| The BRE rs7572644 and NRG3 rs1649942 genetic variants were validated in an independent cohort of EOC Portuguese patients. | Pharmacogenomics in epithelial ovarian cancer first-line treatment outcome: validation of GWAS-associated NRG3 rs1649942 and BRE rs7572644 variants in an independent cohort.
Pinto R, Assis J, Nogueira A, Pereira C, Coelho S, Brandão M, Dias J, Alves S, Pereira D, Medeiros R. | 03/23/2019 |
| C-terminal BRE might be an important contributor to this program because in a case with relapsed AML, we observed an ins(11;2) fusing CHORDC1 to BRE at the region where intragenic transcription starts in KMT2A-rearranged and KAT6A-CREBBP AML. | C-terminal BRE overexpression in 11q23-rearranged and t(8;16) acute myeloid leukemia is caused by intragenic transcription initiation.
Marneth AE, Prange KHM, Al Hinai ASA, Bergevoet SM, Tesi N, Janssen-Megens EM, Kim B, Sharifi N, Yaspo ML, Kuster J, Sanders MA, Stoetman ECG, Knijnenburg J, Arentsen-Peters TCJM, Zwaan CM, Stunnenberg HG, van den Heuvel-Eibrink MM, Haferlach T, Fornerod M, Jansen JH, Valk PJM, van der Reijden BA, Martens JHA. | 02/9/2019 |
| show that BRE facilitates deubiquitylation of CDC25A by recruiting ubiquitin-specific-processing protease 7 (USP7) in the presence of DNA damage | BRE/BRCC45 regulates CDC25A stability by recruiting USP7 in response to DNA damage.
Biswas K, Philip S, Yadav A, Martin BK, Burkett S, Singh V, Babbar A, North SL, Chang S, Sharan SK., Free PMC Article | 09/22/2018 |
| Results show that BRE expression is regulated by HOTTIP LncRNA. Its over-expression promotes cell proliferation and cell cycle progression inhibiting apoptosis of glioma cells. | Over-expression of the long non-coding RNA HOTTIP inhibits glioma cell growth by BRE.
Xu LM, Chen L, Li F, Zhang R, Li ZY, Chen FF, Jiang XD., Free PMC Article | 12/23/2017 |
| High BRE and high EVI1 expression are mutually exclusive in MLL-AF9-positive acute myeloid leukemia patients. | Improved classification of MLL-AF9-positive acute myeloid leukemia patients based on BRE and EVI1 expression.
Noordermeer SM, Monteferrario D, Sanders MA, Bullinger L, Jansen JH, van der Reijden BA. | 07/21/2012 |
| High BRE expression defines a novel subtype of adult acute myeloid leukemia characterized by a favorable prognosis. | High BRE expression predicts favorable outcome in adult acute myeloid leukemia, in particular among MLL-AF9-positive patients.
Noordermeer SM, Sanders MA, Gilissen C, Tönnissen E, van der Heijden A, Döhner K, Bullinger L, Jansen JH, Valk PJ, van der Reijden BA. | 01/21/2012 |
| NBA1/MERIT40 and BRE interaction is required for the integrity of two distinct deubiquitinating enzyme BRCC36-containing complexes | NBA1/MERIT40 and BRE interaction is required for the integrity of two distinct deubiquitinating enzyme BRCC36-containing complexes.
Hu X, Kim JA, Castillo A, Huang M, Liu J, Wang B., Free PMC Article | 06/4/2011 |
| overexpression of the BRE gene is predominantly found in MLL-rearranged AML with t(9;11)(p22;q23). | High BRE expression in pediatric MLL-rearranged AML is associated with favorable outcome.
Balgobind BV, Zwaan CM, Reinhardt D, Arentsen-Peters TJ, Hollink IH, de Haas V, Kaspers GJ, de Bont ES, Baruchel A, Stary J, Meyer C, Marschalek R, Creutzig U, den Boer ML, Pieters R, van den Heuvel-Eibrink MM. | 01/15/2011 |
| Clinical trial of gene-disease association and gene-environment interaction. (HuGE Navigator) | Personalized smoking cessation: interactions between nicotine dose, dependence and quit-success genotype score.
Rose JE, Behm FM, Drgon T, Johnson C, Uhl GR., Free PMC Article | 06/30/2010 |
| A novel stress-responsive gene called BRE which interacts with TNF-receptor-1 and blocks the apoptotic effect of TNF-alpha, was identified. | Differential expression of a novel gene BRE (TNFRSF1A modulator/BRCC45) in response to stress and biological signals.
Chan JY, Li L, Miao J, Cai DQ, Lee KK, Chui YL. | 03/15/2010 |
| These results show that BRE over-expression can indeed promote growth, though not initiation, of liver tumors. | BRE over-expression promotes growth of hepatocellular carcinoma.
Chui YL, Ching AK, Chen S, Yip FP, Rowlands DK, James AE, Lee KK, Chan JY. | 03/1/2010 |
| results implied that BRE plays a significant role in mediating antiapoptotic and proliferative responses in esophageal carcinoma cells | Comparative proteomic analysis reveals differentially expressed proteins regulated by a potential tumor promoter, BRE, in human esophageal carcinoma cells.
Chen HB, Pan K, Tang MK, Chui YL, Chen L, Su ZJ, Shen ZY, Li EM, Xie W, Lee KK. | 01/21/2010 |
| Antiapoptotic in vivo; Bre levels are regulated post-transcriptionally in the liver, which is not observed in human hepatocellular carcinoma (HCC) and non-HCC cell lines. | BRE is an antiapoptotic protein in vivo and overexpressed in human hepatocellular carcinoma.
Chan BC, Ching AK, To KF, Leung JC, Chen S, Li Q, Lai PB, Tang NL, Shaw PC, Chan JY, James AE, Lai KN, Lim PL, Lee KK, Chui YL. | 01/21/2010 |
| the enhanced tumor growth is more likely due to the antiapoptotic activity of BRE than any direct effect of the protein on cell proliferation | BRE enhances in vivo growth of tumor cells.
Chan BC, Li Q, Chow SK, Ching AK, Liew CT, Lim PL, Lee KK, Chan JY, Chui YL. | 01/21/2010 |
| BRE mediates antiapoptosis by inhibiting the mitochondrial apoptotic machinery | A death receptor-associated anti-apoptotic protein, BRE, inhibits mitochondrial apoptotic pathway.
Li Q, Ching AK, Chan BC, Chow SK, Lim PL, Ho TC, Ip WK, Wong CK, Lam CW, Lee KK, Chan JY, Chui YL. | 01/21/2010 |