|1.||Wang, Shaomeng: 6 articles (05/2012 - 12/2007)|
|2.||Sun, Haiying: 5 articles (03/2012 - 12/2007)|
|3.||Lu, Jianfeng: 5 articles (03/2012 - 12/2007)|
|4.||McEachern, Donna: 4 articles (03/2012 - 11/2008)|
|5.||Bai, Longchuan: 4 articles (03/2012 - 11/2008)|
|6.||Sun, Yi: 3 articles (05/2012 - 11/2008)|
|7.||Qiu, Su: 3 articles (05/2011 - 12/2007)|
|8.||Yang, Chao-Yie: 2 articles (03/2012 - 12/2007)|
|9.||Yi, Han: 2 articles (05/2011 - 11/2008)|
|10.||Meagher, Jennifer L: 2 articles (11/2008 - 12/2007)|
|1.||Head and Neck Neoplasms (Head and Neck Cancer)
05/01/2011 - "This study provides a strong rationale to develop the combination of SM-164 and TRAIL as a new therapeutic strategy for the treatment of human cancer."
05/01/2011 - "Therapeutic potential and molecular mechanism of a novel, potent, nonpeptide, Smac mimetic SM-164 in combination with TRAIL for cancer treatment."
11/15/2008 - "Although SM-164 is modestly more effective than SM-122 in induction of cIAP-1/2 degradation, SM-164 is 1,000 times more potent than SM-122 as an inducer of apoptosis in tumor cells, which is attributed to its much higher potency in binding to and antagonizing XIAP. "
11/15/2008 - "SM-164: a novel, bivalent Smac mimetic that induces apoptosis and tumor regression by concurrent removal of the blockade of cIAP-1/2 and XIAP."
04/01/2011 - "Finally, SM-164 also radiosensitized human tumor xenograft while causing minimal toxicity. "
|3.||Breast Neoplasms (Breast Cancer)
05/01/2012 - "Our study demonstrates that IAPs are valid radiosensitizing targets in breast cancer cells and SM-164 could be further developed as a novel class of radiosensitizers for the treatment of radioresistant breast cancer."
05/01/2012 - "We found that SM-164 at nanomolar concentrations promoted degradation of cIAP-1, disrupted the inhibitory binding of XIAP to active caspase-9, and sensitized breast cancer cells to radiation with a sensitization enhancement ratio (SER) of 1.7-1.8. "
05/01/2012 - "Smac-mimetic compound SM-164 induces radiosensitization in breast cancer cells through activation of caspases and induction of apoptosis."
05/01/2011 - "Furthermore, the combination of SM-164 with TRAIL induces rapid tumor regression in vivo in a breast cancer xenograft model in which either agent is ineffective. "
05/01/2012 - "In one line of breast cancer cells resistant to SM-164 as a single agent, SM-164 radiosensitization was mediated by intrinsic apoptosis pathway through activation of caspases-9 and -3. In a line of breast cancer cells sensitive to SM-164 as a single agent, SM-164 radiosensitization was mediated by both extrinsic and intrinsic apoptosis pathways through activation of caspases-9, -8, and -3. Consistently, blockage of caspase activation, through siRNA knockdown or treatment with a pan-caspase inhibitor z-VAD-fmk, inhibited apoptosis and abrogated SM-164 radiosensitization. "
|4.||Colonic Neoplasms (Colon Cancer)
|5.||Pancreatic Neoplasms (Pancreatic Cancer)
|3.||Caspase 3 (Caspase-3)
|4.||Inhibitor of Apoptosis Proteins
|5.||Small Interfering RNA (siRNA)
|6.||Mitochondrial Proteins (Mitochondrial Protein)
|7.||Protein-Tyrosine Kinases (Tyrosine Kinase)
|10.||benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone
|1.||Heterologous Transplantation (Xenotransplantation)