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Source: Cancer Research
Drug: Velcade

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Total 8 results found since Jan 2013.

Abstract P6-11-10: Preclinical efficacy of the novel PIM2 kinase inhibitor, JP11646 in triple negative breast cancer models
Conclusions: PIM2 upregulation in TNBC cell line resulted in more aggressive phenotype. JP11646, through novel mechanism of action resulting in degradation of PIM2, showed robust activity in TNBC cell lines both in vitro and in vivo. Further correlative studies in tumors harvested from in vivo experiments are ongoing. These results encourage further exploration of use of JP11646 as a targeted agent in treatment of TNBC.Citation Format: Mehta R, Kothai Guruswamy Sangameswaran D, Bezbatchenko K, Moore J, Gil M, Khoury T, Baldino C, Caserta J, Fetterly, Jr. G, Lee K, Adjei A, Opyrchal M. Preclinical efficacy of the novel PIM2...
Source: Cancer Research - February 28, 2017 Category: Cancer & Oncology Authors: R Mehta, D Kothai Guruswamy Sangameswaran, K Bezbatchenko, J Moore, M Gil, T Khoury, C Baldino, J Caserta, G Fetterly, Jr., K Lee, A Adjei, M Opyrchal Tags: Poster Session Abstracts Source Type: research

Abstract P3-13-28: Lipofilling of the axilla to reduce secondary lymphedema after axillary lymph node dissection
Conclusions: PIM2 upregulation in TNBC cell line resulted in more aggressive phenotype. JP11646, through novel mechanism of action resulting in degradation of PIM2, showed robust activity in TNBC cell lines both in vitro and in vivo. Further correlative studies in tumors harvested from in vivo experiments are ongoing. These results encourage further exploration of use of JP11646 as a targeted agent in treatment of TNBC.Citation Format: Vandermeeren L, Belgrado J-P, Vankerckhove S, Valsamis J-B, Feipel V, Rooze M, Moraine J-J, Hertens D, Carly B, Liebens F. Lipofilling of the axilla to reduce secondary lymphedema after axil...
Source: Cancer Research - February 13, 2017 Category: Cancer & Oncology Authors: L Vandermeeren, J-P Belgrado, S Vankerckhove, J-B Valsamis, V Feipel, M Rooze, J-J Moraine, D Hertens, B Carly, F Liebens Tags: Poster Session Abstracts Source Type: research

Abstract 5472: Selinexor, a selective inhibitor of nuclear export (SINE), acts through NF-{kappa}B deactivation and combines with proteasome inhibitors to synergistically induce tumor cell death
Conclusion: Inhibition of NF-κB transcriptional activity through forced nuclear retention of IκB appears to be an important mechanism in the selective tumor cell cytotoxicity of selinexor and related SINE compounds. Furthermore, the combination of selinexor and proteasome inhibitors, which are also known to act at least in part through inhibition of NF-κB, leads to synergistic activity in vitro and in vivo, suggesting that such combinations may provide clinically more effective than the single agents. A Phase 1 trial to study the safety and efficacy of selinexor in combination with carfilzomib in multiple myeloma is ong...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Landesman, Y., Kashyap, T., Crochiere, M., Klebanov, B., Friedlander, S., Senapedis, W., Carlson, R., Kauffman, M., Shacham, S. Tags: Experimental and Molecular Therapeutics Source Type: research

Abstract 4969: Metformin causes AR degradation via Skp2-mediated ubiquitination
This study supports that use of metformin in combination with Enza or other ARSI drugs may not only block autophagy survival but also cause AR degradation that leads to PC cell death.Citation Format: Joy C. Yang, Allen C. Gao, Christopher P. Evans. Metformin causes AR degradation via Skp2-mediated ubiquitination. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4969. doi:10.1158/1538-7445.AM2015-4969
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Yang, J. C., Gao, A. C., Evans, C. P. Tags: Molecular and Cellular Biology Source Type: research

Abstract P2-06-04: Proteosome inhibitor bortezomib inhibits NF{kappa}B and effectively overcomes cancer stem cell escape triggered by Wnt inhibitor therapy in FOXC1+ basal-Like/claudin-low breast cancer
In this study, we sought to investigate the link between Wnt signaling and FOXC1 and its potential in regulating CSC biology in basal-Like/claudin-low breast cancer. We observed that exposure of the MDA-MB-231 basal-like/claudin-low cell line (low constitutive FOXC1 expressor) to Wnt3a (a canonical Wnt signaling ligand), resulted in increased expression of FOXC1. Reciprocally, overexpression of FOXC1 in MCF10A human mammary epithelial cells led to a pronounced increase in Wnt signaling activity, strongly suggestive of a direct or indirect positive feedback loop between Wnt signaling and FOXC1. More importantly, BT549 and H...
Source: Cancer Research - April 30, 2015 Category: Cancer & Oncology Authors: Ray, P. S., Tsai, C. Y., Ray, T., Kim, B., Jensen, T. W. Tags: Poster Session Abstracts Source Type: research

Abstract 5112: Histone deacetylase and proteasome inhibitors synergistically induce apoptosis in colon cancer, multiple myeloma and CTCL cells through induction of the immediate early genes ATF3 and JUN
Conclusions: This study provides insight into the mechanistic basis by which combination treatment with HDAC and proteasome inhibitors synergistically induces apoptosis in tumour cells. Citation Format: Janson WT Tse, Anderly C. Chueh, Ian Y. Luk, Fiona Chionh, Yvonne Yeung, Georgia A. Corner, Dominic CH Ng, Hoanh Tran, Amardeep S. Dhillon, John M. Mariadason. Histone deacetylase and proteasome inhibitors synergistically induce apoptosis in colon cancer, multiple myeloma and CTCL cells through induction of the immediate early genes ATF3 and JUN. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Associ...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Tse, J. W., Chueh, A. C., Luk, I. Y., Chionh, F., Yeung, Y., Corner, G. A., Ng, D. C., Tran, H., Dhillon, A. S., Mariadason, J. M. Tags: Molecular and Cellular Biology Source Type: research

Abstract 2739: Specific interaction of human MGMT with ER-{alpha} in breast cancer cells: Co-degradation of MGMT and ER- {alpha} proteins by either fulvestrant or O6-benzylguanine and its therapeutic significance
This study investigated whether i) MGMT is modulated by endocrine therapies, ii) MGMT interacts with ER-signaling components and iii) if such findings are exploitable for improved breast cancer treatment. The ER-α positive cell lines MCF-7, T47D and ER- α negative MDAMB 468 cells, all MGMT-proficient, were treated with Fulvestrant (Faslodex, ICI 182, 780) or O6-benzylguanine (BG) in various experiments. Fulvestrant is a pure antiestrogen that binds to ER without eliciting any transcriptional effects, but leads to the receptor degradation through the ubiquitin-proteasome (ub-P) pathway. BG is a specific pseudosubstrate fo...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Srivenugopal, K. S., Paranjpe, A. Tags: Experimental and Molecular Therapeutics Source Type: research

Abstract 2254: Pro-angiogenic CXCL8 signalling underpins microenvironment-induced relapse to anti-androgen therapy of prostate cancer
Conclusion: Our data suggests that targeting CXCL8 signalling may therefore be a relevant strategy to enhance tumor response to anti-androgen therapies. Inhibiting signalling of this chemokine attenuates key transcriptional approaches induced in the hypoxic microenvironment of bicalutamide-treated tumors. Moreover, inhibition of CXCL8 signalling may prevent the re-vascularization previously observed in hypoxic LNCaP tumors. Citation Format: Melanie McKechnie, Pamela J. Maxwell, David J. J. Waugh. Pro-angiogenic CXCL8 signalling underpins microenvironment-induced relapse to anti-androgen therapy of prostate cancer. [abstrac...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: McKechnie, M., Maxwell, P. J., Waugh, D. J. J. Tags: Molecular and Cellular Biology Source Type: research