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Pten breast

Sarah A Altınoğlu, Ming Wang, Kathleen Q Li, Yuyang Li, Qiaobing Xu
The phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is a tumor suppressor, mutated or inactive in a large percentage of human cancers. Restoring PTEN activity in cancer cells through gene therapy has shown to inhibit cell growth and induce apoptosis, particularly in cells with a PTEN deficiency. Gene therapy, however, comes with some inherent risks such as triggering an immune response and permanent off target effects. Nanoparticle assisted protein delivery could mitigate these liabilities while maintaining therapeutic integrity...
October 17, 2016: Biomaterials Science
Hongyu Shen, Dandan Wang, Liangpeng Li, Sujin Yang, Xiu Chen, Siying Zhou, Shanliang Zhong, Jianhua Zhao, Jinhai Tang
BACKGROUND AND PURPOSE: Acquisition of resistance to adriamycin (ADR) is one of the most important clinical obstacles in the treatment of breast cancer, but the molecular mechanisms underlying sensitivity to ADR remain elusive. In our previous study, through miRNA microarray and experiments, we have emphasized that miR-222 could promote the ADR-resistance in breast cancer cells. The aim of this study was to explore the possible mechanism by which miR-222 affects sensitivity to ADR. METHODS: Through pathway enrichment analyses for miR-222, we found that PTEN/Akt/FOXO1 signaling pathway may be of importance...
October 13, 2016: Gene
Jiawei Guan, Qian Zhao, Weifeng Mao
PTEN is a tumor suppressor gene characterized as a phosphatase that antagonizes the phosphatidylinositol 3-kinase signaling pathway in the cytoplasm. Nuclear PTEN plays roles in chromosomal stability, in which the double-strand breaks (DSB) repair mediated by homologous recombination (HR) and non-homologous end joining (NHEJ) is critical. Herein, the role of nuclear PTEN in DSB repair and the underlying molecular mechanism was investigated in this study. Using human breast cancer BT549 and MDA-MB-231 cell lines, we reveal a specific feature of PTEN that controls poly(ADP-ribosyl)ation of Ku70 and interferes with binding of Ku70 at DSB...
October 11, 2016: Biochimica et Biophysica Acta
Kaye Showler, Mayumi Nishimura, Kazuhiro Daino, Tatsuhiko Imaoka, Yukiko Nishimura, Takamitsu Morioka, Benjamin J Blyth, Toshiaki Kokubo, Masaru Takabatake, Maki Fukuda, Hitomi Moriyama, Shizuko Kakinuma, Masahiro Fukushi, Yoshiya Shimada
The PI3K/AKT pathway is one of the most important signaling networks in human breast cancer, and since it was potentially implicated in our preliminary investigations of radiation-induced rat mammary carcinomas, our aim here was to verify its role. We included mammary carcinomas induced by the chemical carcinogen 1-methyl-1-nitrosourea to determine whether any changes were radiation-specific. Most carcinomas from both groups showed activation of the PI3K/AKT pathway, but phosphorylation of AKT1 was often heterogeneous and only present in a minority of carcinoma cells...
October 13, 2016: Journal of Radiation Research
Rossella Graffeo, Luca Livraghi, Olivia Pagani, Aron Goldhirsch, Ann H Partridge, Judy E Garber
PURPOSE: Genetic evaluation is increasingly becoming an integral part of the management of women with newly diagnosed breast and ovarian cancer (OC), and of individuals at high risk for these diseases. Genetic counseling and testing have been incorporated into oncological care to help and complete management and treatment strategies. Risk assessment and early detection strategies in individuals with BRCA1/2 mutations and with Lynch syndrome have been quite extensively studied, whereas much less is known about the management of mutation carriers with less common high-penetrance cancer susceptibility genes (PTEN, TP53, STK11, CDH1), and particularly those who carry mutations in moderate-penetrance genes (e...
October 12, 2016: Breast Cancer Research and Treatment
Surya Narayan Rath, Debasrita Das, V Badireenath Konkimalla, Sukanta Kumar Pradhan
Solid tumor is generally observed in tissues of epithelial or endothelial cells of lung, breast, prostate, pancreases, colorectal, stomach, and bladder, where several genes transcription is regulated by the microRNAs (miRNAs). Argonaute (AGO) protein is a family of protein which assists in miRNAs to bind with mRNAs of the target genes. Hence, study of the binding mechanism between AGO protein and miRNAs, and also with miRNAs-mRNAs duplex is crucial for understanding the RNA silencing mechanism. In the current work, 64 genes and 23 miRNAs have been selected from literatures, whose deregulation is well established in seven types of solid cancer like lung, breast, prostate, pancreases, colorectal, stomach, and bladder cancer...
September 2016: Genomics & Informatics
Felipe C Geyer, Samuel H Berman, Caterina Marchiò, Kathleen A Burke, Elena Guerini-Rocco, Salvatore Piscuoglio, Charlotte Ky Ng, Fresia Pareja, Hannah Y Wen, Zoltan Hodi, Stuart J Schnitt, Emad A Rakha, Ian O Ellis, Larry Norton, Britta Weigelt, Jorge S Reis-Filho
Acinic cell carcinoma is an indolent form of invasive breast cancer, whereas microglandular adenosis has been shown to be a neoplastic proliferation. Both entities display a triple-negative phenotype, and may give rise to and display somatic genomic alterations typical of high-grade triple-negative breast cancers. Here we report on a comparison of previously published data on eight carcinoma-associated microglandular adenosis and eight acinic cell carcinomas subjected to targeted massively parallel sequencing targeting all exons of 236 genes recurrently mutated in breast cancer and/or DNA repair-related...
October 7, 2016: Modern Pathology: An Official Journal of the United States and Canadian Academy of Pathology, Inc
Dan-Dan Wang, Su-Jin Yang, Xiu Chen, Hong-Yu Shen, Long-Ji Luo, Xiao-Hui Zhang, Shan-Liang Zhong, Jian-Hua Zhao, Jin-Hai Tang
The high resistant rate of Adriamycin (Adr) is associated with a poor prognosis of breast cancer in women worldwide. Since miR-222 might contribute to chemoresistance in many cancer types, in this study, we aimed to investigate its efficacy in breast cancer through PTEN/Akt/p27 (kip1) pathway. Firstly, in vivo, we verified that miR-222 was upregulated in chemoresistant tissues after surgery compared with the paired preneoadjuvant samples of 21 breast cancer patients. Then, human breast cancer Adr-resistant cell line (MCF-7/Adr) was constructed to validate the pathway from the parental sensitive cell line (MCF-7/S)...
October 4, 2016: Tumour Biology: the Journal of the International Society for Oncodevelopmental Biology and Medicine
Qiao Tang, Yajun Liu, Tao Li, Xiang Yang, Guirong Zheng, Hongning Chen, Lee Jia, Jingwei Shao
Metastasis currently remains the predominant cause of breast carcinoma treatment failure. The effective targeting of metastasis-related-pathways in cancer holds promise for a new generation of therapeutics. In this study, we developed an novel Asp-UA conjugate, which was composed of classical "old drug" aspirin and low toxicity natural product ursolic acid for targeting breast cancer metastasis. Our results showed that Asp-UA could attenuate the adhesion, migration and invasion of breast cancer MCF-7 and MDA-MB-231 cells in a more safe and effective manner in vitro...
September 24, 2016: Oncotarget
Shanshan Luo, Jiansi Chen, Xianwei Mo
OBJECTIVE: Phosphatase and tensin homolog (PTEN) deleted on chromosome 10, as a tumor suppressor gene, is crucial for the development of both familial and sporadic breast cancer (BC). The aim of this study was to perform a meta-analysis to evaluate the clinicopathological significance of PTEN promoter hypermethylation in BC. METHODS: A comprehensive literature search was made in PubMed, Embase, Google Scholar, Chinese database (China National Knowledge Infrastructure [CNKI]), and Web of Science...
2016: OncoTargets and Therapy
A Patnaik, L J Appleman, A W Tolcher, K P Papadopoulos, M Beeram, D W Rasco, G J Weiss, J C Sachdev, M Chadha, M Fulk, S Ejadi, J M Mountz, M T Lotze, F G S Toledo, E Chu, M Jeffers, C Peña, C Xia, S Reif, I Genvresse, R K Ramanathan
BACKGROUND: To evaluate the safety, tolerability, pharmacokinetics, and maximum tolerated dose (MTD) of copanlisib, a phosphatidylinositol 3-kinase inhibitor, in patients with advanced solid tumors or non-Hodgkin's lymphoma (NHL). PATIENTS AND METHODS: Phase I dose-escalation study including patients with advanced solid tumors or NHL, and a cohort of patients with type 2 diabetes mellitus. Patients received three weekly intravenous infusions of copanlisib per 28-day cycle over the dose range 0...
October 2016: Annals of Oncology: Official Journal of the European Society for Medical Oncology
Marcel Smid, F Germán Rodríguez-González, Anieta M Sieuwerts, Roberto Salgado, Wendy J C Prager-Van der Smissen, Michelle van der Vlugt-Daane, Anne van Galen, Serena Nik-Zainal, Johan Staaf, Arie B Brinkman, Marc J van de Vijver, Andrea L Richardson, Aquila Fatima, Kim Berentsen, Adam Butler, Sancha Martin, Helen R Davies, Reno Debets, Marion E Meijer-Van Gelder, Carolien H M van Deurzen, Gaëtan MacGrogan, Gert G G M Van den Eynden, Colin Purdie, Alastair M Thompson, Carlos Caldas, Paul N Span, Peter T Simpson, Sunil R Lakhani, Steven Van Laere, Christine Desmedt, Markus Ringnér, Stefania Tommasi, Jorunn Eyford, Annegien Broeks, Anne Vincent-Salomon, P Andrew Futreal, Stian Knappskog, Tari King, Gilles Thomas, Alain Viari, Anita Langerød, Anne-Lise Børresen-Dale, Ewan Birney, Hendrik G Stunnenberg, Mike Stratton, John A Foekens, John W M Martens
A recent comprehensive whole genome analysis of a large breast cancer cohort was used to link known and novel drivers and substitution signatures to the transcriptome of 266 cases. Here, we validate that subtype-specific aberrations show concordant expression changes for, for example, TP53, PIK3CA, PTEN, CCND1 and CDH1. We find that CCND3 expression levels do not correlate with amplification, while increased GATA3 expression in mutant GATA3 cancers suggests GATA3 is an oncogene. In luminal cases the total number of substitutions, irrespective of type, associates with cell cycle gene expression and adverse outcome, whereas the number of mutations of signatures 3 and 13 associates with immune-response specific gene expression, increased numbers of tumour-infiltrating lymphocytes and better outcome...
2016: Nature Communications
Sai-Qi Wang, Cong Wang, Li-Ming Chang, Kai-Rui Zhou, Jun-Wei Wang, Yu Ke, Dong-Xiao Yang, Hong-Ge Shi, Ran Wang, Xiao-Li Shi, Li-Ying Ma, Hong-Min Liu
Paclitaxel, a taxane, is a cytotoxic chemotherapeutic agent that targets microtubules. It has become a front-line therapy for a broad range of malignancies, including lung, breast, gastric, esophageal, and bladder carcinomas. Although paclitaxel can inhibit tumor development and improve survival, poor solubility, myelotoxicity, allergic reactions, and drug resistance have restricted its clinical application. Paclitaxel is frequently combined with other chemotherapeutics to enhance the antitumor effects and reduce side effects...
September 21, 2016: Oncotarget
Chen Zhang, Bingfei Xu, Pian Liu
Breast cancer is one of the leading causes of death for women worldwide. Among various subtypes of breast cancer, human epidermal growth factor receptor 2 (HER2)-positive and phosphatase and tensin homolog (PTEN) loss breast cancer is a cause of great concern in terms of its resistance to HER2-targeted therapies and its poor prognosis. Phosphatidylinositol 3-kinase (PI3K)/AKT hyperphosphorylation is considered one of key mechanisms leading to this resistance, thus combination therapy of PI3K inhibitors and HER2 antibodies is promising for overcoming this problem, and more specific regimens should be designed in this age of precision medicine...
September 17, 2016: Tumour Biology: the Journal of the International Society for Oncodevelopmental Biology and Medicine
Nnennaya Kanu, Maria Antonietta Cerone, Gerald Goh, Lykourgos-Panagiotis Zalmas, Jirina Bartkova, Michelle Dietzen, Nicholas McGranahan, Rebecca Rogers, Emily K Law, Irina Gromova, Maik Kschischo, Michael I Walton, Olivia W Rossanese, Jiri Bartek, Reuben S Harris, Subramanian Venkatesan, Charles Swanton
BACKGROUND: The APOBEC3 family of cytidine deaminases mutate the cancer genome in a range of cancer types. Although many studies have documented the downstream effects of APOBEC3 activity through next-generation sequencing, less is known about their upstream regulation. In this study, we sought to identify a molecular basis for APOBEC3 expression and activation. RESULTS: HER2 amplification and PTEN loss promote DNA replication stress and APOBEC3B activity in vitro and correlate with APOBEC3 mutagenesis in vivo...
2016: Genome Biology
Juan Miguel Cejalvo, J Alejandro Pérez-Fidalgo, Gloria Ribas, Octavio Burgués, Cristina Mongort, Elisa Alonso, Maider Ibarrola-Villava, Begoña Bermejo, María Teresa Martínez, Andrés Cervantes, Ana Lluch
BACKGROUND: There is increasing interest in the molecular profiling of tumour tissues in order to investigate alternative breast cancer (BC) therapies. However, the impact of genomic screening for druggable mutations with targeted gene panel sequencing (TGPS) in routine practice remains controversial. METHODS: This is a retrospective analysis of data from a genomic screening programme at our institution, in which we performed simplified TGPS for mutations in PIK3CA, AKT1, KRAS, NRAS, and BRAF in order to select patients for targeted therapy clinical trials...
November 2016: Breast Cancer Research and Treatment
Warapen Treekitkarnmongkol, Hiroshi Katayama, Kazuharu Kai, Kaori Sasai, Jennifer Carter Jones, Jing Wang, Li Shen, Aysegul A Sahin, Mihai Gagea, Naoto T Ueno, Chad J Creighton, Subrata Sen
Recent data from The Cancer Genome Atlas analysis have revealed that Aurora kinase A (AURKA) amplification and overexpression characterize a distinct subset of human tumors across multiple cancer types. Although elevated expression of AURKA has been shown to induce oncogenic phenotypes in cells in vitro, findings from transgenic mouse models of Aurora-A overexpression in mammary glands have been distinct depending on the models generated. In the present study, we report that prolonged overexpression of AURKA transgene in mammary epithelium driven by ovine β-lactoglobulin promoter, activated through multiple pregnancy and lactation cycles, results in the development of mammary adenocarcinomas with alterations in cancer-relevant genes and epithelial-to-mesenchymal transition...
September 13, 2016: Carcinogenesis
Yi-Min Lu, Feng Cheng, Li-Song Teng
The Phosphatase and tensin homolog (PTEN) protein is a negative regulator of the Akt pathway, leading to suppression of apoptois and increased cell survival. Its role as a tumor-suppressor gene has been adequately substantiated, and PTEN hypermethylation has been demonstrated in familial and sporadic cancers. However, the association and clinical significance between PTEN hypermethylation and breast cancer remains unclear. In this study, we systematically reviewed studies of PTEN hypermethylation and breast cancer and quantify the association between PTEN hypermethylation and breast cancer using meta-analysis methods...
2016: Scientific Reports
Willemina R R Geurts-Giele, Victorien M T van Verschuer, Carolien H M van Deurzen, Paul J van Diest, Rute M S M Pedrosa, J Margriet Collée, Linetta B Koppert, Caroline Seynaeve, Winand N M Dinjens
Female BRCA1/2 mutation carriers affected with breast and/or ovarian cancer may develop new tumor deposits over time. It is of utmost importance to know the clonal relationships between multiple tumor localizations, enabling differentiation between multiple primaries or metastatic disease with consequences for therapy and prognosis. We evaluated the value of targeted next generation sequencing in the diagnostic workup of BRCA1/2 mutation carriers with ≥2 tumor localizations and uncertain tumor origins. Forty-two female BRCA1/2 mutation carriers with ≥2 tumor localizations were selected...
September 9, 2016: Modern Pathology: An Official Journal of the United States and Canadian Academy of Pathology, Inc
Fei Ma, Wenjie Zhu, Yanfang Guan, Ling Yang, Xuefeng Xia, Shanshan Chen, Qiao Li, Xiuwen Guan, Zongbi Yi, Haili Qian, Xin Yi, Binghe Xu
BACKGROUND: Most studies utilizing circulating tumor DNA (ctDNA) to monitor disease interrogated only one or a few genes and failed to develop workable criteria to inform clinical practice. We evaluated the feasibility of detecting resistance to anti-HER2 therapy by serial gene-panel ctDNA sequencing. RESULTS: Primary therapeutic resistance was identified in 6 out of 14 patients with events of progressive disease. For this subset comparison of pre- and post-treatment ctDNA assay results revealed that HER2 amplification concurred with disease progression (4/6, 66...
September 1, 2016: Oncotarget
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