| Shih-Hsin Tu |
------>authors3_c=??? ------>paper_class1=1 ------>Impact_Factor=4.453 ------>paper_class3=2 ------>paper_class2=1 ------>vol= ------>confirm_bywho=chenchho ------>insert_bywho=hoyuansn ------>Jurnal_Rank=25.8 ------>authors4_c=??? ------>comm_author=1 ------>patent_EDate=None ------>authors5_c=??? ------>publish_day=1 ------>paper_class2Letter=None ------>page2= ------>medlineContent= ------>unit=E0310 ------>insert_date=20090718 ------>iam=7 ------>update_date=None ------>author=??? ------>change_event=4 ------>ISSN= ------>authors_c=??? ------>score=470 ------>journal_name=Breast Cancer Research and Treatment ------>paper_name=Increased expression of enolase ? in human breast cancer confers tamoxifen resistance in human breast cancer cells ------>confirm_date=20091116 ------>tch_id=084007 ------>pmid=19655245 ------>page1= ------>fullAbstract=Enolase-alpha (ENO-1) is a key glycolytic enzyme that has been used as a diagnostic marker to identify human lung cancers. To investigate the role of ENO-1 in breast cancer diagnosis and therapy, the mRNA levels of ENO-1 in 244 tumor and normal paired tissue samples and 20 laser capture-microdissected cell clusters were examined by quantitative real-time PCR analysis. Increased ENO-1 mRNA expression was preferentially detected in estrogen receptor-positive (ER+) tumors (tumor/normal ratio >90-fold) when compared to ER-negative (tumor/normal ratio >20-fold) tumor tissues. The data presented here demonstrate that those patients whose tumors highly expressed ENO-1 had a poor prognosis with greater tumor size (>2 cm, *P = .017), poor nodal status (N > 3, *P = .018), and a shorter disease-free interval (<==1 year, *P < .009). We also found that higher-expressing ENO-1 tumors confer longer distance relapse (tumor/normal ratio = 82.8-92.4-fold) when compared to locoregional relapse (tumor/normal ratio = 43.4-fold) in postsurgical 4-hydroxy-tamoxifen (4-OHT)-treated ER+ patients (*P = .014). These data imply that changes in tumor ENO-1 levels are related to clinical 4-OHT therapeutic outcome. In vitro studies demonstrated that decreasing ENO-1 expression using small interfering RNA (siRNA) significantly augmented 4-OHT (100 nM)-induced cytotoxicity in tamoxifen-resistant (Tam-R) breast cancer cells. These results suggest that downregulation of ENO-1 could be utilized as a novel pharmacological approach for overcoming 4-OHT resistance in breast cancer therapy. ------>tmu_sno=None ------>sno=22039 ------>authors2=Chih-Chiang Chang ------>authors3=Ching-Shyang Chen ------>authors4=Ka-Wai Tam ------>authors5=Ying-Jan Wang ------>authors6=Chia-Hwa Lee, Hsiao-Wei LinTzu-Chun Cheng3, Ching-Shui Huang1,2, Jan-Show Chu6, Neng-Yao Shih7, Li-C ------>authors6_c=???, ???, ???, ???, ???, ???, ???, ???, ???, ??? ------>authors=Shih-Hsin Tu ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c=??? ------>publish_area=0 ------>updateTitle=Increased expression of enolase alpha in human breast cancer confers tamoxifen resistance in human breast cancer cells. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no= ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2009 ------>submit_flag=None ------>publish_month=1 |