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Hallmarks, cancer

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https://www.readbyqxmd.com/read/28230863/oncogenic-role-of-rab-escort-protein-1-through-egfr-and-stat3-pathway
#1
Un-Jung Yun, Jee Young Sung, Seog-Yun Park, Sang-Kyu Ye, Jaegal Shim, Jae-Seon Lee, Masahiko Hibi, Young-Ki Bae, Yong-Nyun Kim
Rab escort protein-1 (REP1) is linked to choroideremia (CHM), an X-linked degenerative disorder caused by mutations of the gene encoding REP1 (CHM). REP1 mutant zebrafish showed excessive cell death throughout the body, including the eyes, indicating that REP1 is critical for cell survival, a hallmark of cancer. In the present study, we found that REP1 is overexpressed in human tumor tissues from cervical, lung, and colorectal cancer patients, whereas it is expressed at relatively low levels in the normal tissue counterparts...
February 23, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28228863/medulloblastoma-and-ependymoma-cells-display-increased-levels-of-5-carboxylcytosine-and-elevated-tet1-expression
#2
Ashley Ramsawhook, Lara Lewis, Beth Coyle, Alexey Ruzov
BACKGROUND: Alteration of DNA methylation (5-methylcytosine, 5mC) patterns represents one of the causes of tumorigenesis and cancer progression. Tet proteins can oxidise 5mC to 5-hydroxymethylcytosine (5hmC), 5-formylcytosine and 5-carboxylcytosine (5caC). Although the roles of these oxidised forms of 5mC (oxi-mCs) in cancer pathogenesis are still largely unknown, there are indications that they may be involved in the mechanisms of malignant transformation. Thus, reduction of 5hmC content represents an epigenetic hallmark of human tumours, and according to our recent report, 5caC is enriched in a proportion of breast cancers and gliomas...
2017: Clinical Epigenetics
https://www.readbyqxmd.com/read/28228643/a-chemical-probe-toolbox-for-dissecting-the-cancer-epigenome
#3
REVIEW
Jake Shortt, Christopher J Ott, Ricky W Johnstone, James E Bradner
Cancer cell hallmarks are underpinned by transcriptional programmes operating in the context of a dynamic and complicit epigenomic environment. Somatic alterations of chromatin modifiers are among the most prevalent cancer perturbations. There is a pressing need for targeted chemical probes to dissect these complex, interconnected gene regulatory circuits. Validated chemical probes empower mechanistic research while providing the pharmacological proof of concept that is required to translate drug-like derivatives into therapy for cancer patients...
February 23, 2017: Nature Reviews. Cancer
https://www.readbyqxmd.com/read/28223427/calcium-dependent-enhancement-by-extracellular-acidity-of-the-cytotoxicity-of-mitochondrial-inhibitors-against-melanoma
#4
Fumihito Noguchi, Shigeki Inui, Clare Fedele, Mark Shackleton, Satoshi Itami
Extracellular acidity is a hallmark of cancers and is independent of hypoxia. Since acidity potentiates malignant phenotypes, therapeutic strategies that enhance the targeting of oncogenic mechanisms in an acidic microenvironment should be effective. We report here that drugs which abrogate mitochondrial respiration show enhanced cytotoxicity against melanoma cells in a normoxic but acidic extracellular pH, independent from P53 mutations, BRAF (V600E) mutations and/or resistance against BRAF inhibitors. Conversely, the cytotoxicity against melanoma cells of mitochondrial inhibitors is impaired by a neutral or alkaline extracellular pH and in vivo systemic alkalinization with NaHCO3 enhanced subcutaneous tumor growth and lung metastasis of B16F10 cells in mice treated with the mitochondrial inhibitor phenformin...
February 21, 2017: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/28218421/frameshift-mutational-target-gene-analysis-identifies-similarities-and-differences-in-constitutional-mismatch-repair-deficiency-and-lynch-syndrome
#5
Claudia Maletzki, Maja Huehns, Ingrid Bauer, Tim Ripperger, Maureen M Mork, Eduardo Vilar, Sabine Klöcking, Heike Zettl, Friedrich Prall, Michael Linnebacher
Mismatch-repair deficient (MMR-D) malignancies include Lynch Syndrome (LS), which is secondary to germline mutations in one of the MMR genes, and the rare childhood-form of constitutional mismatch repair-deficiency (CMMR-D); caused by bi-allelic MMR gene mutations. A hallmark of LS-associated cancers is microsatellite instability (MSI), characterized by coding frameshift mutations (cFSM) in target genes. By contrast, tumors arising in CMMR-D patients are thought to display a somatic mutation pattern differing from LS...
February 20, 2017: Molecular Carcinogenesis
https://www.readbyqxmd.com/read/28216603/use-of-mature-mirna-strand-selection-in-mirnas-families-in-cervical-cancer-development
#6
REVIEW
Angelica Judith Granados-López, José Luis Ruiz-Carrillo, Luis Steven Servín-González, José Luis Martínez-Rodríguez, Claudia Araceli Reyes-Estrada, Rosalinda Gutiérrez-Hernández, Jesús Adrián López
Aberrant miRNA expression is well recognized as a cancer hallmark, nevertheless miRNA function and expression does not always correlate in patients tissues and cell lines studies. In addition to this issue, miRNA strand usage conduces to increased cell signaling pathways modulation diversifying cellular processes regulation. In cervical cancer, 20 miRNA families are involved in carcinogenesis induction and development to this moment. These families have 5p and 3p strands with different nucleotide (nt) chain sizes...
February 14, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28212750/conformational-rigidity-and-protein-dynamics-at-distinct-timescales-regulate-ptp1b-activity-and-allostery
#7
Meng S Choy, Yang Li, Luciana E S F Machado, Micha B A Kunze, Christopher R Connors, Xingyu Wei, Kresten Lindorff-Larsen, Rebecca Page, Wolfgang Peti
Protein function originates from a cooperation of structural rigidity, dynamics at different timescales, and allostery. However, how these three pillars of protein function are integrated is still only poorly understood. Here we show how these pillars are connected in Protein Tyrosine Phosphatase 1B (PTP1B), a drug target for diabetes and cancer that catalyzes the dephosphorylation of numerous substrates in essential signaling pathways. By combining new experimental and computational data on WT-PTP1B and ≥10 PTP1B variants in multiple states, we discovered a fundamental and evolutionarily conserved CH/π switch that is critical for positioning the catalytically important WPD loop...
February 16, 2017: Molecular Cell
https://www.readbyqxmd.com/read/28210916/a-multiscale-mathematical-model-of-tumour-invasive-growth
#8
Lu Peng, Dumitru Trucu, Ping Lin, Alastair Thompson, Mark A J Chaplain
Known as one of the hallmarks of cancer (Hanahan and Weinberg in Cell 100:57-70, 2000) cancer cell invasion of human body tissue is a complicated spatio-temporal multiscale process which enables a localised solid tumour to transform into a systemic, metastatic and fatal disease. This process explores and takes advantage of the reciprocal relation that solid tumours establish with the extracellular matrix (ECM) components and other multiple distinct cell types from the surrounding microenvironment. Through the secretion of various proteolytic enzymes such as matrix metalloproteinases or the urokinase plasminogen activator (uPA), the cancer cell population alters the configuration of the surrounding ECM composition and overcomes the physical barriers to ultimately achieve local cancer spread into the surrounding tissue...
February 16, 2017: Bulletin of Mathematical Biology
https://www.readbyqxmd.com/read/28210711/intergenically-spliced-chimeric-rnas-in-cancer
#9
Yuemeng Jia, Zhongqiu Xie, Hui Li
Gene fusions and their encoded products (fusion RNAs and proteins) are viewed as one of the hallmarks of cancer. Traditionally, they were thought to be generated solely by chromosomal rearrangements. However, recent discoveries of trans-splicing and cis-splicing events between neighboring genes, suggest that there are other mechanisms to generate chimeric fusion RNAs without corresponding changes in DNA. In addition, chimeric RNAs have been detected in normal physiology, complicating the use of fusions in cancer detection and therapy...
September 2016: Trends in Cancer
https://www.readbyqxmd.com/read/28210259/resolution-of-cancer-promoting-inflammation-a-new-approach-for-anticancer-therapy
#10
REVIEW
Qi Zhang, Bo Zhu, Yongsheng Li
Inflammation is a protective response that eliminates harmful stimuli and restores tissue homeostasis, whereas the failure to resolve inflammation leads to the development of malignancies. Immune cells in the tumor inflammatory microenvironment endow cancer cells with their specific hallmarks, including mutations, metabolic reprograming, angiogenesis, invasion, and metastasis. Targeting the inflammatory microenvironment with anti-inflammatory drugs (e.g., aspirin) or by enhancing antitumor immunity (e.g., chimeric antigen receptor T cell therapy) has been extensively investigated and has achieved promising results in many cancers...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28209486/vasodilator-stimulated-phosphoprotein-vasp-depletion-from-breast-cancer-mda-mb-231-cells-inhibits-tumor-spheroid-invasion-through-downregulation-of-migfilin-%C3%AE-catenin-and-urokinase-plasminogen-activator-upa
#11
Vasiliki Gkretsi, Andreas Stylianou, Triantafyllos Stylianopoulos
A hallmark of cancer cells is their ability to invade surrounding tissues and form metastases. Cell-extracellular matrix (ECM)-adhesion proteins are crucial in metastasis, connecting tumor ECM with actin cytoskeleton thus enabling cells to respond to mechanical cues. Vasodilator-stimulated phosphoprotein (VASP) is an actin-polymerization regulator which interacts with cell-ECM adhesion protein Migfilin, and regulates cell migration. We compared VASP expression in MCF-7 and MDA-MB-231 breast cancer (BC) cells and found that more invasive MDA-MB-231 cells overexpress VASP...
February 13, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28209166/intra-tumor-heterogeneity-from-a-cancer-stem-cell-perspective
#12
REVIEW
Pramudita R Prasetyanti, Jan Paul Medema
Tumor heterogeneity represents an ongoing challenge in the field of cancer therapy. Heterogeneity is evident between cancers from different patients (inter-tumor heterogeneity) and within a single tumor (intra-tumor heterogeneity). The latter includes phenotypic diversity such as cell surface markers, (epi)genetic abnormality, growth rate, apoptosis and other hallmarks of cancer that eventually drive disease progression and treatment failure. Cancer stem cells (CSCs) have been put forward to be one of the determining factors that contribute to intra-tumor heterogeneity...
February 16, 2017: Molecular Cancer
https://www.readbyqxmd.com/read/28208102/oncogenic-growth-factor-signaling-mediating-tumor-escape-from-cellular-immunity
#13
REVIEW
Fernando Concha-Benavente, Robert L Ferris
Unrestrained growth factor signals can promote carcinogenesis, as well as other hallmarks of cancer such as immune evasion. Our understanding of the function and complex regulation of HER family of receptors has led to the development of targeted therapeutic agents that suppress tumor growth. However, these receptors also mediate escape from recognition by the host immune system. We discuss how HER family of oncogenic receptors downregulate tumor antigen presentation and upregulate suppressive membrane-bound or soluble secreted inhibitory molecules that ultimately lead to impaired cellular immunity mediated by cytotoxic T lymphocyte (CTL) recognition...
February 13, 2017: Current Opinion in Immunology
https://www.readbyqxmd.com/read/28207501/pd-l1-pd-1-check-point-in-gastric-carcinoma-with-lymphoid-stroma-case-report-with-immunochemical-study
#14
Anna Crescenzi, Chiara Taffon, Michele Donati, Michele Pier Luca Guarino, Sergio Valeri, Roberto Coppola
INTRODUCTION: Gastric carcinoma with lymphoid stroma is an unusual type of gastric tumor associated with a better prognosis than typical gastric carcinomas. The hallmark of this cancer is a prominent lymphoid infiltration of the stroma that represents an intense host lymphocytic response. The programmed death 1-programmed death-ligand 1 (PD-1/PD-L1) axis has recently emerged as a master immune checkpoint that controls antitumor immune responses against many neoplasms. PATIENT'S CONCERNS CASE STUDY AND OUTCOME: We report the case of a male patient with gastric carcinoma with lymphoid stroma with a large mass infiltrating the gastric wall without nodal metastasis...
February 2017: Medicine (Baltimore)
https://www.readbyqxmd.com/read/28206758/structural-optimization-and-pharmacological-evaluation-of-inhibitors-targeting-dual-specificity-tyrosine-phosphorylation-regulated-kinases-dyrk-and-cdc-like-kinases-clk-in-glioblastoma
#15
Qing-Qing Zhou, Athena F Phoa, Ramzi H Abbassi, Monira Hoque, Tristan A Reekie, Josep S Font, Renae M Ryan, Brett W Stringer, Bryan W Day, Terrance G Johns, Lenka Munoz, Michael Kassiou
The DYRK family contains kinases that are up-regulated in malignancy and control several cancer hallmarks. To assess the anti-cancer potential of inhibitors targeting DYRK kinases, we developed a series of novel DYRK inhibitors based on the 7-azaindole scaffold. All compounds were tested for their ability to inhibit DYRK1A, DYRK1B, DYRK2 and the structurally related CLK1. The library was screened for anti-cancer efficacy in established and stem cell-like glioblastoma cell lines. The most potent inhibitors (IC50 ≤ 50 nM) significantly decreased viability, clonogenic survival, migration and invasion of glioblastoma cells...
February 16, 2017: Journal of Medicinal Chemistry
https://www.readbyqxmd.com/read/28203301/progress-with-palbociclib-in-breast-cancer-latest-evidence-and-clinical-considerations
#16
REVIEW
Andrea Rocca, Alessio Schirone, Roberta Maltoni, Sara Bravaccini, Lorenzo Cecconetto, Alberto Farolfi, Giuseppe Bronte, Daniele Andreis
Deregulation of the cell cycle is a hallmark of cancer, and research on cell cycle control has allowed identification of potential targets for anticancer treatment. Palbociclib is a selective inhibitor of the cyclin-dependent kinases 4 and 6 (CDK4/6), which are involved, with their coregulatory partners cyclin D, in the G1-S transition. Inhibition of this step halts cell cycle progression in cells in which the involved pathway, including the retinoblastoma protein (Rb) and the E2F family of transcription factors, is functioning, although having been deregulated...
February 2017: Therapeutic Advances in Medical Oncology
https://www.readbyqxmd.com/read/28202690/a-rhog-mediated-signaling-pathway-that-modulates-invadopodia-dynamics-in-breast-cancer-cells
#17
Silvia M Goicoechea, Ashtyn Zinn, Sahezeel S Awadia, Kyle Snyder, Rafael Garcia-Mata
One of the hallmarks of cancer is the ability of tumor cells to invade surrounding tissues and metastasize. During metastasis, cancer cells degrade the extracellular matrix, which acts as a physical barrier, by developing a specialized actin-rich membrane protrusion structure called invadopodia. The formation of invadopodia is regulated by Rho GTPases, a family of proteins that regulates the actin cytoskeleton. Here, we describe a novel role for RhoG in the regulation of invadopodia disassembly in human breast cancer cells...
February 15, 2017: Journal of Cell Science
https://www.readbyqxmd.com/read/28202516/modeling-the-genetic-regulation-of-cancer-metabolism-interplay-between-glycolysis-and-oxidative-phosphorylation
#18
Linglin Yu, Mingyang Lu, Dongya Jia, Jianpeng Ma, Eshel Ben-Jacob, Herbert Levine, Benny A Kaipparettu, Jose' N Onuchic
Abnormal metabolism is a hallmark of cancer, yet its regulation remains poorly understood. Cancer cells were considered to utilize primarily glycolysis for ATP production, referred to as the Warburg effect. However, recent evidence suggests that oxidative phosphorylation (OXPHOS) plays a crucial role during cancer progression. Here we utilized a systems biology approach to decipher the regulatory principle of glycolysis and OXPHOS. Integrating information from literature, we constructed a regulatory network of genes and metabolites from which we extracted a core circuit containing HIF-1, AMPK, and ROS...
February 15, 2017: Cancer Research
https://www.readbyqxmd.com/read/28199202/racial-disparity-in-metabolic-regulation-of-cancer
#19
Kuldeep S Attri, Divya Murthy, Pankaj K Singh
Genetic mutations and metabolic reprogramming are two key hallmarks of cancer, required for proliferation, invasion, and metastasis of the disease. While genetic mutations, whether inherited or acquired, are critical for the initiation of tumor development, metabolic reprogramming is an effector mechanism imperative for adaptational transition during the progression of cancer. Recent findings in the literature emphasize the significance of molecular cross-talk between these two cellular processes in regulating signaling and differentiation of cancer cells...
March 1, 2017: Frontiers in Bioscience (Landmark Edition)
https://www.readbyqxmd.com/read/28199186/potential-of-redox-therapies-in-neurodegenerative-disorders
#20
Elzbieta Miller, Lukasz Markiewicz, Jacek Kabzinski, Dominik Odrobina, Ireneusz Majsterek
Recently significant advances have been made to understand the pathophysiological mechanisms of neurodegenerative disorders to provide real therapeutic benefits. There is evidence that persistent inflammation and oxidative stress are the crucial factors of ongoing cell damage in neurodegenerative complex etiology. The variety of reactive oxygen and nitrogen species are the cause of both axonal and neuronal destruction, which is pathological hallmark of neurodegeneration. Therefore, the reduction of oxidative stress is currently one of the main neuroprotective strategies...
March 1, 2017: Frontiers in Bioscience (Elite Edition)
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