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Total 70 results found since Jan 2013.

Matrix Metalloproteinase and Tissue Inhibitor of Metalloproteinases Is Associated with Multiple Myeloma Progression, Prognosis and Extramedullary Plasmacytoma
Conclusions: Our results suggest that TIMP1, 2 and MMP14, 24 were associated with EMP formation. Among those factors, TIMP1 is the one which may play a key role for MM progression and chemo-resistance based on the results revealing its upregulation by antineoplastic agents and association with poor prognosis of MM patients. Our results is consistent with a previous report describing that high serum TIMP1 concentration was associated with poor prognosis of MM. TIMP is recently shown to play another role besides negative regulator for MMP, so further study to elucidate its specific role for chemo-resistance contributes to de...
Source: Blood - November 21, 2018 Category: Hematology Authors: Ishihara, R., Murakami, Y., Homma, K., Watanabe, S., Oda, T., Sunaga, M., Yamane, E., Kobayashi, N., Osaki, Y., Ishizaki, T., Shimizu, H., Iriuchishima, H., Koiso, H., Tsukamoto, N., Yokohama, A., Nanami, G., Ino, R., Saitoh, T., Murakami, H., Handa, H. Tags: 651. Myeloma: Biology and Pathophysiology, excluding Therapy: Poster II Source Type: research

Blockade of Ubiquitin Receptor PSMD4/Rpn10 Triggers Cytotoxicity and Overcomes Bortezomib-Resistance in Multiple Myeloma
ConclusionOur preclinical data validates targeting 19S proteasome ubiquitin receptor Rpn10 upstream of the proteasome in the ubiquitin proteasomal cascade, and provides the framework for clinical evaluation of Rpn10 inhibitors to overcome PI resistance and improve patient outcome in MM.DisclosuresAnderson: C4 Therapeutics: Equity Ownership, Other: Scientific founder; Celgene: Consultancy; Bristol Myers Squibb: Consultancy; Gilead: Membership on an entity's Board of Directors or advisory committees; Millennium Takeda: Consultancy; OncoPep: Equity Ownership, Other: Scientific founder.
Source: Blood - November 21, 2018 Category: Hematology Authors: Song, Y., Ray, A., Chauhan, D., Anderson, K. Tags: 652. Myeloma: Pathophysiology and Pre-Clinical Studies, excluding Therapy: Poster II Source Type: research

Targeting Insulin-like Growth Factor in Multiple Myeloma: Novel Strategies in the Treatment of Proteasome Inhibitor Resistant Cells
Conclusion: The IGF1 signaling pathway is involved in proteasome inhibitor sensitivity and plays a key role in chemokine production of the HUVEC. Our data also suggested that administration of IGF1R inhibitor, linsitinib, might be a powerful strategy against myeloma cells and enhance cytotoxic effects of proteasome inhibitors in those residual MM cells.DisclosuresOhyashiki: MSD,: Honoraria, Research Funding; Bristol Meyer Squibb KK,: Honoraria, Research Funding; Kyowakko Kirin KK,: Research Funding; Celegene KK,: Honoraria, Research Funding; Pfizer KK,: Honoraria, Research Funding; Novartis KK,: Honoraria, Research Funding...
Source: Blood - November 21, 2018 Category: Hematology Authors: Tanaka, Y., Okabe, S., Tauchi, T., Ito, Y., Ohyashiki, K. Tags: 605. Molecular Pharmacology, Drug Resistance-Lymphoid and Other Diseases Source Type: research

Overexpressed Melk Promotes the Stability of EZH2 through Phosphorylation in Natural Killer/T Cell Lymphoma (NKTL)
In this study, we examined EZH2 protein turnover mechanisms in the NKTL context.The serine/threonine kinase Melk is one of the overexpressed genes in NKTL patient samples and cell lines, and the interaction between Melk and EZH2 was established by co-immunoprecipitation. Inhibition of Melk using inhibitor or siRNA both resulted in a decrease of EZH2 protein levels in NKTL cells, whereas there was no change in the mRNA level of EZH2, suggesting that Melk regulated EZH2 at the protein level. Next, we observed a change of EZH2 ubiquitination upon manipulation of Melk expression.Next, in order to confirm that Melk truly affect...
Source: Blood - November 21, 2018 Category: Hematology Authors: Li, B., Kappei, D., Yan, J., Eichhorn, P., Ng, S. B., Chng, W. J. Tags: 622. Lymphoma Biology-Non-Genetic Studies: Poster II Source Type: research

The association of neuronal stress with activating transcription factor 3 in dorsal root ganglion of in vivo and in vitro models of bortezomib-induced neuropathy.
This study exhibited important mechanistic insight into how BTZ induces neurotoxicity through the activation of ATF3 resulting in intracellular oxidative stress, mitochondrial dysfunction, cell apoptosis, and ER stress and provided a novel potential therapeutic target by blocking ATF3 signaling. PMID: 30289077 [PubMed - as supplied by publisher]
Source: Current Cancer Drug Targets - October 3, 2018 Category: Cancer & Oncology Authors: Yin Y, Qi X, Qiao Y, Liu H, Yan Z, Li H, Liu Z Tags: Curr Cancer Drug Targets Source Type: research

Blockade of deubiquitinase USP7 overcomes bortezomib resistance by suppressing NF- κB signaling pathway in multiple myeloma.
Blockade of deubiquitinase USP7 overcomes bortezomib resistance by suppressing NF-κB signaling pathway in multiple myeloma. J Leukoc Biol. 2018 Jul 19;: Authors: Yao Y, Zhang Y, Shi M, Sun Y, Chen C, Niu M, Zhang Q, Zeng L, Yao R, Li H, Yang J, Li Z, Xu K Abstract The treatment of multiple myeloma (MM) with bortezomib (BTZ) is promising; however, the emergence of resistance is challenging in the clinical treatment. Thus, a novel targeted treatment or exploring the mechanism underlying BTZ resistance is an urgent requisite. The current data showed that high expression of USP7 in myeloma was a predicto...
Source: Journal of Leukocyte Biology - July 19, 2018 Category: Hematology Authors: Yao Y, Zhang Y, Shi M, Sun Y, Chen C, Niu M, Zhang Q, Zeng L, Yao R, Li H, Yang J, Li Z, Xu K Tags: J Leukoc Biol Source Type: research

Inhibition of mTOR complex 2 restrains tumor angiogenesis in multiple myeloma.
Authors: Lamanuzzi A, Saltarella I, Desantis V, Frassanito MA, Leone P, Racanelli V, Nico B, Ribatti D, Ditonno P, Prete M, Solimando AG, Dammacco F, Vacca A, Ria R Abstract The mammalian Target of Rapamycin (mTOR) is an intracellular serine/threonine kinase that mediates intracellular metabolism, cell survival and actin rearrangement. mTOR is made of two independent complexes, mTORC1 and mTORC2, activated by the scaffold proteins RAPTOR and RICTOR, respectively. The activation of mTORC1 triggers protein synthesis and autophagy inhibition, while mTORC2 activation promotes progression, survival, actin reorganization...
Source: Oncotarget - May 15, 2018 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

Upregulation of NLRP3 via STAT3-dependent histone acetylation contributes to painful neuropathy induced by bortezomib.
Abstract Painful neuropathy, as a severe side effect of chemotherapeutic bortezomib, is the most common reason for treatment discontinuation. However, the mechanism by which administration of bortezomib leads to painful neuropathy remains unclear. In the present study, we found that application of bortezomib significantly increased the expression of NOD-like receptor family pyrin domain containing 3 (NLRP3) and phosphorylated signal transducer and activator of transcription-3 (STAT3) in dorsal root ganglion (DRG). Intrathecal injection of NLRP3 siRNA significantly prevented the mechanical allodynia induced by bort...
Source: Experimental Neurology - January 12, 2018 Category: Neurology Authors: Liu CC, Huang ZX, Li X, Shen KF, Liu M, Ouyang HD, Zhang SB, Ruan YT, Zhang XL, Wu SL, Xin WJ, Ma C Tags: Exp Neurol Source Type: research

The full-length interleukin-33 (FLIL33)-importin-5 interaction does not regulate nuclear localization of FLIL33 but controls its intracellular degradation Protein Synthesis and Degradation
Human mature IL-33 is a member of the IL-1 family and a potent regulator of immunity through its pro-T helper cell 2 activity. Its precursor form, full-length interleukin-33 (FLIL33), is an intranuclear protein in many cell types, including fibroblasts, and its intracellular levels can change in response to stimuli. However, the mechanisms controlling the nuclear localization of FLIL33 or its stability in cells are not understood. Here, we identified importin-5 (IPO5), a member of the importin family of nuclear transport proteins, as an intracellular binding partner of FLIL33. By overexpressing various FLIL33 protein segme...
Source: Journal of Biological Chemistry - December 29, 2017 Category: Chemistry Authors: Andrew Clerman, Zahid Noor, Rita Fishelevich, Virginia Lockatell, Brian S. Hampton, Nirav G. Shah, Mariah V. Salcedo, Nevins W. Todd, Sergei P. Atamas, Irina G. Luzina Tags: Cell Biology Source Type: research

The MIP ‐1α autocrine loop contributes to decreased sensitivity to anticancer drugs
This article is protected by copyright. All rights reserved
Source: Journal of Cellular Physiology - October 23, 2017 Category: Cytology Authors: Masanobu Tsubaki, Tomoya Takeda, Yoshika Tomonari, Kenji Mashimo, Yu ‐ichi Koumoto, Sachi Hoshida, Tatsuki Itoh, Motohiro Imano, Takao Satou, Katsuhiko Sakaguchi, Shozo Nishida Tags: ORIGINAL RESEARCH ARTICLE Source Type: research

Pre-Clinical Evaluation of Combined Proteasome and Spliceosome Inhibition in Triple Negative Breast Cancer (TNBC)
TNBC is an aggressive subtype that comprises 15% of breast cancer diagnoses. Non-targeted cytotoxic therapies are prone to resistance, metastasis, and recurrence. siRNA screening has revealed the selective necessity of proteasome and spliceosome function for the survival of TNBC cells arrested in a progenitor-like state. We explore inhibiting these pathways simultaneously, with the proteasome inhibitor Bortezomib and the splicing inhibitor E7107.
Source: Journal of the American College of Surgeons - October 1, 2017 Category: Surgery Authors: Praveen Sridhar, Stefanie Chan, Fabio Petrocca, Ying-Jie Lock Tags: Scientific poster presentation Source Type: research

Preclinical activity of DCZ3301, a novel aryl-guanidino compound in the therapy of multiple myeloma
We synthesized a novel aryl-guanidino compound, DCZ3301, and found that it has potent cytotoxicity against multiple human cancer cell lines. The anticancer activity was most potent against multiple myeloma (MM). DCZ3301 induced cytotoxicity in MM cell lines, as well as patient myeloma cells, in part by decreasing mitochondrial membrane potential to induce apoptosis. In contrast, DCZ3301 had no cytotoxic effect on normal cells. DCZ3301 also inhibited cell cycling and caused a G2/M accumulation that corresponded with downregulation of Cdc25C, CDK1, and Cyclin B1. DCZ3301 retained its activity against MM cells in the presence...
Source: Theranostics - September 12, 2017 Category: Molecular Biology Authors: Minjie Gao, Bo Li, Xi Sun, Yunfei Zhou, Yingcong Wang, Van S. Tompkins, Zhijian Xu, Nekitsing Indima, Houcai Wang, Wenqin Xiao, Lu Gao, Gege Chen, Huiqun Wu, Xiaosong Wu, Yuanyuan Kong, Bingqian Xie, Yiwen Zhang, Gaomei Chang, Liangning Hu, Guang Yang, Bo Tags: Research Paper Source Type: research

Blockade of Deubiquitylating Enzyme USP1 Inhibits DNA Repair and Triggers Apoptosis in Multiple Myeloma Cells.
CONCLUSIONS: Our preclinical studies provide the framework for clinical evaluation of USP1 inhibitors, alone or in combination, as a potential novel MM therapy. PMID: 28270494 [PubMed - as supplied by publisher]
Source: Clinical Cancer Research - March 6, 2017 Category: Cancer & Oncology Authors: Das DS, Das A, Ray A, Song Y, Samur MK, Munshi NC, Chauhan D, Anderson KC Tags: Clin Cancer Res Source Type: research

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