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Genomic instability cancer

Yi Sui, Fuqiang Li, Tingting Wu, Jian Ding, Zeming Lu, Lingyao Wang, Yang Yang, Fei Wang, Linhong Zhao, Huihui Zhu, Tao Wei, Jingji Jin, Yong Cai
The restriction of YY1 at BCCIP transcriptional start site (TSS) proximal region in several human cancer cell lines was found by analyzation of ChIP-Seq database from UCSC Genome Browser(h t t p: //genome. ucsc. edu). However, whether the stabilization of YY1 by BCCIP impacts its recruitment in the BCCIP promoter region is unclear. Here, we present evidence that transcriptional regulation of YY1 on BCCIP is closely related to YY1 stability in HCT116 human colon cancer cells. YY1 stabilization was in turn regulated by BCCIP, suggesting the existence of a BCCIP-YY1 feedback loop in regulating BCCIP transcription by the YY1...
June 22, 2018: FEBS Journal
Soo-Min Kim, Kyung-A Hwang, Kyung-Chul Choi
Reactive oxygen species (ROS) are major sources of cellular oxidative stress. Specifically, cancer cells harbor genetic alterations that promote a continuous and elevated production of ROS. While such oxidative stress conditions could be harmful to normal cells, they facilitate cancer cell growth in multiple ways by causing DNA damage and genomic instability, and ultimately, by reprogramming cancer cell metabolism. This review provides up to date findings regarding the role of ROS generation induced by diverse biological molecules and chemicals in representative women's' cancer...
June 20, 2018: BMB Reports
Eleonora Sementino, Craig W Menges, Yuwaraj Kadariya, Suraj Peri, Jinfei Xu, Zemin Liu, Richard G Wilkes, Kathy Q Cai, Frank J Rauscher, Andres J Klein-Szanto, Joseph R Testa
Malignant mesothelioma (MM) is a therapy-resistant cancer arising primarily from the lining of the pleural and peritoneal cavities. The most frequently altered genes in human MM are cyclin-dependent kinase inhibitor 2A (CDKN2A), which encodes components of the p53 (p14ARF) and RB (p16INK4A) pathways, BRCA1-associated protein 1 (BAP1), and neurofibromatosis 2 (NF2). Furthermore, the p53 gene (TP53) itself is mutated in ~15% of MMs. In many MMs, the PI3K-PTEN-AKT-mTOR signaling node is hyperactivated, which contributes to tumor cell survival and therapeutic resistance...
June 15, 2018: Journal of Cellular Physiology
Aaron M Goodman, David Piccioni, Shumei Kato, Amélie Boichard, Huan-You Wang, Garrett Frampton, Scott M Lippman, Caitlin Connelly, David Fabrizio, Vincent Miller, Jason K Sicklick, Razelle Kurzrock
Importance: Copy number alterations in programmed cell death ligand 1 (PDL1 or CD274), programmed cell death 1 ligand 2 (PDCD1LG2 or PDL2), and Janus kinase 2 (JAK2) genes (chromosome 9p24.1) characterize Hodgkin lymphoma, resulting in high response rates to programmed cell death 1 (PD-1)/programmed cell death ligand 1 (PD-L1) blockade. The prevalence and utility of PDL1 amplification as a response biomarker to PD-1/PD-L1 blockade are unknown in other tumors. Objectives: To examine the prevalence of PDL1 amplification and its utility as a response biomarker to PD-1/PD-L1 blockade in solid tumors...
June 14, 2018: JAMA Oncology
Yu Jiang, Gang Liu, Li Zhang, Sheng Cheng, Chun Luo, Yang Liao, Shuliang Guo
The aim of the present study was to investigate the effects of combination therapy of LY294002, a specific inhibitor of phosphatidylinositol 3‑kinase (PI3K), with hydrogen‑rich saline on the proliferation and apoptosis of the non‑small cell lung cancer (NSCLC) A549 cell line and the mechanisms underpinning this. Excessive production of reactive oxygen species (ROS) may induce DNA mutations, DNA damage, genomic instability and cell proliferation, and ROS are involved in several types of cancer, particularly lung cancer...
June 14, 2018: Molecular Medicine Reports
Emilio Lecona, Oscar Fernandez-Capetillo
The chemical treatment of cancer started with the realization that DNA damaging agents such as mustard gas present notable antitumoural properties. Consequently, early drug development focused on genotoxic chemicals, some of which are still widely used in the clinic. However, the efficacy of such therapies is often limited by the side effects of these drugs on healthy cells. A refinement to this approach is to use compounds that can exploit the presence of DNA damage in cancer cells. Given that replication stress (RS) is a major source of genomic instability in cancer, targeting the RS-response kinase ataxia telangiectasia and Rad3-related protein (ATR) has emerged as a promising alternative...
June 13, 2018: Nature Reviews. Cancer
Keiichi Hatakeyama, Takeshi Nagashima, Kenichi Urakami, Keiichi Ohshima, Masakuni Serizawa, Sumiko Ohnami, Yuji Shimoda, Shumpei Ohnami, Koji Maruyama, Akane Naruoka, Yasuto Akiyama, Masatoshi Kusuhara, Tohru Mochizuki, Ken Yamaguchi
Tumor mutational burden (TMB) is an emerging characteristic in cancer and has been associated with microsatellite instability, defective DNA replication/repair, and response to PD-1 and PD-L1 blockade immunotherapy. When estimating TMB, targeted panel sequencing is performed using a few hundred genes; however, a comparison of TMB results obtained with this platform and with whole exome sequencing (WES) has not been performed for various cancer types. In the present study, we compared TMB results using the above two platforms in 2,908 solid tumors that were obtained from Japanese patients...
2018: Biomedical Research
Yong-Kook Kang
In human cancers, histone methyltransferase SETDB1 (SET domain, bifurcated 1) is frequently overexpressed but its significance in carcinogenesis remains elusive. A recent study shows that SETDB1 downregulation induces de-repression of retroelements and innate immunity in cancer cells. The possibility of SETDB1 functioning as a surveillant of retroelement expression is discussed in this study: the cytoplasmic presence of retroelement-derived nucleic acids (RdNAs) drives SETDB1 into the nucleus by the RNA-interference route, rendering the corresponding retroelement transcriptionally inert...
June 13, 2018: BioEssays: News and Reviews in Molecular, Cellular and Developmental Biology
Georgia Velimezi, Lydia Robinson-Garcia, Francisco Muñoz-Martínez, Wouter W Wiegant, Joana Ferreira da Silva, Michel Owusu, Martin Moder, Marc Wiedner, Sara Brin Rosenthal, Kathleen M Fisch, Jason Moffat, Jörg Menche, Haico van Attikum, Stephen P Jackson, Joanna I Loizou
Defects in DNA repair can cause various genetic diseases with severe pathological phenotypes. Fanconi anemia (FA) is a rare disease characterized by bone marrow failure, developmental abnormalities, and increased cancer risk that is caused by defective repair of DNA interstrand crosslinks (ICLs). Here, we identify the deubiquitylating enzyme USP48 as synthetic viable for FA-gene deficiencies by performing genome-wide loss-of-function screens across a panel of human haploid isogenic FA-defective cells (FANCA, FANCC, FANCG, FANCI, FANCD2)...
June 11, 2018: Nature Communications
Carine Pecqueux, Aysenur Arslan, Martina Heller, Michael Falkenstein, Adam Kaczorowski, Yanis Tolstov, Holger Sültmann, Carsten Grüllich, Esther Herpel, Anette Duensing, Glen Kristiansen, Markus Hohenfellner, Nora M Navone, Stefan Duensing
BACKGROUND: There is mounting evidence to suggest that stromal cells play an integral role in the progression of prostate cancer (PCa). One of the most frequently altered growth factors in PCa is fibroblast growth factor-2 (FGF-2). It has previously been proposed that early stages of PCa are characterized by a primarily exogenous, that is, stromal cell-derived FGF-2 production, whereas advanced tumors rely more on an autocrine FGF-2 production. Prostate cancer progression is characterized by an increase of genomic instability including aneuploidy and structural chromosomal alterations...
June 7, 2018: Urologic Oncology
Xiaonian Zhu, Zhigang Wang, Xiaoqiang Qiu, Weiwei Wang, Chunhua Bei, Chao Tan, Linyuan Qin, Yuan Ren, Shengkui Tan
The defects of DNA repair genes may lead to genomic instability and cancer. As an important DNA mismatch repair gene that maintains genomic stability from DNA replication errors, genetic variants of mutS homolog 2 (MSH2) are associated with some cancers. In this study, 1021 hepatocellular carcinoma (HCC) cases and 1021 non-HCC controls from Guangxi were included to explore the association between MSH2 single-nucleotide polymorphisms (SNPs) and HCC. Among the eight MSH2 SNPs, only genotype distribution of rs2303428 was significantly different from HCC and non-HCC patients (p < 0...
June 6, 2018: DNA and Cell Biology
Le-Xing Yu, Yan Ling, Hong-Yang Wang
Hepatocellular carcinoma (HCC) has become a leading cause of cancer-related death, making the elucidation of its underlying mechanisms an urgent priority. Inflammation is an adaptive response to infection and tissue injury under strict regulations. When the host regulatory machine runs out of control, nonresolving inflammation occurs. Nonresolving inflammation is a recognized hallmark of cancer that substantially contributes to the development and progression of HCC. The HCC-associated inflammation can be initiated and propagated by extrinsic pathways through activation of pattern-recognition receptors (PRRs) by pathogen-associated molecule patterns (PAMPs) derived from gut microflora or damage-associated molecule patterns (DAMPs) released from dying liver cells...
2018: NPJ Precision Oncology
Huihong Zeng, Gayani K Nanayakkara, Ying Shao, Hangfei Fu, Yu Sun, Ramon Cueto, William Y Yang, Qian Yang, Haitao Sheng, Na Wu, Luqiao Wang, Wuping Yang, Hongping Chen, Lijian Shao, Jianxin Sun, Xuebin Qin, Joon Y Park, Konstantinos Drosatos, Eric T Choi, Qingxian Zhu, Hong Wang, Xiaofeng Yang
Under inflammatory conditions, inflammatory cells release reactive oxygen species (ROS) and reactive nitrogen species (RNS) which cause DNA damage. If not appropriately repaired, DNA damage leads to gene mutations and genomic instability. DNA damage checkpoint factors (DDCF) and DNA damage repair factors (DDRF) play a vital role in maintaining genomic integrity. However, how DDCFs and DDRFs are modulated under physiological and pathological conditions are not fully known. We took an experimental database analysis to determine the expression of 26 DNA DD C Fs and 42 DNA DD R Fs in 21 human and 20 mouse tissues in physiological/pathological conditions...
2018: Frontiers in Physiology
Mohamed E Salem, Alberto Puccini, Joanne Xiu, Derek Raghavan, Heinz-Josef Lenz, W Michael Korn, Anthony F Shields, Philip A Philip, John L Marshall, Richard M Goldberg
BACKGROUND: Gastroesophageal cancers are often grouped together even though cancers that originate in the esophagus often exhibit different histological features, geographical distribution, risk factors, and clinical characteristics than those originating in the stomach. Herein, we aimed to compare the molecular characteristics of three different gastroesophageal cancer types: esophageal squamous cell carcinoma (ESCC), esophageal adenocarcinoma (EAC), and gastric adenocarcinoma (GAC)...
June 4, 2018: Oncologist
Shinji Tanaka
Accumulated evidence suggests that multiple molecular and cellular interactions promote cancer evolution in vivo. Surgical oncology is of growing significance to a comprehensive understanding of the malignant diseases for therapeutic application. We have analyzed more than 1000 clinical samples from surgically resected tissue to identify molecular biomarkers and therapeutic targets for advanced malignancies. Cancer stemness and mitotic instability were then determined as the essential predictors of aggressive phenotype with poor prognosis...
March 2018: Annals of gastroenterological surgery
Mayuko Furuta, Hiroko Tanaka, Yuichi Shiraishi, Takuro Unida, Michio Imamura, Akihiro Fujimoto, Masahi Fujita, Aya Sasaki-Oku, Kazuhiro Maejima, Kaoru Nakano, Yoshiiku Kawakami, Koji Arihiro, Hiroshi Aikata, Masaki Ueno, Shinya Hayami, Shun-Ichi Ariizumi, Masakazu Yamamoto, Kunihito Gotoh, Hideki Ohdan, Hiroki Yamaue, Satoru Miyano, Kazuaki Chayama, Hidewaki Nakagawa
Integration of Hepatitis B virus (HBV) into the human genome can cause genetic instability, leading to selective advantages for HBV-induced liver cancer. Despite the large number of studies for HBV integration into liver cancer, little is known about the mechanism of initial HBV integration events owing to the limitations of materials and detection methods. We conducted an HBV sequence capture, followed by ultra-deep sequencing, to screen for HBV integrations in 111 liver samples from human-hepatocyte chimeric mice with HBV infection and human clinical samples containing 42 paired samples from non-tumorous and tumorous liver tissues...
May 18, 2018: Oncotarget
Quan Zhu, Nien Hoong, Aaron Aslanian, Toshiro Hara, Christopher Benner, Sven Heinz, Karen H Miga, Eugene Ke, Sachin Verma, Jan Soroczynski, John R Yates, Tony Hunter, Inder M Verma
Heterochromatic repetitive satellite RNAs are extensively transcribed in a variety of human cancers, including BRCA1 mutant breast cancer. Aberrant expression of satellite RNAs in cultured cells induces the DNA damage response, activates cell cycle checkpoints, and causes defects in chromosome segregation. However, the mechanism by which satellite RNA expression leads to genomic instability is not well understood. Here we provide evidence that increased levels of satellite RNAs in mammary glands induce tumor formation in mice...
June 7, 2018: Molecular Cell
Yuki Tanoue, Takeshi Toyoda, Jinghua Sun, Md Kawsar Mustofa, Chie Tateishi, Shinya Endo, Noboru Motoyama, Kimi Araki, Di Wu, Yutaka Okuno, Tetsuya Tsukamoto, Motohiro Takeya, Hironobu Ihn, Cyrus Vaziri, Satoshi Tateishi
Defects in DNA polymerase Eta (Polη) cause the sunlight-sensitivity and skin cancer-propensity disorder xeroderma pigmentosum variant (XP-V). The extent to which Polη function depends on the upstream E3 ubiquitin ligase Rad18 is controversial and has not been investigated using mouse models. Therefore, we tested the role of Rad18 in UV-inducible skin tumorigenesis. Because Rad18-deficiency leads to compensatory DNA damage signaling by Chk2, we also investigated genetic interactions between Rad18 and Chk2 in vivo...
May 31, 2018: Journal of Investigative Dermatology
Giacomo Diaz, Ronald E Engle, Ashley Tice, Marta Melis, Stephanie Montenegro, Jaime Rodriguez-Canales, Jeffrey Hanson, Michael R Emmert-Buck, Kevin W Bock, Ian N Moore, Fausto Zamboni, Sugantha Govindarajan, David Kleiner, Patrizia Farci
There is limited data on the molecular mechanisms whereby hepatitis D virus (HDV) promotes liver cancer. Therefore, serum and liver specimens obtained at the time of liver transplantation from well-characterized patients with HDV-HCC (n-5) and with non-HCC HDV cirrhosis (n=7) were studied using an integrated genomic approach. Transcriptomic profiling was performed using laser capture-microdissected (LCM) malignant and non-malignant hepatocytes, tumorous and non-tumorous liver tissue from patients with HDV-HCC, and liver tissue from patients with non-HCC HDV cirrhosis...
June 1, 2018: Molecular Cancer Research: MCR
Sergej Skvortsov, Ira-Ida Skvortsova, Dean G Tang, Anna Dubrovska
Prostate cancer (PCa) is heterogeneous harboring phenotypically diverse cancer cell types. PCa cell heterogeneity is caused by genomic instability that leads to the clonal competition and evolution of the cancer genome, and by epigenetic mechanisms that result in subclonal cellular differentiation. The process of tumor cell differentiation is initiated from a population of prostate cancer stem cells (PCSCs) that possess many phenotypic and functional properties of normal stem cells. Since the initial reports on PCSCs in 2005, there has been much effort to elucidate their biological properties including unique metabolic characteristics...
May 30, 2018: Stem Cells
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