
0.100 |
GeneticVariation
|
disease |
GWASCAT |
Genome-wide association analysis of chronic lymphocytic leukaemia, Hodgkin lymphoma and multiple myeloma identifies pleiotropic risk loci.
|
28112199 |
2017 |
|
Multiple Myeloma
|
0.100 |
GeneticVariation
|
disease |
GWASCAT |
Genome-wide association analysis of chronic lymphocytic leukaemia, Hodgkin lymphoma and multiple myeloma identifies pleiotropic risk loci.
|
28112199 |
2017 |
|
Small Lymphocytic Lymphoma
|
0.100 |
GeneticVariation
|
disease |
GWASCAT |
Genome-wide association analysis of chronic lymphocytic leukaemia, Hodgkin lymphoma and multiple myeloma identifies pleiotropic risk loci.
|
28112199 |
2017 |
|
Neoplasms
|
0.040 |
Biomarker
|
group |
BEFREE |
Subtoxic concentrations of the MEK inhibitor MEK162 and the PI3Kα-specific inhibitor BYL719 synergized to trigger apoptosis in <i>NRAS</i>-mutated RMS cells <i>in vitro</i> and <i>in vivo</i><i>NRAS</i>- or <i>HRAS</i>-mutated cell lines were more vulnerable to MEK162/BYL719 cotreatment than <i>RAS</i> wild-type cell lines, and MEK162/BYL719 cotreatment was more effective to trigger apoptosis in <i>NRAS</i>-mutated than <i>RAS</i> wild-type RMS tumors <i>in vivo</i> We identified BCL-2-modifying factor (BMF) as an inhibitory target of oncogenic NRAS, with either NRAS silencing or MEK inhibition upregulating BMF mRNA and protein levels, which BYL719 further increased.
|
29437705 |
2018 |
|
Neoplasms
|
0.040 |
AlteredExpression
|
group |
BEFREE |
Initial tumor response was associated with apoptosis mediated via upregulation of BMF and BIM.
|
26914605 |
2016 |
|
Neoplasms
|
0.040 |
Biomarker
|
group |
BEFREE |
In conclusion, we have identified repression of BMF as a major cue that underpins anoikis resistance and tumour dissemination in E-cadherin-deficient metastatic breast cancer.
|
27035620 |
2016 |
|
Neoplasms
|
0.040 |
AlteredExpression
|
group |
BEFREE |
We showed that the introduction of Gas5 by plasmid transfection increased the expression of tumor suppressor Bcl-2-modifying factor (bmf) and Plexin C1 via directly targeting and reducing the expression of miR-222.
|
26370254 |
2015 |
|
Autoimmune Diseases
|
0.020 |
GeneticVariation
|
group |
BEFREE |
We have previously reported that deletion of BIM or BMF stabilizes donor stem cell numbers during transplantation and improves cellular fitness and transplantation outcomes, albeit posing a risk for lymphoma and autoimmunity in recipient mice.
|
30156339 |
2018 |
|
Autoimmune Diseases
|
0.020 |
Biomarker
|
group |
BEFREE |
Bcl-2 modifying factor (Bmf) is one such BH3-only protein that is implicated in various death paradigms such as anoikis, seizures, cancer and autoimmunity.
|
29499358 |
2018 |
|
Lymphoma
|
0.020 |
Biomarker
|
group |
BEFREE |
We have previously reported that deletion of BIM or BMF stabilizes donor stem cell numbers during transplantation and improves cellular fitness and transplantation outcomes, albeit posing a risk for lymphoma and autoimmunity in recipient mice.
|
30156339 |
2018 |
|
Adult Lymphoma
|
0.020 |
Biomarker
|
disease |
BEFREE |
We have previously reported that deletion of BIM or BMF stabilizes donor stem cell numbers during transplantation and improves cellular fitness and transplantation outcomes, albeit posing a risk for lymphoma and autoimmunity in recipient mice.
|
30156339 |
2018 |
|
Childhood Lymphoma
|
0.020 |
Biomarker
|
disease |
BEFREE |
We have previously reported that deletion of BIM or BMF stabilizes donor stem cell numbers during transplantation and improves cellular fitness and transplantation outcomes, albeit posing a risk for lymphoma and autoimmunity in recipient mice.
|
30156339 |
2018 |
|
B-Cell Lymphomas
|
0.020 |
GeneticVariation
|
group |
BEFREE |
SNP rs539846 C>A, the most highly associated variant (p = 1.42 × 10(-13), odds ratio = 1.35), localizes to a super-enhancer defined by extensive histone H3 lysine 27 acetylation in intron 3 of B cell lymphoma 2 (BCL2)-modifying factor (BMF).
|
27524613 |
2016 |
|
Lymphoma
|
0.020 |
Biomarker
|
group |
BEFREE |
Moreover, apoptosis was initiated at drug concentrations insufficient to antagonize PI3K/mTORC2-regulated AKT phosphorylation. p53-independent induction of the proapoptotic BH3-only protein BMF was identified as a mechanism by which dual DDR/mTORC1 inhibition caused lymphoma cell death.
|
23403624 |
2013 |
|
Adult Lymphoma
|
0.020 |
Biomarker
|
disease |
BEFREE |
Moreover, apoptosis was initiated at drug concentrations insufficient to antagonize PI3K/mTORC2-regulated AKT phosphorylation. p53-independent induction of the proapoptotic BH3-only protein BMF was identified as a mechanism by which dual DDR/mTORC1 inhibition caused lymphoma cell death.
|
23403624 |
2013 |
|
Childhood Lymphoma
|
0.020 |
Biomarker
|
disease |
BEFREE |
Moreover, apoptosis was initiated at drug concentrations insufficient to antagonize PI3K/mTORC2-regulated AKT phosphorylation. p53-independent induction of the proapoptotic BH3-only protein BMF was identified as a mechanism by which dual DDR/mTORC1 inhibition caused lymphoma cell death.
|
23403624 |
2013 |
|
B-Cell Lymphomas
|
0.020 |
Biomarker
|
group |
BEFREE |
BCL-2 modifying factor (BMF) is a sentinel considered to register damage at the cytoskeleton and to convey a death signal to B-cell lymphoma 2.
|
21673109 |
2011 |