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Genomic instability cancer

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https://www.readbyqxmd.com/read/27910065/pathology-of-endometrial-carcinoma
#1
Sigurd F Lax
On a clinicopathological and molecular level, two distinctive types of endometrial carcinoma, type I and type II, can be distinguished. Endometrioid carcinoma, the typical type I carcinoma, seems to develop through an estrogen-driven "adenoma carcinoma" pathway from atypical endometrial hyperplasia/endometrioid intraepithelial neoplasia (AEH/EIN). It is associated with elevated serum estrogen and high body mass index and expresses estrogen and progesterone receptors. They are mostly low grade and show a favorable prognosis...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/27908669/cellular-responses-to-replication-stress-implications-in-cancer-biology-and-therapy
#2
REVIEW
Hui-Ju Hsieh, Guang Peng
DNA replication is essential for cell proliferation. Any obstacles during replication cause replication stress, which may lead to genomic instability and cancer formation. In this review, we summarize the physiological DNA replication process and the normal cellular response to replication stress. We also outline specialized therapies in clinical trials based on current knowledge and future perspectives in the field.
November 22, 2016: DNA Repair
https://www.readbyqxmd.com/read/27908614/a-critical-discussion-on-diet-genomic-mutations-and-repair-mechanisms-in-colon-carcinogenesis
#3
Juliana Yumi Sakita, Bianca Gasparotto, Sergio Britto Garcia, Sergio Akira Uyemura, Vinicius Kannen
Colon cancer is one of the most common malignancies and its etiology closely tied to dietary habits. Recent epidemiological data shows that colon cancer incidence is shifting to a much younger population. In this regard, some dietary components from a regular human meal might have various DNA-damaging compounds. Given that not every person endure cancer, the colonic malignancy develops throughout decades, and persistent DNA damage promotes cancer when induced at the proper intensity, a critical discussion of possible novel mechanisms by which carcinogens promote these tumors is urgently needed...
November 28, 2016: Toxicology Letters
https://www.readbyqxmd.com/read/27908234/sustained-early-disruption-of-mitochondrial-function-contributes-to-arsenic-induced-prostate-tumorigenesis
#4
B Singh, M Kulawiec, K M Owens, A Singh, K K Singh
Arsenic is a well-known human carcinogen that affects millions of people worldwide, but the underlying mechanisms of carcinogenesis are unclear. Several epidemiological studies have suggested increased prostate cancer incidence and mortality due to exposure to arsenic. Due to lack of an animal model of arsenic-induced carcinogenesis, we used a prostate epithelial cell culture model to identify a role for mitochondria in arsenic-induced prostate cancer. Mitochondrial morphology and membrane potential was impacted within a few hours of arsenic exposure of non-neoplastic prostate epithelial cells...
October 2016: Biochemistry. Biokhimii︠a︡
https://www.readbyqxmd.com/read/27907175/p53-specifically-binds-triplex-dna-in-vitro-and-in-cells
#5
Marie Brázdová, Vlastimil Tichý, Robert Helma, Pavla Bažantová, Alena Polášková, Aneta Krejčí, Marek Petr, Lucie Navrátilová, Olga Tichá, Karel Nejedlý, Martin L Bennink, Vinod Subramaniam, Zuzana Bábková, Tomáš Martínek, Matej Lexa, Matej Adámik
Triplex DNA is implicated in a wide range of biological activities, including regulation of gene expression and genomic instability leading to cancer. The tumor suppressor p53 is a central regulator of cell fate in response to different type of insults. Sequence and structure specific modes of DNA recognition are core attributes of the p53 protein. The focus of this work is the structure-specific binding of p53 to DNA containing triplex-forming sequences in vitro and in cells and the effect on p53-driven transcription...
2016: PloS One
https://www.readbyqxmd.com/read/27904700/detection-of-gene-copy-number-alterations-in-dcis-and-invasive-breast-cancer-by-qm-fish
#6
Aifeng Pan, Yawei Zhou, Kun Mu, Yansong Liu, Feifei Sun, Peng Li, Li Li
The exact roles of copy number alteration (CNA) in initiation, progression and immunotherapy of breast cancer and the genomic alterations behind progression from ductal carcinoma in situ (DCIS) to invasive carcinoma remain unknown. Quantitative multi-gene fluorescence in situ hybridization (QM-FISH) opens a possibility of large scale genomic analysis of specific deletions and amplifications with high-resolution at one cell level. We detected CNAs of 30 genes using QM-FISH and analyzed their association with clinicopathological parameters and patients' outcomes in 66 breast cancers with synchronous invasive carcinoma and DCIS...
2016: American Journal of Translational Research
https://www.readbyqxmd.com/read/27900199/effects-of-exercise-on-markers-of-oxidative-stress-an-ancillary-analysis-of-the-alberta-physical-activity-and-breast-cancer-prevention-trial
#7
Christine M Friedenreich, Vincent Pialoux, Qinggang Wang, Eileen Shaw, Darren R Brenner, Xavier Waltz, Shannon M Conroy, Rhys Johnson, Christy G Woolcott, Marc J Poulin, Kerry S Courneya
BACKGROUND: Oxidative stress may contribute to cancer aetiology through several mechanisms involving damage to DNA, proteins and lipids leading to genetic mutations and genomic instability. The objective of this study was to determine the effects of aerobic exercise on markers of oxidative damage and antioxidant enzymes in postmenopausal women. METHODS: The Alberta Physical Activity and Breast Cancer Prevention Trial (ALPHA) was a two-centre, two-armed randomised trial of 320 inactive, healthy, postmenopausal women aged 50-74 years...
2016: BMJ Open Sport & Exercise Medicine
https://www.readbyqxmd.com/read/27898099/clinical-and-molecular-rationale-to-retain-the-cancer-descriptor-for-gleason-score-6-disease
#8
REVIEW
Chad A Reichard, Eric A Klein
Treatment choices for men with indolent prostate cancer include active surveillance or definitive local therapy. Overtreatment of these patients is an important current problem. Treatment decisions are often made jointly by the clinician and the patient, partly based on the tumour's Gleason score. To reduce the burden of overtreatment, the clinical significance of Gleason score 3 + 3 = 6 prostate cancer has been questioned and some have advocated that Gleason pattern 3 should be stripped of its cancer status...
November 29, 2016: Nature Reviews. Urology
https://www.readbyqxmd.com/read/27896849/cytoplasmic-msh2-immunoreactivity-in-a-patient-with-lynch-syndrome-with-an-epcam-msh2-fusion
#9
Shigeki Sekine, Reiko Ogawa, Shinya Saito, Mineko Ushiama, Dai Shida, Takeshi Nakajima, Hirokazu Taniguchi, Nobuyoshi Hiraoka, Teruhiko Yoshida, Kokichi Sugano
AIMS: Immunohistochemistry for mismatch repair (MMR) proteins is being increasingly used to examine MMR status in tumours. The aim of the present article was to report the case of a colon cancer patient with Lynch syndrome who showed unusual cytoplasmic MMR protein localization. METHODS AND RESULTS: Histologically, the colon cancer was diagnosed as medullary carcinoma associated with prominent tumour-infiltrating lymphocytes and a Crohn's-like reaction. Immunohistochemistry revealed cytoplasmic and nuclear expression of MSH2 in non-neoplastic cells, and exclusively cytoplasmic expression in tumour cells...
October 19, 2016: Histopathology
https://www.readbyqxmd.com/read/27896456/dna-copy-number-profiling-in-microsatellite-stable-and-microsatellite-unstable-hereditary-non-polyposis-colorectal-cancers-by-targeted-cnv-array
#10
Weixiang Chen, Jun Ding, Long Jiang, Zebing Liu, Xiaoyan Zhou, Daren Shi
About half of hereditary non-polyposis colorectal cancers (HNPCCs) fulfilling the Amsterdam criteria (AC) do not display evidence of mismatch repair defects, and the difference between microsatellite-stable (MSS) and microsatellite-unstable HNPCC remains poorly understood. The study was to compare overall copy number variation (CNV) and loss of heterozygosity (LOH) of the entire genome in HNPCCs with MSS and microsatellite-instability (MSI) using the Cytoscan HD Array. This was a study carried out in samples from 20 patients with MSS HNPCC and four patients with MSI HNPCC from the Fudan University Shanghai Cancer Center (China)...
November 28, 2016: Functional & Integrative Genomics
https://www.readbyqxmd.com/read/27895396/genetic-alterations-in-hepatocellular-carcinoma-an-update
#11
REVIEW
Zhao-Shan Niu, Xiao-Jun Niu, Wen-Hong Wang
Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths worldwide. Although recent advances in therapeutic approaches for treating HCC have improved the prognoses of patients with HCC, this cancer is still associated with a poor survival rate mainly due to late diagnosis. Therefore, a diagnosis must be made sufficiently early to perform curative and effective treatments. There is a need for a deeper understanding of the molecular mechanisms underlying the initiation and progression of HCC because these mechanisms are critical for making early diagnoses and developing novel therapeutic strategies...
November 7, 2016: World Journal of Gastroenterology: WJG
https://www.readbyqxmd.com/read/27894690/a-systematic-review-of-the-association-between-occupational-exposure-to-formaldehyde-and-effects-on-chromosomal-dna-damage-measured-using-the-cytokinesis-block-micronucleus-assay-in-lymphocytes
#12
REVIEW
Michael Fenech, Armen Nersesyan, Siegfried Knasmueller
Formaldehyde (FAL) is classified as a Class I carcinogen by the WHO International Agency for Research on Cancer. Therefore, there is a need to validate appropriate methods for detecting its genotoxic effects in vivo in humans. One of the most commonly used methods to measure the genotoxic effects of exposure to environmental chemicals is the lymphocyte cytokinesis-block micronucleus (L-CBMN assay). We performed a systematic review and statistical analysis of the results from all of the published studies in which the L-CBMN assay was used to measure the genotoxic effects of human exposure to FAL...
October 2016: Mutation Research
https://www.readbyqxmd.com/read/27893964/aneuploidy-in-cancer-and-aging
#13
Ryan M Naylor, Jan M van Deursen
Chromosomal instability (CIN), the persistent inability of a cell to faithfully segregate its genome, is a feature of many cancer cells. It stands to reason that CIN enables the acquisition of multiple cancer hallmarks; however, there is a growing body of evidence suggesting that CIN impairs cellular fitness and prevents neoplastic transformation. Here, we suggest a new perspective to reconcile this apparent paradox and share an unexpected link between aneuploidy and aging that was discovered through attempts to investigate the CIN-cancer relationship...
November 23, 2016: Annual Review of Genetics
https://www.readbyqxmd.com/read/27893783/role-of-pten-in-oxidative-stress-and-dna-damage-in-the-liver-of-whole-body-pten-haplodeficient-mice
#14
Ezgi Eyluel Bankoglu, Oliver Tschopp, Johannes Schmitt, Philipp Burkard, Daniel Jahn, Andreas Geier, Helga Stopper
Type 2 diabetes (T2DM) and obesity are frequently associated with non-alcoholic fatty liver disease (NAFLD) and with an elevated cancer incidence. The molecular mechanisms of carcinogenesis in this context are only partially understood. High blood insulin levels are typical in early T2DM and excessive insulin can cause elevated reactive oxygen species (ROS) production and genomic instability. ROS are important for various cellular functions in signaling and host defense. However, elevated ROS formation is thought to be involved in cancer induction...
2016: PloS One
https://www.readbyqxmd.com/read/27891063/cell-division-cycle-7-kinase-inhibitor-pha-767491-hydrochloride-suppresses-glioblastoma-growth-and-invasiveness
#15
Zubeyde Erbayraktar, Begum Alural, Resat Serhat Erbayraktar, Erdogan Pekcan Erkan
BACKGROUND: Genomic instability is a hallmark of cancer cells, and this cellular phenomenon can emerge as a result of replicative stress. It is possible to take advantage of replicative stress, and enhance it in a targeted way to fight cancer cells. One of such strategies involves targeting the cell division cycle 7-related protein kinase (CDC7), a protein with key roles in regulation of initiation of DNA replication. CDC7 overexpression is present in different cancers, and small molecule inhibitors of the CDC7 have well-documented anti-tumor effects...
2016: Cancer Cell International
https://www.readbyqxmd.com/read/27890638/aberrant-base-excision-repair-pathway-of-oxidatively-damaged-dna-implications-for-degenerative-diseases
#16
Ibtissam Talhaoui, Bakhyt T Matkarimov, Thierry Tchenio, Dmitry O Zharkov, Murat K Saparbaev
In cellular organisms composition of DNA is constrained to only four nucleobases A, G, T and C, except for minor DNA base modifications such as methylation which serves for defence against foreign DNA or gene expression regulation. Interestingly, this severe evolutionary constraint among other things demands DNA repair systems to discriminate between regular and modified bases. DNA glycosylases specifically recognize and excise damaged bases among vast majority of regular bases in the base excision repair (BER) pathway...
November 24, 2016: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/27888635/lncrnas-the-bridge-linking-rna-and-colorectal-cancer
#17
Yanfei Yang, Linjie Zhao, Lingzi Lei, Wayne Bond Lau, Bonnie Lau, Qilian Yang, Xiaobing Le, Huiliang Yang, Chenlu Wang, Zhongyue Luo, Yu Xuan, Yi Chen, Xiangbing Deng, Lian Xu, Min Feng, Tao Yi, Xia Zhao, Yuquan Wei, Shengtao Zhou
Long noncoding RNAs (lncRNAs) are transcribed by genomic regions (exceeding 200 nucleotides in length) that do not encode proteins. While the exquisite regulation of lncRNA transcription can provide signals of malignant transformation, lncRNAs control pleiotropic cancer phenotypes through interactions with other cellular molecules including DNA, protein, and RNA. Recent studies have demonstrated that dysregulation of lncRNAs is influential in proliferation, angiogenesis, metastasis, invasion, apoptosis, stemness, and genome instability in colorectal cancer (CRC), with consequent clinical implications...
November 24, 2016: Oncotarget
https://www.readbyqxmd.com/read/27886675/pathogenic-germline-mcm9-variants-are-rare-in-australian-lynch-like-syndrome-patients
#18
Qing Liu, Luke B Hesson, Andrea C Nunez, Deborah Packham, Nicholas J Hawkins, Robyn L Ward, Mathew A Sloane
Lynch syndrome is a hereditary cancer syndrome caused by the autosomal dominant inheritance of loss-of-function mutations in DNA mismatch repair (MMR) genes. Approximately one quarter of clinically suspected cases have no identifiable germline mutation in any MMR gene, a condition known as Lynch-like syndrome (LLS). MCM9 was recently identified as the DNA helicase in the mammalian MMR complex and loss of helicase activity results in microsatellite instability. We hypothesized that pathogenic variants in MCM9 may account for LLS...
November 2016: Cancer Genetics
https://www.readbyqxmd.com/read/27886118/natural-compound-histone-deacetylase-inhibitors-hdaci-synergy-with-inflammatory-signaling-pathway-modulators-and-clinical-applications-in-cancer
#19
REVIEW
Hélène Losson, Michael Schnekenburger, Mario Dicato, Marc Diederich
The remarkable complexity of cancer involving multiple mechanisms of action and specific organs led researchers Hanahan and Weinberg to distinguish biological capabilities acquired by cancer cells during the multistep development of human tumors to simplify its understanding. These characteristic hallmarks include the abilities to sustain proliferative signaling, evade growth suppressors, resist cell death, enable replicative immortality, induce angiogenesis, activate invasion and metastasis, avoid immune destruction, and deregulate cellular energetics...
November 23, 2016: Molecules: a Journal of Synthetic Chemistry and Natural Product Chemistry
https://www.readbyqxmd.com/read/27884198/use-of-poly-adp-ribose-polymerase-parp-inhibitors-in-cancer-cells-bearing-ddr-defects-the-rationale-for-their-inclusion-in-the-clinic
#20
REVIEW
Aniello Cerrato, Francesco Morra, Angela Celetti
BACKGROUND: DNA damage response (DDR) defects imply genomic instability and favor tumor progression but make the cells vulnerable to the pharmacological inhibition of the DNA repairing enzymes. Targeting cellular proteins like PARPs, which cooperate and complement molecular defects of the DDR process, induces a specific lethality in DDR defective cancer cells and represents an anti-cancer strategy. Normal cells can tolerate the DNA damage generated by PARP inhibition because of an efficient homologous recombination mechanism (HR); in contrast, cancer cells with a deficient HR are unable to manage the DSBs and appear especially sensitive to the PARP inhibitors (PARPi) effects...
November 24, 2016: Journal of Experimental & Clinical Cancer Research: CR
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