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https://www.readbyqxmd.com/read/29666625/dying-to-be-noticed-epigenetic-regulation-of-immunogenic-cell-death-for-cancer-immunotherapy
#1
REVIEW
Brianne Cruickshank, Michael Giacomantonio, Paola Marcato, Sherri McFarland, Jonathan Pol, Shashi Gujar
Immunogenic cell death (ICD) activates both innate and adaptive arms of the immune system during apoptotic cancer cell death. With respect to cancer immunotherapy, the process of ICD elicits enhanced adjuvanticity and antigenicity from dying cancer cells and consequently, promotes the development of clinically desired antitumor immunity. Cancer ICD requires the presentation of various "hallmarks" of immunomodulation, which include the cell-surface translocation of calreticulin, production of type I interferons, and release of high-mobility group box-1 and ATP, which through their compatible actions induce an immune response against cancer cells...
2018: Frontiers in Immunology
https://www.readbyqxmd.com/read/29666324/microrna-197-induces-epithelial-mesenchymal-transition-and-invasion-through-the-downregulation-of-hipk2-in-lung-adenocarcinoma
#2
Nan Zhang, Liang Tian, Zhigang Miao, Nan Guo
The major cause of cancer-related deaths in patients with lung adenocarcinoma (LAD) is due to distant metastasis. Many reports have indicated that miRNA plays a key role in tumour metastasis. The expression of miR-197 is correlated with LADprogression, however, the mechanism of miR-197 is still unknown in the processing of LAD. A Boyden chamber migration/invasion assay was used for the metastatic function study in vitro. Real-time PCR andWestern blot assays were employed to analyse the EMT hallmark changes in both the mRNA and protein levels...
March 2018: Journal of Genetics
https://www.readbyqxmd.com/read/29665859/morphology-and-genomic-hallmarks-of-breast-tumours-developed-by-atm-deleterious-variant-carriers
#3
Anne-Laure Renault, Noura Mebirouk, Laetitia Fuhrmann, Guillaume Bataillon, Eve Cavaciuti, Dorothée Le Gal, Elodie Girard, Tatiana Popova, Philippe La Rosa, Juana Beauvallet, Séverine Eon-Marchais, Marie-Gabrielle Dondon, Catherine Dubois d'Enghien, Anthony Laugé, Walid Chemlali, Virginie Raynal, Martine Labbé, Ivan Bièche, Sylvain Baulande, Jacques-Olivier Bay, Pascaline Berthet, Olivier Caron, Bruno Buecher, Laurence Faivre, Marc Fresnay, Marion Gauthier-Villars, Paul Gesta, Nicolas Janin, Sophie Lejeune, Christine Maugard, Sébastien Moutton, Laurence Venat-Bouvet, Hélène Zattara, Jean-Pierre Fricker, Laurence Gladieff, Isabelle Coupier, Georgia Chenevix-Trench, Janet Hall, Anne Vincent-Salomon, Dominique Stoppa-Lyonnet, Nadine Andrieu, Fabienne Lesueur
BACKGROUND: The ataxia telangiectasia mutated (ATM) gene is a moderate-risk breast cancer susceptibility gene; germline loss-of-function variants are found in up to 3% of hereditary breast and ovarian cancer (HBOC) families who undergo genetic testing. So far, no clear histopathological and molecular features of breast tumours occurring in ATM deleterious variant carriers have been described, but identification of an ATM-associated tumour signature may help in patient management. METHODS: To characterise hallmarks of ATM-associated tumours, we performed systematic pathology review of tumours from 21 participants from ataxia-telangiectasia families and 18 participants from HBOC families, as well as copy number profiling on a subset of 23 tumours...
April 17, 2018: Breast Cancer Research: BCR
https://www.readbyqxmd.com/read/29665004/thiostrepton-degrades-mutant-p53-by-eliciting-an-autophagic-response-in-sw480-cells
#4
Dhanya Kalathil, Manu Prasad, Maharrish Chelladurai, Samu John, Asha S Nair
Mutations in p53 gene are one of the hallmarks of tumor development. Specific targeting of mutant p53 protein has a promising role in cancer therapeutics. Our preliminary observation showed destabilization of mutant p53 protein in SW480, MiaPaCa and MDAMB231 cell lines upon thiostrepton treatment. In order to elucidate the mechanism of thiostrepton triggered mutant p53 degradation, we explored the impact of proteasome inhibition on activation of autophagy. Combined treatment of thiostrepton and cycloheximide/chloroquine prevented the degradation of mutant p53 protein, reinforcing autophagy as the means of mutant p53 destabilization...
April 17, 2018: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/29664569/fatty-acid-metabolism-in-cd8-t-cell-memory-challenging-current-concepts
#5
REVIEW
Brenda Raud, Peter J McGuire, Russell G Jones, Tim Sparwasser, Luciana Berod
CD8+ T cells are key members of the adaptive immune response against infections and cancer. As we discuss in this review, these cells can present diverse metabolic requirements, which have been intensely studied during the past few years. Our current understanding suggests that aerobic glycolysis is a hallmark of activated CD8+ T cells, while naive and memory (Tmem ) cells often rely on oxidative phosphorylation, and thus mitochondrial metabolism is a crucial determinant of CD8+ Tmem cell development. Moreover, it has been proposed that CD8+ Tmem cells have a specific requirement for the oxidation of long-chain fatty acids (LC-FAO), a process modulated in lymphocytes by the enzyme CPT1A...
May 2018: Immunological Reviews
https://www.readbyqxmd.com/read/29662626/store-operated-calcium-entry-is-altered-by-the-inhibition-of-receptors-tyrosine-kinase
#6
Noémie Emeriau, Marie de Clippele, Philippe Gailly, Nicolas Tajeddine
SOCE (Store-Operated Calcium Entry) is the main mechanism by which external Ca2+ enters into non-excitable cells after endoplasmic reticulum emptying. It is implicated in several processes such as proliferation and migration. Alterations in SOCE could initiate or support the development of hallmarks of cancer. In this project, we showed that disruption of the EGFR/ErbB2-dependent signalling by lapatinib and CP-724714, two inhibitors of the receptor tyrosine kinase (RTK), dramatically reduced the amplitude of the SOCE in breast cancer cells...
March 23, 2018: Oncotarget
https://www.readbyqxmd.com/read/29662619/uev1a-ubc13-promotes-colorectal-cancer-metastasis-through-regulating-cxcl1-expression-via-nf-%C3%B0%C2%BAb-activation
#7
Zhaojia Wu, Heather Neufeld, Eminao Torlakovic, Wei Xiao
Colorectal cancer is the second most common cause of cancer-related death worldwide. Uncontrolled growth and distant metastasis are hallmarks of colorectal cancer. However, the precise etiological factors and the mechanisms are diverse and still largely unclear. The potential proto-oncogene UEV1A encodes a ubiquitin conjugating enzyme variant, which is required for Ubc13-catalyzed K63-linked poly-ubiquitination of target proteins and the activation of NF-кB, a transcription factor known to be involved in innate immunity, anti-apoptosis, inflammation and cancer...
March 23, 2018: Oncotarget
https://www.readbyqxmd.com/read/29661224/notch-signals-modulate-lgl-mediated-tumorigenesis-by-the-activation-of-jnk-signaling
#8
Maimuna Sali Paul, Ankita Singh, Debdeep Dutta, Mousumi Mutsuddi, Ashim Mukherjee
OBJECTIVES: Oncogenic potential of Notch signaling and its cooperation with other factors to affect proliferation are widely established. Notch exhibits a cooperative effect with loss of a cell polarity gene, scribble to induce neoplastic overgrowth. Oncogenic Ras also show cooperative effect with loss of cell polarity genes such as scribble (scrib), lethal giant larvae (lgl) and discs large to induce neoplastic overgrowth and invasion. Our study aims at assessing the cooperation of activated Notch with loss of function of lgl in tumor overgrowth, and the mode of JNK signaling activation in this context...
April 16, 2018: BMC Research Notes
https://www.readbyqxmd.com/read/29661172/mth1-deficiency-selectively-increases-non-cytotoxic-oxidative-dna-damage-in-lung-cancer-cells-more-bad-news-than-good
#9
Hussein H K Abbas, Kheloud M H Alhamoudi, Mark D Evans, George D D Jones, Steven S Foster
BACKGROUND: Targeted therapies are based on exploiting cancer-cell-specific genetic features or phenotypic traits to selectively kill cancer cells while leaving normal cells unaffected. Oxidative stress is a cancer hallmark phenotype. Given that free nucleotide pools are particularly vulnerable to oxidation, the nucleotide pool sanitising enzyme, MTH1, is potentially conditionally essential in cancer cells. However, findings from previous MTH1 studies have been contradictory, meaning the relevance of MTH1 in cancer is still to be determined...
April 16, 2018: BMC Cancer
https://www.readbyqxmd.com/read/29661159/active-dna-end-processing-in-micronuclei-of-ovarian-cancer-cells
#10
Zizhi Tang, Juan Yang, Xin Wang, Ming Zeng, Jing Wang, Ao Wang, Mingcai Zhao, Liandi Guo, Cong Liu, Dehua Li, Jie Chen
BACKGROUND: Ovarian cancer is one of the most deadly gynecological malignancies and inclined to recurrence and drug resistance. Previous studies showed that the tumorigenesis of ovarian cancers and their major histotypes are associated with genomic instability caused by defined sets of pathogenic mutations. In contrast, the mechanism that influences the development of drug resistance and disease recurrence is not well elucidated. Solid tumors are prone to chromosomal instability (CIN) and micronuclei formation (MN)...
April 16, 2018: BMC Cancer
https://www.readbyqxmd.com/read/29657328/non-canonical-functions-of-enzymes-facilitate-cross-talk-between-cell-metabolic-and-regulatory-pathways
#11
REVIEW
Marteinn T Snaebjornsson, Almut Schulze
The metabolic rewiring that occurs during cell transformation is a hallmark of cancer. It is diverse in different cancers as it reflects different combinations of oncogenic drivers, tumor suppressors, and the microenvironment. Metabolic rewiring is essential to cancer as it enables uncontrolled proliferation and adaptation to the fluctuating availability of nutrients and oxygen caused by poor access to the vasculature due to tumor growth and a foreign microenvironment encountered during metastasis. Increasing evidence now indicates that the metabolic state in cancer cells also plays a causal role in tumor growth and metastasis, for example through the action of oncometabolites, which modulate cell signaling and epigenetic pathways to promote malignancy...
April 16, 2018: Experimental & Molecular Medicine
https://www.readbyqxmd.com/read/29655550/proteomic-investigating-the-cooperative-lethal-effect-of-egfr-and-mdm2-inhibitors-on-ovarian-carcinoma
#12
Shing-Jyh Chang, En-Chi Liao, Hsin-Yueh Yeo, Wen-Hong Kuo, Hsin-Yi Chen, Yi-Ting Tsai, Yu-Shan Wei, Ying-Jen Chen, Yi-Shiuan Wang, Ji-Min Li, Chuan-Chi Shih, Chia-Hao Chan, Hsiu-Chuan Chou, Yung-Jen Chuang, Hong-Lin Chan
With the concept of precision medicine, combining multiple molecular-targeting therapies has brought new approaches to current cancer treatments. Malfunction of the tumor suppressor protein, p53 is a universal hallmark in human cancers. Under normal conditions, p53 is degraded through an ubiquitin-proteosome pathway regulated by its negative regulator, MDM2. In contrast, cellular stress such as DNA damage will activate p53 to carry out DNA repair, cell cycle arrest, and apoptosis. In this study, we focused on ovarian carcinoma with high EGFR and MDM2 overexpression rate...
April 12, 2018: Archives of Biochemistry and Biophysics
https://www.readbyqxmd.com/read/29652061/bevacizumab-and-near-infrared-probe-conjugated-iron-oxide-nanoparticles-for-vascular-endothelial-growth-factor-targeted-mr-and-optical-imaging
#13
Run Lin, Jing Huang, Liya Wang, Yuancheng Li, Malgorzata Lipowska, Hui Wu, Jianyong Yang, Hui Mao
Vascular endothelial growth factor (VEGF) plays a pivotal role in the cascade of development and progression of cancers. Targeting this cancer hallmark is a logical strategy for imaging based cancer detection and monitoring the anti-angiogenesis treatment. Using Bevacizumab (Avastin®), which is a recombinant humanized monoclonal antibody directly against VEGF and an angiogenesis inhibitor, as a targeting ligand, a multimodal VEGF targeted molecular imaging probe was developed by conjugating near infrared dye (NIR830) labeled bevacizumab to magnetic iron oxide nanoparticles (IONP) for optical and magnetic resonance (MR) imaging of cancers over-expressing VEGF...
April 13, 2018: Biomaterials Science
https://www.readbyqxmd.com/read/29650553/enduring-epigenetic-landmarks-define-the-cancer-microenvironment
#14
Ruth Pidsley, Mitchell G Lawrence, Elena Zotenko, Birunthi Niranjan, Aaron Statham, Jenny Song, Roman M Chabanon, Wenjia Qu, Hong Wang, Michelle Richards, Shalima S Nair, Nicola J Armstrong, Hieu T Nim, Melissa Papargiris, Preetika Balanathan, Hugh French, Timothy Peters, Sam Norden, Andrew Ryan, John Pedersen, James Kench, Roger J Daly, Lisa G Horvath, Phillip Stricker, Mark Frydenberg, Renea A Taylor, Clare Stirzaker, Gail P Risbridger, Susan J Clark
The growth and progression of solid tumors involves dynamic cross-talk between cancer epithelium and the surrounding microenvironment. To date, molecular profiling has largely been restricted to the epithelial component of tumors; therefore, features underpinning the persistent protumorigenic phenotype of the tumor microenvironment are unknown. Using whole-genome bisulfite sequencing, we show for the first time that cancer-associated fibroblasts (CAFs) from localized prostate cancer display remarkably distinct and enduring genome-wide changes in DNA methylation, significantly at enhancers and promoters, compared to nonmalignant prostate fibroblasts (NPFs)...
April 12, 2018: Genome Research
https://www.readbyqxmd.com/read/29649096/defining-driver-dna-methylation-changes-in-human-cancer
#15
REVIEW
Gerd P Pfeifer
Human malignant tumors are characterized by pervasive changes in the patterns of DNA methylation. These changes include a globally hypomethylated tumor cell genome and the focal hypermethylation of numerous 5'-cytosine-phosphate-guanine-3' (CpG) islands, many of them associated with gene promoters. It has been challenging to link specific DNA methylation changes with tumorigenesis in a cause-and-effect relationship. Some evidence suggests that cancer-associated DNA hypomethylation may increase genomic instability...
April 12, 2018: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29643204/l1-retrotransposition-is-a-common-feature-of-mammalian-hepatocarcinogenesis
#16
Stephanie N Schauer, Patricia E Carreira, Ruchi Shukla, Daniel J Gerhardt, Patricia Gerdes, Francisco J Sanchez-Luque, Paola Nicoli, Michaela Kindlova, Serena Ghisletti, Alexandre Dos Santos, Delphine Rapoud, Didier Samuel, Jamila Faivre, Adam D Ewing, Sandra R Richardson, Geoffrey J Faulkner
The retrotransposon Long Interspersed Element 1 (LINE-1 or L1) is a continuing source of germline and somatic mutagenesis in mammals. Deregulated L1 activity is a hallmark of cancer, and L1 mutagenesis has been described in numerous human malignancies. We previously employed retrotransposon capture sequencing (RC-seq) to analyze hepatocellular carcinoma (HCC) samples from patients infected with hepatitis B or hepatitis C virus and identified L1 variants responsible for activating oncogenic pathways. Here, we have applied RC-seq and whole-genome sequencing (WGS) to an Abcb4 (Mdr2) -/- mouse model of hepatic carcinogenesis and demonstrated for the first time that L1 mobilization occurs in murine tumors...
April 11, 2018: Genome Research
https://www.readbyqxmd.com/read/29629339/metabolic-reprogramming-in-thyroid-carcinoma
#17
REVIEW
Raquel Guimaraes Coelho, Rodrigo S Fortunato, Denise P Carvalho
Among all the adaptations of cancer cells, their ability to change metabolism from the oxidative to the glycolytic phenotype is a hallmark called the Warburg effect. Studies on tumor metabolism show that improved glycolysis and glutaminolysis are necessary to maintain rapid cell proliferation, tumor progression, and resistance to cell death. Thyroid neoplasms are common endocrine tumors that are more prevalent in women and elderly individuals. The incidence of thyroid cancer has increased in the Past decades, and recent findings describing the metabolic profiles of thyroid tumors have emerged...
2018: Frontiers in Oncology
https://www.readbyqxmd.com/read/29628997/cancer-metabolism-new-insights-into-classic-characteristics
#18
REVIEW
Yasumasa Kato, Toyonobu Maeda, Atsuko Suzuki, Yuh Baba
Initial studies of cancer metabolism in the early 1920s found that cancer cells were phenotypically characterized by aerobic glycolysis, in that these cells favor glucose uptake and lactate production, even in the presence of oxygen. This property, called the Warburg effect, is considered a hallmark of cancer. The mechanism by which these cells acquire aerobic glycolysis has been uncovered. Acidic extracellular fluid, secreted by cancer cells, induces a malignant phenotype, including invasion and metastasis...
February 2018: Japanese Dental Science Review
https://www.readbyqxmd.com/read/29628979/isomangiferin-a-novel-potent-vascular-endothelial-growth-factor-receptor-2-kinase-inhibitor-suppresses-breast-cancer-growth-metastasis-and-angiogenesis
#19
Banghua Wang, Jia Shen, Zexia Wang, Jianxia Liu, Zhifeng Ning, Meichun Hu
Purpose: Vascular endothelial growth factor (VEGF) signal transduction mainly depends on its binding to VEGF receptor 2 (VEGFR-2). VEGF downstream signaling proteins mediate several of its effects in cancer progression, including those on tumor growth, metastasis, and blood vessel formation. The activation of VEGFR-2 signaling is a hallmark of and is considered a therapeutic target for breast cancer. Here, we report a study of the regulation of the VEGFR-2 signaling pathway by a small molecule, isomangiferin...
March 2018: Journal of Breast Cancer
https://www.readbyqxmd.com/read/29628794/surface-markers-of-cancer-stem-like-cells-of-ovarian-cancer-and-their-clinical-relevance
#20
REVIEW
Aleksandra Klemba, J Karolina Purzycka-Olewiecka, Gabriel Wcisło, Anna M Czarnecka, Sławomir Lewicki, Bogdan Lesyng, Cezary Szczylik, Claudine Kieda
Cancer stem-like cells (CSLCs) are defined as cancer cells with stem cell characteristics. Although CSLCs constitute no more than a few percent of the tumor mass, they play important roles in cancer chemo-resistance, metastasis and disease recurrence. Ovarian cancer (OC) is considered the most aggressive gynecological malignancy in which the role of CSLCs is of major significance, although it remains to be specified. The studies describing ovarian CSLC phenotype vary in the definition of the molecular pattern of expression of the main markers such as CD133, CD44, CD117, and CD24...
March 2018: Contemporary Oncology Współczesna Onkologia
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