|1.||Benbrook, Doris M: 9 articles (07/2013 - 07/2003)|
|2.||Berlin, K Darrell: 7 articles (01/2015 - 07/2003)|
|3.||Benbrook, Doris Mangiaracina: 7 articles (01/2015 - 05/2009)|
|4.||Chengedza, Shylet: 4 articles (03/2010 - 05/2009)|
|5.||Nammalwar, Baskar: 2 articles (01/2015 - 06/2014)|
|6.||Bunce, Richard A: 2 articles (01/2015 - 06/2014)|
|7.||Rao, Chinthalapally V: 2 articles (09/2013 - 07/2012)|
|8.||Kapetanovic, Izet M: 2 articles (07/2013 - 07/2012)|
|9.||Masamha, Chioniso Patience: 2 articles (08/2009 - 05/2009)|
|10.||Lightfoot, Stan: 2 articles (08/2009 - 05/2009)|
08/01/2009 - "The hypothesis of this study was that the lead Flex-Het, SHetA2, inhibits angiogenesis by blocking cytokine release from cancer cells. "
06/01/2014 - "SHetA2 is a small molecule flexible heteroarotinoid (Flex-Het) with promising cancer prevention and therapeutic activity. "
05/01/2009 - "Structure function analysis of related Flex-Hets for potential improvement of SHetA2 pharmaceutical properties showed that compounds with increased hydrophilicity slightly reduced the growth inhibition efficacy, but retained the differential effect on cancer over normal cells. "
05/01/2009 - "Potential chemopreventive and therapeutic value of the lead Flexible Heteroarotinoid (Flex-Het), SHetA2, was indicated by growth inhibition of multiple cancer cell lines. "
01/01/2015 - "The objectives of this structure activity relationship (SAR) study were to determine if a 4-atom acrylamide linker and various substitutions on the terminal aryl ring altered the anti-cancer activity of these second generation Flex-Het compounds compared to the parent Flex-Het compound, SHetA2, which has a thiourea linker and a nitro substituent. "
|2.||Ovarian Neoplasms (Ovarian Cancer)
01/01/2007 - "One objective of this study was to synthesize a series of heteroarotinoids structurally related to SHetA2 and to measure the effect of structural alterations on the cytotoxicity activities of the compounds on A2780 ovarian cancer cells. "
08/15/2009 - "The objective of this study was to determine if a flexible heteroarotinoid anticancer compound, SHetA2, regulates cell cycle proteins and cell cycle progression in ovarian cancer cells. "
03/01/2010 - "The flexible heteroarotinoid, SHetA2, sensitizes resistant ovarian cancer cells to TNF-alpha-induced extrinsic apoptosis, and also induces intrinsic apoptosis as a single agent. "
08/15/2009 - "In conclusion, we show that loss of cyclin D1 in ovarian cancer cells treated with SHetA2 is sufficient to induce G(1) cell cycle arrest and this strategy is not impeded by the presence of cyclin E2. "
10/01/2005 - "Oral administration of Flex-Hets (SHetA2 and SHetA4) inhibited growth of OVCAR-3 ovarian cancer xenografts to similar extents as administration of a RAR/RXR-panagonist (SHet50) and Fenretinide (4-HPR) in vivo. "
|3.||Kidney Neoplasms (Kidney Cancer)
05/01/2009 - "The objective of this study was to evaluate the SHetA2 mechanism and in vivo activity in kidney cancer. "
05/01/2009 - "In conclusion, SHetA2 regulates growth, differentiation, and apoptosis in kidney cancer cells through multiple molecular events downstream of nuclear factor-κB repression. "
08/01/2009 - "SHetA2 inhibition of in vivo angiogenesis was observed in Caki-1 renal cancer xenografts. "
05/01/2009 - "SHetA2 induced apoptosis in the Caki-1 kidney cancer cell line through reduction of Bcl-2 protein and induction of PARP-1 and caspase 3 cleavages, whereas normal kidney epithelial cells exhibited resistance. "
05/01/2009 - "Oral SHetA2 inhibited growth in one of two renal cancer xenograft models without causing mortality or weight loss. "
09/01/2013 - "SHetA2 modulation of biomarkers in colon polyps identifies potential pharmacodynamic endpoints for SHetA2 clinical trials."
09/01/2013 - "Immunohistochemical and Western blot analysis of polyps showed reduced levels of cyclin D1 and proliferating cell nuclear antigen in both SHetA2 treatment groups. "
|5.||Weight Loss (Weight Reduction)
|2.||Cell Cycle Proteins
|3.||Biological Markers (Surrogate Marker)
|4.||Carrier Proteins (Binding Protein)
|5.||Caspase 3 (Caspase-3)
|6.||Retinoic Acid Receptors (Retinoic Acid Receptor)
|8.||Tumor Necrosis Factor-alpha (Tumor Necrosis Factor)
|10.||TNF-Related Apoptosis-Inducing Ligand
|1.||Heterologous Transplantation (Xenotransplantation)