|
Prostatic Neoplasms
|
0.350 |
AlteredExpression
|
group |
BEFREE |
These results suggest that increased expression of BAD provides a proliferative advantage to prostate tumors, while BAD dephosphorylation increases sensitivity of prostate cancer cells to apoptosis.
|
19593445 |
2009 |
|
Prostatic Neoplasms
|
0.350 |
Biomarker
|
group |
BEFREE |
DHA also inhibits AKT(T308) but not AKT(S473) phosphorylation, alters PI(3,4,5)P3 (PIP3) and phospho-AKT(S473) protein localization, decreases pPDPK1(S241)-AKT and AKT-BAD interaction and suppresses prostate tumor growth.
|
23633519 |
2013 |
|
Malignant neoplasm of prostate
|
0.320 |
PosttranslationalModification
|
disease |
BEFREE |
Using pharmacological inhibitors and dominant-negative proteins, we showed that VIP-induced cytoprotection and BAD phosphorylation are mediated via both Ras/MAPK and PKA pathways in CSCs of prostate cancer LNCaP and C4-2 cells, but only PKA signaling was involved in CSCs of DUVIPR (DU145 prostate cancer cells ectopically expressing VIP receptor) and breast cancer MCF7 cells.
|
28569785 |
2017 |
|
Malignant neoplasm of prostate
|
0.320 |
AlteredExpression
|
disease |
BEFREE |
Combination of proliferative and apoptotic properties prompts prostate cancer cells to be "addicted" to increased levels of phosphorylated BAD.
|
19593445 |
2009 |
|
Glioma
|
0.240 |
Biomarker
|
disease |
BEFREE |
Thus, our data suggest that glioma cell survival occurs through a novel PI (3)-kinase/PDK1/PKC-ι/BAD mediated pathway.
|
21419810 |
2011 |
|
Glioma
|
0.240 |
Biomarker
|
disease |
BEFREE |
Surprisingly, although siRNA-mediated depletion of BAD in glioma cells abrogates cytotoxic- and chemotherapy-induced apoptosis, TWEAK still displays a strong protective effect, suggesting that BAD serine 136 phosphorylation plays a minor role in TWEAK-Akt2-induced glioma cell survival.
|
19861406 |
2009 |
|
Glioma
|
0.240 |
AlteredExpression
|
disease |
BEFREE |
The apoptotic death in the glioma cell lines treated with PPARgamma agonists was correlated with the transient up-regulation of Bax and Bad protein levels.
|
12065618 |
2002 |
|
Glioma
|
0.240 |
Biomarker
|
disease |
BEFREE |
Inhibition of either PPARgamma or MEK1/2 blocked the Troglitazone-mediated phosphorylation of BAD and further increased the synergistic induction of glioma cell death by TRAIL and Troglitazone.
|
19158480 |
2008 |
|
Malignant tumor of colon
|
0.220 |
GeneticVariation
|
disease |
BEFREE |
Using principal component analysis to derive a numeric score representing pathway expression, we evaluated clinico-genomic datasets (n=427) from corresponding normal, pre-invasive and invasive cancers of different types, such as ovarian, endometrial, breast and colon cancers in order to determine the associations between the BAD-mediated apoptotic pathway and cancer development.
|
25653146 |
2015 |
|
Malignant tumor of colon
|
0.220 |
GeneticVariation
|
disease |
BEFREE |
This is the first report on Bad gene mutation in human malignancies, and our data suggest that Bad gene is occasionally mutated in colon cancers and that somatic mutation of Bad may contribute to the development of colon cancers.
|
15033904 |
2004 |
|
Obesity
|
0.210 |
GeneticVariation
|
disease |
BEFREE |
Common BAD and SERPINA6 variants were associated (p<0.05) with obesity and insulin resistance, respectively.
|
29126409 |
2017 |
|
Malignant Neoplasms
|
0.080 |
GeneticVariation
|
group |
BEFREE |
Inequality in genetic cancer risk suggests bad genes rather than bad luck.
|
29079851 |
2017 |
|
Malignant Neoplasms
|
0.080 |
AlteredExpression
|
group |
BEFREE |
These findings indicate that AF1q up-regulation of BAD is through its effect on NF-kappaB and this may hint of its oncogenic mechanism in cancer.
|
20596645 |
2010 |
|
Malignant Neoplasms
|
0.080 |
AlteredExpression
|
group |
BEFREE |
Phospho-BAD expression in the non-tumour hepatocytes was seen in all of the hepatocellular carcinomas, while the expression in the cancer cells was observed in 15% (3 of the 20) of the hepatocellular carcinomas.
|
16807152 |
2006 |
|
Malignant Neoplasms
|
0.080 |
Biomarker
|
group |
BEFREE |
In addition, the WTS implicated the BCL-2/BAX/BAD apoptotic pathway as a potential mechanism for this enhanced combination effect.Clin Cancer Res; 23(1); 171-80.©2016 AACR.
|
27370604 |
2017 |
|
Malignant Neoplasms
|
0.080 |
AlteredExpression
|
group |
BEFREE |
Higher pBAD protein levels were observed in the cancer cells compared to the immortalized normal cells, whereas PP2C gene expression was lower in the cancer compared to the ovarian tumor tissue samples (n=76, p<0.001).
|
25653146 |
2015 |
|
Malignant Neoplasms
|
0.080 |
Biomarker
|
group |
BEFREE |
The good oncogene: When bad genes identify good outcome in cancer.
|
21050670 |
2011 |
|
Malignant Neoplasms
|
0.080 |
GeneticVariation
|
group |
BEFREE |
This is the first report on Bad gene mutation in human malignancies, and our data suggest that Bad gene is occasionally mutated in colon cancers and that somatic mutation of Bad may contribute to the development of colon cancers.
|
15033904 |
2004 |
|
Malignant Neoplasms
|
0.080 |
PosttranslationalModification
|
group |
BEFREE |
Upregulated DNMTs (DNMT1, DNMT3A, and DNMT3B) mediated downregulation and hypermethylation of BAD and INPPL1 in CAC and CRC cells.
|
31802101 |
2019 |
|
B-Cell Lymphomas
|
0.080 |
Biomarker
|
group |
BEFREE |
In addition to increased B-cell lymphoma 2 (Bcl-2) phosphorylation through JNK signaling in response to docetaxel, si-Vav3 enhanced docetaxel-induced apoptosis, as characterized by the accumulation of sub-G1 phase cells and DNA fragmentation, through Bcl-xL/Bcl-2-associated death promoter (Bad) dephosphorylation, resulting in increased caspase-9, caspase-3, and cleaved poly(ADP-ribose) polymerase activation.
|
23566222 |
2013 |
|
B-Cell Lymphomas
|
0.080 |
GeneticVariation
|
group |
BEFREE |
Western blot analysis was performed in order to determine the differential expression levels of Janus kinase (JAK), signal transducer and activator of transcription 3 (STAT3) and apoptosis associated proteins B-cell lymphoma 2 (Bcl-2), Bcl-2 associated X protein (Bax) and Bcl-2 associated agonist of cell death (Bad).
|
28599489 |
2017 |
|
B-Cell Lymphomas
|
0.080 |
Biomarker
|
group |
BEFREE |
OGD/R-mediated DNA fragmentation and Casp3 expression could be prevented as well as resolved by the addition of hWJ-MSC-derived EV before and after OGD, respectively. hWJ-MSC-derived EV also tended to increase the phosphorylation of the B cell lymphoma 2 (Bcl2) family member Bcl-2-antagonist of cell death (BAD) in N2a cells, when added prior or post OGD, thereby inactivating the proapoptotic function of BAD.
|
29562785 |
2018 |
|
B-Cell Lymphomas
|
0.080 |
GeneticVariation
|
group |
BEFREE |
We conclude that mutations in the BAD gene do not play a role in the pathogenesis of the major subtypes of human B-cell lymphomas.
|
16646081 |
2006 |
|
B-Cell Lymphomas
|
0.080 |
AlteredExpression
|
group |
BEFREE |
Anti-apoptosis B-cell lymphoma (Bcl)-2 and Bcl-w genes were downregulated and pro-apoptotic Bcl-2-associated agonist of cell death and caspase-3 genes were upregulated in U-2OS cells following treatment with β-elemene-paclitaxel.
|
30008912 |
2018 |
|
B-Cell Lymphomas
|
0.080 |
AlteredExpression
|
group |
BEFREE |
Apoptosis was triggered through the intrinsic pathway by upregulating the expression of several B-cell lymphoma-2 (Bcl-2) family proapoptotic proteins, including p53-upregulated modulator of apoptosis (PUMA), Bcl-2-associated X protein and Bcl-2-associated agonist of cell death, and by downregulating the antiapoptotic protein Bcl-extra large.
|
28529565 |
2017 |