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Molecular Cancer Therapeutics

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https://www.readbyqxmd.com/read/28069878/malat1-is-associated-with-poor-response-to-oxaliplatin-based-chemotherapy-in-colorectal-cancer-patients-and-promotes-chemoresistance-through-ezh2
#1
Peilong Li, Xin Zhang, Haiyan Wang, Lili Wang, Tong Liu, Lutao Du, Yongmei Yang, Chuanxin Wang
A major reason for oxaliplatin chemoresistance in colorectal cancer (CRC) is the acquisition of epithelial-mesenchymal transition (EMT) in cancer cells. The long non-coding RNA, MALAT1, is a highly conserved nuclear ncRNA and a key regulator of metastasis development in several cancers. However, its role in oxaliplatin-induced metastasis and chemo-resistance is not well known. In this study, we aim to investigate the prognostic and therapeutic role of MALAT1 in CRC patients receiving oxaliplatin-based therapy, and further explore the potential transcriptional regulation through interaction with EZH2 based on the established HT29 oxaliplatin-resistant cells...
January 9, 2017: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/28069877/bone-seeking-matrix-metalloproteinase-2-inhibitors-prevent-bone-metastatic-breast-cancer-growth
#2
Marilena Tauro, Gemma Shay, Samer S Sansil, Antonio Laghezza, Paolo Tortorella, Anthony M Neuger, Hatem Soliman, Conor C Lynch
Bone metastasis is common during breast cancer progression. Matrix metalloproteinase-2 (MMP-2) is significantly associated with aggressive breast cancer and poorer overall survival. In bone, tumor or host derived MMP-2 contributes to breast cancer growth and does so by processing substrates including type I collagen and transforming growth factorβ (TGFβ) latency proteins. These data provide strong rationale for the application of MMP-2 inhibitors to treat the disease. However, in vivo, MMP-2 is systemically expressed...
January 9, 2017: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/28069876/targeting-plk1-to-enhance-efficacy-of-olaparib-in-castration-resistant-prostate-cancer
#3
Xiaoqi Liu, Jie Li, Ruixin Wang, Yifan Kong, Meaghan M Broman, Colin Carlock, Long Chen, Zhiguo Li, Elia Farah, Timothy L Ratliff
Olaparib is a FDA-approved PARP inhibitor (PARPi) that has shown promise as a synthetic lethal treatment approach for BRCA-mutant castration-resistant prostate cancer (CRPC) in clinical use. However, emerging data has also shown that even BRCA-mutant cells may be resistant to PARPi. The mechanistic basis for these drug resistances is poorly understood. Polo-like kinase 1 (Plk1), a critical regulator of many cell cycle events, is significantly elevated upon castration of mice carrying xenograft prostate tumors...
January 9, 2017: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/28069875/15%C3%A2-methoxypuupehenol-induces-antitumor-effects-in-vitro-and-in-vivo-against-human-glioblastoma-and-breast-cancer-models
#4
Tyvette Hilliard, Gabriella Miklossy, Christopher Chock, Peibin Yue, Philip Williams, James Turkson
Studies with 15∝-methoxypuupehenol (15∝-MP), obtained from the extracts of Hyrtios sp., identified putative targets that are associated with its antitumor effects against human glioblastoma (GBM) and breast cancer. In the human GBM (U251MG) or breast cancer (MDA-MB-231) cells, treatment with 15∝-MP repressed pY705Stat3 (Signal Transducer and Activator of Transcription 3), pErk1/2 (extracellular signal-regulated kinase), pS147CyclinB1, pY507Alk (Anaplastic lymphoma kinase), and pY478ezrin levels, and induced pS10merlin, without inhibiting pJAK2 (Janus kinase) or pAkt induction...
January 9, 2017: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/28069874/dimethyl-fumarate-controls-the-nrf2-dj-1-axis-in-cancer-cells-therapeutic-applications
#5
Nathaniel Edward Bennett Saidu, Gaëlle Noé, Olivier Cerles, Luc Cabel, Niloufar Kavian-Tessler, Sandrine Chouzenoux, Mathilde Bahuaud, Christiane Chéreau, Carole Nicco, Karen Leroy, Bruno Borghese, Francois Goldwasser, Frédéric Batteux, Jerome Alexandre
The transcription factor NRF2 (NFE2L2), regulates important antioxidant and cytoprotective genes. It enhances cancer cell proliferation and promotes chemoresistance in several cancers. Dimethyl fumarate (DMF) is known to promote NRF2 activity in non-cancer models. We combined in vitro and in vivo methods to examine the effect of DMF on cancer cell death and the activation of the NRF2 antioxidant pathway. We demonstrated that at lower concentrations (< 25 μM), DMF has a cytoprotective role through activation of the NRF2 antioxidant pathway...
January 9, 2017: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/28003325/nanoparticle-based-celecoxib-and-plumbagin-for-the-synergistic-treatment-of-melanoma
#6
Raghavendra Gowda, Gregory Kardos, Arati Sharma, Sanjay Singh, Gavin P Robertson
Using multiple drugs to kill cancer cells can decrease drug resistance development. However, this approach is frequently limited by the bioavailability and toxicity of the combined agents and delivery at ratios to specific locations that synergistically kill the cancer cells. Loading the individual agents into a nanoparticle that releases the drugs at synergizing ratios at a single location is one approach to resolve this concern. Celecoxib and Plumbagin are two drugs that were identified from a screen to synergistically kill melanoma cells compared to normal cells...
December 21, 2016: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/27980109/folate-hapten-mediated-immunotherapy-synergizes-with-vascular-endothelial-growth-factor-receptor-inhibitors-in-treating-murine-models-of-cancer
#7
N Achini Bandara, Cody D Bates, Yingjuan Lu, Emily K Hoylman, Philip S Low
The over-expression of folate receptors (FR) on many human cancers has led to the development of folate-linked drugs for the imaging and therapy of FR-expressing cancers. In a recent phase 1 clinical trial of late stage renal cell carcinoma patients, folate was exploited to deliver an immunogenic hapten, fluorescein, to FR+ tumor cells in an effort to render the cancer cells more immunogenic. Although >50% of the patients showed prolonged stable disease, all patients eventually progressed, suggesting that the folate-hapten immunotherapy was insufficient by itself to treat the cancer...
December 15, 2016: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/27980108/dual-hdac-and-pi3k-inhibitor-cudc-907-downregulates-myc-and-suppresses-growth-of-myc-dependent-cancers
#8
Kaiming Sun, Ruzanna Atoyan, Mylissa A Borek, Steven DellaRocca, Maria Elena S Samson, Anna W Ma, Guang-Xin Xu, Troy Patterson, David P Tuck, Jaye L Viner, Ali Fattaey, Jing Wang
Upregulation of MYC is a common driver event in human cancers, and some tumors depend on MYC to maintain transcriptional programs that promote cell growth and proliferation. Preclinical studies have suggested that individually targeting upstream regulators of MYC, such as histone deacetylases (HDACs) and phosphoinositide 3-kinases (PI3Ks), can reduce MYC protein levels and suppress the growth of MYC-driven cancers. Synergy between HDAC and PI3K inhibition in inducing cancer cell death has also been reported, but the involvement of MYC regulation is unclear...
December 15, 2016: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/27980107/niclosamide-inhibits-oxaliplatin-neurotoxicity-while-improving-colorectal-cancer-therapeutic-response
#9
Olivier Cerles, Evelyne Benoit, Christiane Chéreau, Sandrine Chouzenoux, Florence Morin, Marie-Anne Guillaumot, Romain Coriat, Niloufar Kavian, Thomas Loussier, Pietro Santulli, Louis Marcellin, Nathaniel E B Saidu, Bernard Weill, Frederic Batteux, Carole Nicco
Neuropathic pain is a limiting-factor of platinum-based chemotherapies. We sought to investigate the neuroprotective potential of niclosamide in peripheral neuropathies induced by oxaliplatin. Normal neuron-like and cancer cells were treated in vitro with oxaliplatin associated or not with an inhibitor of STAT3 and NF-кB, niclosamide. Cell production of reactive oxygen species and viability were measured by 2',7'-dichlorodihydrofluorescein diacetate and crystal violet. Peripheral neuropathies were induced in mice by oxaliplatin with or without niclosamide...
December 15, 2016: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/27980106/imatinib-spares-ckit-expressing-prostate-neuroendocrine-tumors-whereas-kills-seminal-vesicle-epithelial-stromal-tumors-targeting-pdgfr-%C3%AE
#10
Elena Jachetti, Alice Rigoni, Lucia Bongiovanni, Ivano Arioli, Laura Botti, Mariella Parenza, Valeria Cancila, Claudia Chiodoni, Fabrizio Festinese, Matteo Bellone, Regina Tardanico, Claudio Tripodo, Mario P Colombo
Prostate cancer is a leading cause of death by cancer in male worldwide. Indeed, advanced and metastatic disease characterized by androgen resistance and often associated with neuroendocrine (NE) differentiation remains incurable. Using the spontaneous prostate cancer TRAMP model, we have shown that mast cells (MCs) support in vivo the growth of prostate adenocarcinoma, whereas their genetic or pharmacologic targeting favours prostate NE cancer arousal. Aiming at simultaneously targeting prostate NE tumor cells and MCs, both expressing the cKit tyrosine kinase receptor, we have tested the therapeutic effect of Imatinib in TRAMP mice...
December 15, 2016: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/27980104/the-fa-brca-pathway-identified-as-the-major-predictor-of-cisplatin-response-in-head-and-neck-cancer-by-functional-genomics
#11
Sanne R Martens-de Kemp, Arjen Brink, Ida H van der Meulen, Renee X De Menezes, Dennis E Te Beest, C Rene Leemans, Victor W van Beusechem, Boudewijn J M Braakhuis, Ruud H Brakenhoff
Patients with advanced stage head and neck squamous cell carcinoma (HNSCC) are often treated with cisplatin-containing chemoradiation protocols. Although cisplatin is an effective radiation sensitizer, it causes severe toxicity and not all patients benefit from the combination treatment. HNSCCs expectantly not responding to cisplatin may better be treated with surgery and postoperative radiation or cetuximab and radiation, but biomarkers to personalize chemoradiotherapy, are not available. We performed an unbiased genome-wide functional genetic screen in vitro to identify genes that influence the response to cisplatin in HNSCC cells...
December 15, 2016: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/27980103/repositioning-fda-approved-drugs-in-combination-with-epigenetic-drugs-to-reprogram-colon-cancer-epigenome
#12
Noël J-M Raynal, Elodie M Da Costa, Justin T Lee, Vazganush Gharibyan, Saira Ahmed, Hanghang Zhang, Takahiro Sato, Gabriel G Malouf, Jean-Pierre J Issa
Epigenetic drugs, such as DNA methylation inhibitors (DNMTi) or histone deacetylase inhibitors (HDACi), are approved in monotherapy for cancer treatment. These drugs reprogram gene expression profiles, reactivate tumor suppressor genes (TSG) producing cancer cell differentiation and apoptosis. Epigenetic drugs have been shown to synergize with other epigenetic drugs or various anticancer drugs. To discover new molecular entities that enhance epigenetic therapy, we performed a high-throughput screening using FDA-approved libraries in combination with DNMTi or HDACi...
December 15, 2016: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/27980102/blocking-the-ccl2-ccr2-axis-using-ccl2-neutralizing-antibody-is-an-effective-therapy-for-hepatocellular-cancer-in-a-mouse-model
#13
Kun-Yu Teng, Jianfeng Han, Xiaoli Zhang, Shu-Hao Hsu, Shun He, Nissar Wani, Juan Barajas, Linda A Snyder, Wendy L Frankel, Michael A Caligiuri, Samson T Jacob, Jianhua Yu, Kalpana Ghoshal
Hepatocellular carcinoma (HCC), a deadly disease, commonly arises in the setting of chronic inflammation. C-C motif chemokine ligand2 (CCL2/MCP1), a chemokine that recruits CCR2-positive immune cells to promote inflammation, is highly upregulated in HCC patients. Here, we examined the therapeutic efficacy of CCL2-CCR2 axis inhibitors against hepatitis and HCC in the miR-122 knockout (aka KO) mouse model. This mouse model displays upregulation of hepatic CCL2 expression, which correlates with hepatitis that progress to HCC with age...
December 15, 2016: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/27980101/evaluation-of-nonpeptidic-ligand-conjugates-for-treatment-of-hypoxic-and-carbonic-anhydrase-ix-expressing-cancers
#14
Peng-Cheng Lv, Jyoti Roy, Karson S Putt, Philip S Low
The majority of tumors contain regions of hypoxia which cause marked phenotypic changes to resident cells. This altered gene expression often leads to increased resistance to anti-cancer treatments. Therefore, elimination of these resistant hypoxic cells is crucial to prevent disease recurrence. Herein, we describe the selective delivery of imaging and chemotherapeutic agents to cells expressing carbonic anhydrase IX (CA IX), a highly upregulated hypoxia receptor. These agents were conjugated to a potent divalent CA IX ligand through a hydrophilic PEG linker...
December 15, 2016: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/27956521/dual-targeting-nanoparticles-for-in-vivo-delivery-of-suicide-genes-to-chemotherapy-resistant-ovarian-cancer-cells
#15
Emiliano Cocco, Yang Deng, Erik M Shapiro, Ileana Bortolomai, Salvatore Lopez, Ken Lin, Stefania Bellone, Jiajia Cui, Gulden Menderes, Jonathan D Black, Carlton L Schwab, Elena Bonazzoli, Fan Yang, Federica Predolini, Luca Zammataro, Gary Altwerger, Christopher de Haydu, Mitchell Clark, Julio Alvarenga, Elena Ratner, Masoud Azodi, Dan-Arin Silasi, Peter E Schwartz, Babak Litkouhi, W Mark Saltzman, Alessandro D Santin
Ovarian cancer is the most lethal gynecologic cancer. Claudin-3 and-4, the receptors for Clostridium Perfringens Enterotoxin (CPE), are overexpressed in over 70% of these tumors. Here we synthesized and characterized poly(lactic-co-glycolic-acid) (PLGA) nanoparticles (NP) modified with the carboxi-terminal binding domain of CPE (c-CPE-NP) for the delivery of suicide gene therapy to chemotherapy-resistant ovarian cancer cells. As a therapeutic payload we generated a plasmid encoding for the Diphteria Toxin subunit-A (DT-A) under the transcriptional control of the p16 promoter, a gene highly differentially expressed in ovarian cancer cells...
December 12, 2016: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/27956520/dual-inhibition-of-key-proliferation-signaling-pathways-in-triple-negative-breast-cancer-cells-by-a-novel-derivative-of-taiwanin-a
#16
Yueh-Hsiung Kuo, En-Pei Isabel Chiang, Che-Yi Chao, Raymond L Rodriguez, Pei-Yu Chou, Shu-Yao Tsai, Man-Hui Pai, Feng-Yao Tang
The treatment of breast cancer cells obtained by blocking the aberrant activation of the proliferation signaling pathways PI-3K/Akt/mTOR and MEK/ERK has received considerable attention in recent years. Previous studies showed that Taiwanin A inhibited the proliferation of several types of cancer cells. In this study, we report that 3,4-bis-3,4,5- trimethoxybenzylidene-dihydrofuran (BTMB), a novel derivative of Taiwanin A, significantly inhibited the proliferation of triple negative breast cancer (TNBC) cells both in vitro and in vivo...
December 12, 2016: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/27913578/characterization-of-egfr-t790m-l792f-and-c797s-mutations-as-mechanisms-of-acquired-resistance-to-afatinib-in-lung-cancer
#17
Yoshihisa Kobayashi, Koichi Azuma, Hiroki Nagai, Young Hak Kim, Yosuke Togashi, Yuichi Sesumi, Masato Chiba, Masaki Shimoji, Katsuaki Sato, Kenji Tomizawa, Toshiki Takemoto, Kazuto Nishio, Tetsuya Mitsudomi
Lung cancers harboring common EGFR mutations respond to EGFR tyrosine kinase inhibitors (TKIs). We previously reported that tumors with exon 18 mutations are particularly sensitive to irreversible second-generation (2G) afatinib compared with 1G-TKIs. However, data on the mechanisms of acquired resistance to afatinib are limited. We established afatinib-resistant cells by transfecting Ba/F3 cells with common or exon 18 (G719A and Del18) mutations and subjecting them to chronic exposure to increasing concentrations of afatinib...
December 2, 2016: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/27903753/a-novel-lsd1-inhibitor-t-3775440-disrupts-gfi1b-containing-complex-leading-to-transdifferentiation-and-impaired-growth-of-aml-cells
#18
Yoshinori Ishikawa, Kanae Gamo, Masato Yabuki, Shinji Takagi, Kosei Toyoshima, Kazuhide Nakayama, Akiko Nakayama, Megumi Morimoto, Hitoshi Miyashita, Ryo Dairiki, Yukiko Hikichi, Naoki Tomita, Daisuke Tomita, Shinichi Imamura, Misa Iwatani, Yusuke Kamada, Satoru Matsumoto, Ryujiro Hara, Toshiyuki Nomura, Ken Tsuchida, Kazuhide Nakamura
Dysregulation of the histone demethylase LSD1, also known as KDM1A, has been implicated in the development of various cancers, including leukemia. Here we describe the anti-leukemic activity and mechanism of action of T-3775440, a novel irreversible LSD1 inhibitor. Cell growth analysis of leukemia cell lines revealed that acute erythroleukemia (AEL) and acute megakaryoblastic leukemia cells (AMKL) were highly sensitive to this compound. T-3775440 treatment enforced transdifferentiation of erythroid/megakaryocytic lineages into granulomonocytic-like lineage cells...
November 30, 2016: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/27903752/hexim1-as-a-robust-pharmacodynamic-marker-for-monitoring-target-engagement-of-bet-family-bromodomain-inhibitors-in-tumors-and-surrogate-tissues
#19
Xiaoyu Lin, Xiaoli Huang, Tamar Uziel, Paul Hessler, Daniel H Albert, Lisa A Roberts-Rapp, Keith F McDaniel, Warren M Kati, Yu Shen
An increasing number of BET family protein inhibitors have recently entered clinical trials. It has been reported that attempts of monitoring target engagement of the BET bromodomain inhibitor OTX015 using literature-described putative pharmacodynamic (PD) markers such as c-Myc, BRD2, etc. failed to detect PD marker responses in AML patients treated at active dose and those with clinical responses. Here we report the identification and characterization of HEXIM1 and other genes as robust PD markers for BET inhibitors...
November 30, 2016: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/27903751/microdose-induced-drug-dna-adducts-as-biomarkers-of-chemotherapy-resistance-in-humans-and-mice
#20
Maike Zimmermann, Si-Si Wang, Hongyong Zhang, Tzu-Yin Lin, Michael Malfatti, Kurt Haack, Ted Ognibene, Hongyuan Yang, Susan Airhart, Kenneth W Turteltaub, George D Cimino, Clifford G Tepper, Alexandra Drakaki, Karim Chamie, Ralph de Vere White, Chong-Xian Pan, Paul T Henderson
We report progress on predicting tumor response to platinum-based chemotherapy with a novel mass spectrometry approach. Fourteen bladder cancer patients were administered one diagnostic microdose each of [14C]carboplatin (1% of the therapeutic dose). Carboplatin-DNA adducts were quantified by accelerator mass spectrometry (AMS) in blood and tumor samples collected within 24 hours, and compared to subsequent chemotherapy response. Patients with the highest adduct levels were responders, but not all responders had high adduct levels...
November 30, 2016: Molecular Cancer Therapeutics
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