Mutation Research-Reviews in Mutation Research最新文献

{"title":"Lymphocyte micronuclei frequencies in skin, haematological, prostate, colorectal and esophageal cancer cases: A systematic review and meta-analysis","authors":"Varinderpal S. Dhillon ,&nbsp;Permal Deo ,&nbsp;Stefano Bonassi ,&nbsp;Michael Fenech","doi":"10.1016/j.mrrev.2021.108372","DOIUrl":"10.1016/j.mrrev.2021.108372","url":null,"abstract":"<div><p><span>Micronucleus (MN) assay has been widely used as a biomarker of DNA damage, chromosomal instability, cancer risk and accelerated aging in many epidemiological studies. In this narrative review and meta-analysis we assessed the association between lymphocyte micronuclei (MNi) and cancers of the skin, blood, digestive tract, and prostate. The review identified nineteen studies with 717 disease subjects and 782 controls. Significant increases in MRi for MNi were observed in the following groups: subjects with blood cancer (MRi = 3.98; 95 % CI: 1.98–7.99; p = 0.000) and </span>colorectal cancer (excluding IBD) (MRi = 2.69; 95 % CI: 1.82–3.98, p &lt; 0.000). The results of this review suggest that lymphocyte MNi are a biomarker of DNA damage and chromosomal instability in people with haematological or colorectal cancers. However, the MRi for lymphocyte MNi in subjects with cancers of skin, prostate, esophagus was not significantly increased. More case-control and prospective studies are warranted to further verify the observed trends and to better understand the role of lymphocyte MNi as a biomarker of cancer risk in blood, skin, digestive tract and prostate.</p></div>","PeriodicalId":49789,"journal":{"name":"Mutation Research-Reviews in Mutation Research","volume":"787 ","pages":"Article 108372"},"PeriodicalIF":5.3,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.mrrev.2021.108372","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10637853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bruce Nathan Ames - Paradigm shifts inside the cancer research revolution","authors":"Carr J. Smith ,&nbsp;Thomas A. Perfetti ,&nbsp;Sir Colin Berry ,&nbsp;Douglas E. Brash ,&nbsp;James Bus ,&nbsp;Edward Calabrese ,&nbsp;Roger A. Clemens ,&nbsp;John R. Jack Fowle III ,&nbsp;Helmut Greim ,&nbsp;James T. MacGregor ,&nbsp;Robert Maronpot ,&nbsp;Peter Pressman ,&nbsp;Errol Zeiger ,&nbsp;A. Wallace Hayes","doi":"10.1016/j.mrrev.2020.108363","DOIUrl":"10.1016/j.mrrev.2020.108363","url":null,"abstract":"<div><p><span>Dr. Bruce Ames turned 92 on December 16, 2020. He considers his most recent work linking adequate consumption of 30 known vitamins and minerals with successful aging to be his most important contribution. With the passage of time, it is not uncommon for the accomplishments of a well-known scientist to undergo a parsimonious reductionism in the public mind - Pasteur’s vaccine, Mendel’s peas, Pavlov’s dogs, Ames’ test. Those of us in the research generation subsequent to Dr. Ames’ are undoubtedly affected by our own unconscious tendencies toward accepting the outstanding achievements of the past as commonplace. In doing so, seminal advances made by earlier investigators are often inadvertently subsumed into common knowledge. But having followed Ames’ work since the mid-1970s, we are cognizant that the eponymous Ames Test is but a single chapter in a long and rich narrative. That narrative begins with Ames' classic studies on the histidine operon of </span><em>Salmonella</em>, for which he was elected to the National Academy of Sciences.</p><p>A summary of the historical progression of the understanding of chemical carcinogenesis<span> to which Ames and his colleagues contributed is provided. Any summary of a topic as expansive and complex as the ongoing unraveling of the mechanisms underlying chemical carcinogenesis will only touch upon some of the major conceptual advances to which Ames and his colleagues contributed. We hope that scientists of all ages familiar with Ames only through the eponymous Ames Test will further investigate the historical progression of the conceptualization of cancer caused by chemical exposure. As the field of chemical carcinogenesis gradually moves away from primary reliance on animal testing to alternative protocols under the rubric of New Approach Methodologies (NAM) an understanding of where we have been might help to guide where we should go.</span></p></div>","PeriodicalId":49789,"journal":{"name":"Mutation Research-Reviews in Mutation Research","volume":"787 ","pages":"Article 108363"},"PeriodicalIF":5.3,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.mrrev.2020.108363","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39058069","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Micronuclei and upper body cancers (head, neck, breast cancers) a systematic review and meta-analysis","authors":"Claudia Bolognesi ,&nbsp;Marco Bruzzone ,&nbsp;Marcello Ceppi ,&nbsp;Francesca Marcon","doi":"10.1016/j.mrrev.2020.108358","DOIUrl":"10.1016/j.mrrev.2020.108358","url":null,"abstract":"<div><p>A systematic review and a meta-analysis were performed on 19 studies on head and neck cancer<span> (HNC) and 21 studies on breast cancer (BC) to evaluate the application of micronucleus (MN) assay as a predictive and prognostic test for cancer risk. In these studies the MN test was applied in peripheral lymphocytes and buccal cells of patients and healthy subjects with family history of cancer. The meta-analysis on MN applied in buccal cells of HNC patients was performed on two subgroups of studies. A significant increase of MN frequency in patients compared to healthy controls was observed for the subgroup on oral cancer (243 cases/370 controls, meta-MR = 4.71 95 %CI:2.75–8.06) and HNC (204 patients/163 controls metaMR=2.28 95 %CI:2.02–2.58). A metaMR = 3.27 (95 %CI:1.41–7.59) was obtained for MN applied in peripheral lymphocytes on HNC (160 cases/160 controls). For BC, the analysis of MN in peripheral lymphocytes showed significantly higher values in patients (n = 761) than in controls (n = 788) (meta-MR1.90 95 % CI:1.44–2.49). No statistically significant increase of baseline MN was detected in studies on groups of healthy subjects with BC family history (n = 224) or with BRCA1/2 mutations (n = 101) with respect to the controls. After ex-vivo challenge with ionizing radiation, the meta-analysis revealed a slightly statistically significant increase in MN only in BC patients (n = 614) compared to controls (n = 622)(meta-MR = 1.11 95 %CI:1.02–1.21); no increase was observed in healthy subjects with BC family history carrying or not BRCA1/2 mutations. Significant difference between BC patients (n = 183) and controls (n = 165) was observed by the meta-analysis of data on MN in buccal cells (MR = 3.89 95 %CI:1.54–9.78). The MN assay in buccal cells has some perspective of clinical application in HNC.</span></p></div>","PeriodicalId":49789,"journal":{"name":"Mutation Research-Reviews in Mutation Research","volume":"787 ","pages":"Article 108358"},"PeriodicalIF":5.3,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.mrrev.2020.108358","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39074425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role and potential clinical utility of ARID1A in gastrointestinal malignancy","authors":"Ruihua Wang ,&nbsp;Mei Chen ,&nbsp;Xiaojun Ye ,&nbsp;Karen Poon","doi":"10.1016/j.mrrev.2020.108360","DOIUrl":"10.1016/j.mrrev.2020.108360","url":null,"abstract":"<div><p><em>ARID1A</em><span> (AT-rich interactive domain 1A) is a newly discovered tumor suppressor gene<span>, and its encoded product is an important component of the SWI/SNF chromatin remodeling complex. </span></span><em>ARID1A</em><span><span><span> plays an important role in cell proliferation, invasion and metastasis, apoptosis, </span>cell cycle regulation, </span>epithelial mesenchymal transition, and the regulation of other of biological behaviors. Recently, </span><em>ARID1A</em><span> mutations have been increasingly reported in esophageal adenocarcinoma<span><span>, gastric cancer, colorectal cancer<span>, hepatocellular carcinoma, </span></span>cholangiocarcinoma<span>, pancreatic cancer, and other malignant tumors of the digestive system. This article reviews the relationship between </span></span></span><em>ARID1A</em><span><span> mutation and the molecular mechanisms of carcinogenesis, including microsatellite instability and the PI3K/ATK </span>signaling pathway, and relates these mechanisms to the prognostic assessment of digestive malignancy. Further, this review describes the potential for molecular pathologic epidemiology (MPE) to provide new insights into environment-tumor-host interactions.</span></p></div>","PeriodicalId":49789,"journal":{"name":"Mutation Research-Reviews in Mutation Research","volume":"787 ","pages":"Article 108360"},"PeriodicalIF":5.3,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.mrrev.2020.108360","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39074426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of epigenetic mechanisms in propagating off-targeted effects following radiation based therapies – A review","authors":"Swati,&nbsp;Vijayta D. Chadha","doi":"10.1016/j.mrrev.2021.108370","DOIUrl":"10.1016/j.mrrev.2021.108370","url":null,"abstract":"<div><p>Despite being an important diagnostic and treatment modality, ionizing radiation (IR) is also known to cause genotoxicity and multiple side effects leading to secondary carcinogenesis. While modern cancer radiation therapy has improved patient recovery and enhanced survival rates, the risk of radiation-related adverse effects has become a growing challenge. It is now well-accepted that IR-induced side effects are not exclusively restricted to exposed cells but also spread to distant ‘bystander’ cells and even to the unexposed progeny of the irradiated cells. These ‘off-targeted’ effects involve a plethora of molecular events depending on the type of radiation and tumor tissue background. While the mechanisms by which off-targeted effects arise remain obscure, emerging evidence based on the non-mendelian inheritance of various manifestations of them as well as their persistence for longer periods supports a contribution of epigenetic factors. This review focuses on the major epigenetic phenomena including DNA methylation, histone modifications, and small RNA mediated silencing and their versatile role in the manifestation of IR induced off-targeted effects. As short- and long-range communication vehicles respectively, the role of gap junctions and exosomes in spreading these epigenetic-alteration driven off-targeted effects is also discussed. Furthermore, this review emphasizes the possible therapeutic potentials of these epigenetic mechanisms and how beneficial outcomes could potentially be achieved by targeting various signaling molecules involved in these mechanisms.</p></div>","PeriodicalId":49789,"journal":{"name":"Mutation Research-Reviews in Mutation Research","volume":"787 ","pages":"Article 108370"},"PeriodicalIF":5.3,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.mrrev.2021.108370","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39059055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The pathways related to glutamine metabolism, glutamine inhibitors and their implication for improving the efficiency of chemotherapy in triple-negative breast cancer","authors":"Soheila Delgir ,&nbsp;Milad Bastami ,&nbsp;Khandan Ilkhani ,&nbsp;Asma Safi ,&nbsp;Farhad Seif ,&nbsp;Mohammad Reza Alivand","doi":"10.1016/j.mrrev.2021.108366","DOIUrl":"10.1016/j.mrrev.2021.108366","url":null,"abstract":"<div><p>Breast cancer (BC) is a heterogeneous cancer with multiple subtypes affecting women worldwide. Triple-negative breast cancer (TNBC) is a prominent subtype of BC with poor prognosis and an aggressive phenotype. Recent understanding of metabolic reprogramming supports its role in the growth of cancer cells and their adaptation to their microenvironment. The Warburg effect is characterized by the shift from oxidative to reductive metabolism and external secretion of lactate. The Warburg effect prevents the use of the required pyruvate in the tricarboxylic acid (TCA) cycle progressing through pyruvate dehydrogenase inactivation. Therefore, it is a major regulatory mechanism to promote glycolysis and disrupt the TCA cycle. Glutamine (Gln) can supply the complementary energy for cancer cells. Additionally, it is the main substrate to support bioenergetics and biosynthetic activities in cancer cells and plays a vital role in a wide array of other processes such as ferroptosis. Thus, the switching of glucose to Gln in the TCA cycle toward reductive Gln metabolism is carried out by hypoxia-inducible factors (HIFs) conducted through the Warburg effect. The literature suggests that the addiction of TNBC to Gln could facilitate the proliferation and invasiveness of these cancers. Thus, Gln metabolism inhibitors, such as CB-839, could be applied to manage the carcinogenic properties of TNBC. Such inhibitors, along with conventional chemotherapy agents, can potentially improve the efficiency and efficacy of TNBC treatment. In this review, we discuss the associations between glucose and Gln metabolism and control of cancer cell growth from the perspective that Gln metabolism inhibitors could improve the current chemotherapy drug effects.</p></div>","PeriodicalId":49789,"journal":{"name":"Mutation Research-Reviews in Mutation Research","volume":"787 ","pages":"Article 108366"},"PeriodicalIF":5.3,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.mrrev.2021.108366","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39058944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Micronucleus assay for predicting coronary artery disease: A systematic review and meta-analysis","authors":"Maria Grazia Andreassi,&nbsp;Andrea Borghini,&nbsp;Cecilia Vecoli","doi":"10.1016/j.mrrev.2020.108348","DOIUrl":"10.1016/j.mrrev.2020.108348","url":null,"abstract":"<div><p><span>Coronary artery disease (CAD) is the leading cause of morbidity and mortality worldwide. Coronary </span>angiography allows an accurate assessment of the extent and severity of atherosclerotic coronary narrowing, but it provides little characterization of early detection of potentially asymptomatic vulnerable plaque. The identification of the coronary “vulnerable patient” or high-risk plaques remains a major challenge in the treatment of CAD.</p><p><span>Recently, growing evidence shows that DNA damage plays a role in the initiation and progression of atherosclerotic plaque. Cytokinesis-block micronucleus (CBMN) assay is one of the most frequently used and validated method for assessing chromosomal damage and genetic instability. Accordingly, the purpose of this systematic review was to retrieve and discuss existing literature on the studies assessing the association between MN and angiographically-proven CAD. A total of 8 studies published between 2001 and 2017 were included in the meta-analysis. Despite a large heterogeneity between studies (I</span>²<span>= 99.7 %, p &lt; 0.0001), an overall increase of MN frequencies was found in patients with CAD compared with control group (meta-MR = 1.96; 95 % CI, 1.5–3.2, p = 0.009). A subgroup analysis showed an increase in the frequency of MN formation for both two- vessel (MR = 2.13, 95 % CI: 0.9–6.9, p = 0.08) and three-vessel disease (MR = 2.89, 95 % CI: 1.84–4.55, P = 0.06). Overall, the results of this meta-analysis provide evidence of an association between CBMN and presence, extent and severity of angiographically-assessed CAD. However, the small number of papers analyzed requires further large and more rigorously designed studies, carefully considering a series of clinical confounding factors, such as the quality of the metabolic control, the influence of drugs and radiation imaging treatments.</span></p></div>","PeriodicalId":49789,"journal":{"name":"Mutation Research-Reviews in Mutation Research","volume":"787 ","pages":"Article 108348"},"PeriodicalIF":5.3,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.mrrev.2020.108348","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39074430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A review of the genotoxicity of the industrial chemical cumene","authors":"B. Bhaskar Gollapudi ,&nbsp;Amy L. Williams,&nbsp;James S. Bus","doi":"10.1016/j.mrrev.2021.108364","DOIUrl":"10.1016/j.mrrev.2021.108364","url":null,"abstract":"<div><p>The purpose of this review is to evaluate the literature on the genotoxicity of cumene (CAS # 98−82-8) and to assess the role of mutagenicity, if any, in the mode of action for cumene-induced rodent tumors. The studies reviewed included microbial mutagenicity, DNA damage/ repair, cytogenetic effects, and gene mutations. In reviewing these studies, attention was paid to their conformance to applicable OECD test guidelines which are considered as internationally recognized standards for performing these assays. Cumene was not a bacterial mutagen and did not induce <em>Hprt</em> mutations in CHO cell cultures. In the primary rat hepatocyte cultures, cumene induced unscheduled DNA synthesis in one study but this response could not be reproduced in an independent study using a similar protocol. In a study that is not fully compliant to the current OECD guideline, no increase in chromosomal aberrations was observed in CHO cells treated with cumene. The weight of the evidence (WoE) from multiple <em>in vivo</em> studies indicates that cumene is not a clastogen or aneugen. The weak positive response in an <em>in vivo</em> comet assay in the rat liver and mouse lung tissues is of questionable significance due to several study deficiencies. The genotoxicity profile of cumene does not match that of a classic DNA-reactive molecule and the available data does not support a conclusion that cumene is an <em>in vivo</em> mutagen. As such, mutagenicity does not appear to be an early key event in cumene-induced rodent tumors and alternate hypothesized non-mutagenic modes-of-action are presented. Further data are necessary to rule in or rule out a particular MoA.</p></div>","PeriodicalId":49789,"journal":{"name":"Mutation Research-Reviews in Mutation Research","volume":"787 ","pages":"Article 108364"},"PeriodicalIF":5.3,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.mrrev.2021.108364","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39059053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genomic instability in chronic obstructive pulmonary disease and lung cancer: A systematic review and meta-analysis of studies using the micronucleus assay","authors":"Maxim Asanov ,&nbsp;Stefano Bonassi ,&nbsp;Stefania Proietti ,&nbsp;Varvara I. Minina ,&nbsp;Carlo Tomino ,&nbsp;Randa El-Zein","doi":"10.1016/j.mrrev.2020.108344","DOIUrl":"10.1016/j.mrrev.2020.108344","url":null,"abstract":"<div><p><span>Respiratory tissues are highly susceptible to diseases due to the constant exposure to physical and chemical airborne pollutants. Chronic obstructive pulmonary disease (COPD) and lung cancer are among the most common causes of serious illness and death worldwide. The inflammatory environment associated with these respiratory diseases has long been accepted as the major player in the development of airway abnormalities. The presence and relevance of DNA damage and genomic instability makes the micronucleus assay a suitable candidate to quantitatively estimate these early pathogenetic events. A systematic review and meta-analysis were planned to determine underlying common mechanisms that can explain the relationships between COPD and lung cancer. A total of 17 studies from Jan 1999 to Dec 2019 comparing micronucleus frequency in patients affected by respiratory diseases </span><em>vs</em> healthy controls were analysed. Our results confirmed the presence of significant association between MN frequency and the diseases investigated, and suggested a circle of events linking inflammation induced oxidative stress to the risk of disease through genomic instability and hypoxia. Therefore, using non-invasive, robust and cost effective genomic instability assays such as the micronucleus assay, would allow us to capture unique phenotypic and biological changes that would allow the identification of subjects at high risk of developing lung diseases and improve early detection strategies.</p></div>","PeriodicalId":49789,"journal":{"name":"Mutation Research-Reviews in Mutation Research","volume":"787 ","pages":"Article 108344"},"PeriodicalIF":5.3,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.mrrev.2020.108344","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39074428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Histone methylation can either promote or reduce cellular radiosensitivity by regulating DNA repair pathways","authors":"Yuchuan Zhou,&nbsp;Chunlin Shao","doi":"10.1016/j.mrrev.2020.108362","DOIUrl":"10.1016/j.mrrev.2020.108362","url":null,"abstract":"<div><p>Radiotherapy is one of the primary modalities for cancer treatment, and its efficiency usually relies on cellular radiosensitivity. DNA damage repair is a core content of cellular radiosensitivity, and the primary mechanism of which includes non-homologous end-joining (NHEJ) and homologous recombination (HR). By affecting DNA damage repair, histone methylation regulated by histone methyltransferases (HMTs) and histone demethylases (HDMs) participates in the regulation of cellular radiosensitivity via three mechanisms: (a) recruiting DNA repair-related proteins, (b) regulating the expressions of DNA repair genes, and (c) mediating the dynamic change of chromatin. Interestingly, both aberrantly high and low levels of histone methylation could impede DNA repair processes. Here we reviewed the mechanisms of the dual effects of histone methylation on cell response to radiation. Since some inhibitors of HMTs and HDMs are reported to increase cellular radiosensitivity, understanding their molecular mechanisms may be helpful in developing new drugs for the therapy of radioresistant tumors.</p></div>","PeriodicalId":49789,"journal":{"name":"Mutation Research-Reviews in Mutation Research","volume":"787 ","pages":"Article 108362"},"PeriodicalIF":5.3,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.mrrev.2020.108362","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39074431","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}