|1.||Schally, Andrew V: 12 articles (06/2013 - 02/2007)|
|2.||Zarandi, Marta: 6 articles (04/2012 - 11/2008)|
|3.||Rick, Ferenc G: 5 articles (06/2013 - 10/2009)|
|4.||Szalontay, Luca: 5 articles (06/2013 - 10/2009)|
|5.||Hohla, Florian: 5 articles (11/2012 - 02/2007)|
|6.||Buchholz, Stefan: 5 articles (11/2012 - 02/2007)|
|7.||Block, Norman L: 4 articles (06/2013 - 01/2012)|
|8.||Schally, A V: 3 articles (07/2013 - 06/2008)|
|9.||Krishan, Awtar: 3 articles (06/2013 - 10/2009)|
|10.||Seitz, Stephan: 3 articles (11/2012 - 11/2008)|
11/15/2012 - "Our observations indicate that JMR-132 enhances the antiproliferative effect of S-phase-specific cytotoxic drugs by causing accumulation of tumor cells in S-phase."
11/15/2012 - "In vivo, daily treatment with GHRH antagonist JMR-132 decreased the tumor volume by 40-55% (p < 0.001) of HT-29, HCT-116 and HCT-15 tumors xenografted into athymic nude mice. "
01/31/2012 - "JMR-132 suppressed the proliferation of PC-3 cells in vitro in a dose-dependent manner and significantly inhibited growth of PC-3 tumors by 61% (P < 0.05). "
10/01/2009 - "In vivo, JMR-132 decreased the volume of HT-29, HCT-116 and HCT-15 tumors xenografted into athymic mice up to 75% (p < 0.05) and extended tumor doubling time (p < 0.001). "
07/01/2013 - "Treatment with the combination of JMR-132 and docetaxel led to an inhibition of tumor volume by 71.6% (p<0.001). "
|2.||Prostatic Neoplasms (Prostate Cancer)
01/31/2012 - "Our findings indicate that inhibition of PC-3 prostate cancer by JMR-132 involves inactivation of Akt and ERK. "
01/31/2012 - "We evaluated the effects of the GHRH antagonist, JMR-132, on PC-3 human androgen-independent prostate cancer cells in vitro and in vivo. "
02/15/2013 - "This study determined the effect of growth hormone-releasing hormone (GHRH) antagonists, JMR-132 and JV-1-38 on growth of PC3 tumors as well as on angiogenesis and metastasis through the evaluation of various factors that contribute largely to the progression of prostate cancer. "
12/23/2008 - "In this study, we evaluated by Western blot the effects in vitro of GHRH and its antagonist JMR-132 on proliferating cell nuclear antigen, tumor suppressor protein p53, transcription factor NF-kappaB p50 and its phosphorylated form, caspase 3, and cleaved caspase 3 in the LNCaP human prostate cancer cell line. "
|3.||Breast Neoplasms (Breast Cancer)
07/01/2013 - "In this study, we investigated the effectiveness of the treatment of MDA-MB-231 human triple-negative breast cancer (TNBC) with GHRH antagonist JMR-132 alone or in combination with docetaxel. "
11/01/2008 - "In the present study we demonstrate that a novel highly potent GHRH antagonist JMR-132 strongly inhibits the proliferation of both estrogen receptor negative SKBR 3 and estrogen receptor positive ZR 75 human breast cancer cell lines in vitro. "
11/01/2008 - "These in vitro results suggest that JMR-132 is a potent inhibitor of breast cancer growth, independent of the estrogen receptor status. "
|4.||Colonic Neoplasms (Colon Cancer)
10/01/2009 - "Time course studies revealed that the treatment of human HCT-116 colon cancer cells with 10 muM GHRH antagonist JMR-132 causes a significant DNA damage as shown by an increase in olive tail moment (OTM) and loss of inner mitochondrial membrane potential (Delta Psi m). "
10/01/2009 - "Our observations suggest that GHRH antagonist JMR-132 exerts its antiproliferative effect on experimental colon cancer cells through p21(Waf1/Cip1) mediated S-phase arrest along with apoptosis involving the intrinsic pathway."
10/01/2009 - "We investigated the mechanisms of inhibitory effect of growth hormone-releasing hormone (GHRH) antagonist JMR-132 on the growth of HT29, HCT-116 and HCT-15 human colon cancer cells in vitro and in vivo. "
11/01/2008 - "Suppression of p21 expression by siRNA in human HT29 colon cancer cells and non-transformed mouse osteoblasts KS483 also blocked the anti-proliferative effects of JMR-132 suggesting that the regulation of cell proliferation by GHRH is p21 dependent. "
11/15/2012 - "Treatment of colon cancer with an antagonist of growth hormone-releasing hormone (GHRH), JMR-132, results in a cell cycle arrest in S-phase of the tumor cells. "
|5.||Ovarian Neoplasms (Ovarian Cancer)
01/01/2010 - "The present study demonstrates that the inhibitory effect of the GHRH antagonist JMR-132 on proliferation is due, in part, to an interference with the EGFR-Akt pathway in ovarian cancer cells."
01/01/2010 - "In this study, we investigated the effects of a new GHRH antagonist JMR-132, in ovarian cancer cell lines SKOV3 and CaOV3 expressing splice variant (SV)1 of GHRH receptors. "
01/01/2010 - "In addition, JMR-132 treatments decreased significantly the epidermal growth factor receptor (EGFR) level and the phosphorylation of Akt (p-Akt), suggesting that JMR-132 inhibits the EGFR-Akt pathway in ovarian cancer cells. "
10/01/2011 - "Nude mice bearing xenografts on ES-2 and UCI-107 ovarian cancer were treated with JMR-132 and MZ-J-7-118, respectively. "
10/01/2011 - "Our results indicate that GHRHa such as JMR-132 and MZ-J-7-118 can inhibit the growth of human ovarian cancer. "
|2.||Growth Hormone-Releasing Hormone (Somatotropin Releasing Hormone)
|3.||Caspase 3 (Caspase-3)
|4.||Proliferating Cell Nuclear Antigen (PCNA)
|5.||NF-kappa B (NF-kB)
|6.||Tumor Suppressor Protein p53
|7.||Transcription Factors (Transcription Factor)
|10.||somatotropin releasing hormone receptor
|1.||Drug Therapy (Chemotherapy)
|2.||Heterologous Transplantation (Xenotransplantation)