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Human papillomavirus molecular biology. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2017-05-23 Mallory E Harden,Karl Munger
Human papillomaviruses are small DNA viruses with a tropism for squamous epithelia. A unique aspect of human papillomavirus molecular biology involves dependence on the differentiation status of the host epithelial cell to complete the viral lifecycle. A small group of these viruses are the etiologic agents of several types of human cancers, including oral and anogenital tract carcinomas. This review
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Insulin-like growth factor (IGF) axis in cancerogenesis. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2017-05-23 Aldona Kasprzak,Wojciech Kwasniewski,Agnieszka Adamek,Anna Gozdzicka-Jozefiak
Determination of the role of insulin-like growth factor (IGF) family components in carcinogenesis of several human tumors is based on numerous epidemiological and pre-clinical studies, experiments in vivo and in vitro and on attempts at application of drugs affecting the IGF axis. Investigative hypotheses in original studies were based on biological functions manifested by the entire family of IGF
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The IGF axis in HPV associated cancers. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2017-05-23 Adam Pickard,Julia Durzynska,Dennis J McCance,Elisabeth R Barton
Human papillomaviruses (HPV) infect and replicate in stratified epithelium at cutaneous and mucosal surfaces. The proliferation and maintenance of keratinocytes, the cells which make up this epithelium, are controlled by a number of growth factor receptors such as the keratinocyte growth factor receptor (KGFR, also called fibroblast growth factor receptor 2b (FGFR2b)), the epithelial growth factor
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Clinical relevance and implications of HPV-induced neoplasia in different anatomical locations. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2017-05-23 Elena Sophie Prigge,Magnus von Knebel Doeberitz,Miriam Reuschenbach
Human papillomaviruses (HPV) are widespread DNA viruses that can infect epithelial cells of the skin and mucosa. Most HPV infections remain clinically unapparent and clear spontaneously. In few cases, however, HPV infections persist and can cause benign and malignant neoplasms at different anatomic locations. Malignant HPV-induced neoplasms are caused by distinct types of HPV (oncogenic or high-risk
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HPV entry into cells. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2017-05-23 Pinar Aksoy,Elinor Y Gottschalk,Patricio I Meneses
Human papillomavirus (HPV) is a sexually transmitted virus responsible for the development of cervical cancer, anal cancer, head and throat cancers, as well as genital area warts. A major focus of current HPV research is on preventing the virus from entering a cell and transferring its genetic material to the nucleus, thus potentially preventing the development of cancer. Although the available HPV
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Human papillomaviruses in epigenetic regulations. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2017-05-23 Julia Durzynska,Krzysztof Lesniewicz,Elzbieta Poreba
Human Papillomaviruses (HPVs) are double-stranded DNA viruses, that infect epithelial cells and are etiologically involved in the development of human cancer. Today, over 200 types of human papillomaviruses are known. They are divided into low-risk and high-risk HPVs depending on their potential to induce carcinogenesis, driven by two major viral oncoproteins, E6 and E7. By interacting with cellular
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Molecular mechanisms underlying human papillomavirus E6 and E7 oncoprotein-induced cell transformation. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2017-05-23 Suruchi Mittal,Lawrence Banks
Human papillomaviruses (HPVs) are the causative agents of 5% of all human cancers, with cervical cancer being the most important. Two viral oncoproteins, E6 and E7, are essential for the development and maintenance of malignancy. Both proteins function by targeting critical pathways that are essential for maintaining cellular homeostasis. As a consequence of these activities, this produces an environment
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IGF-I deficiency, longevity and cancer protection of patients with Laron syndrome. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2017-05-23 Zvi Laron,Rivka Kauli,Lena Lapkina,Haim Werner
Laron syndrome (LS) is a unique model of congenital IGF-I deficiency. It is characterized by dwarfism and obesity, and is caused by deletion or mutations of the growth hormone receptor (GH-R) gene. It is hypothesized that LS is an old disease originating in Indonesia and that the mutated gene spread to South Asia, the Middle East, the Mediterranean region and South America.
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Clinical studies in humans targeting the various components of the IGF system show lack of efficacy in the treatment of cancer. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2017-05-23 Anastassios Philippou,Panagiotis F Christopoulos,Dr Michael Koutsilieris
The insulin-like growth factors (IGFs) system regulates cell growth, differentiation and energy metabolism and plays crucial role in the regulation of key aspects of tumor biology, such as cancer cell growth, survival, transformation and invasion. The current focus for cancer therapeutic approaches have shifted from the conventional treatments towards the targeted therapies and the IGF system has gained
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Special Issue " HPV and IGF axis in carcinogenesis". Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2017-05-23 Julia Durzynska
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Mutations of myelodysplastic syndromes (MDS): An update. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2016-08-21 Bani Bandana Ganguly,N N Kadam
The plethora of knowledge gained on myelodysplastic syndromes (MDS), a heterogeneous pre-malignant disorder of hematopoietic stem cells, through sequencing of several pathway genes has unveiled molecular pathogenesis and its progression to AML. Evolution of phenotypic classification and risk-stratification based on peripheral cytopenias and blast count has moved to five-tier risk-groups solely concerning
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The ubiquitin family meets the Fanconi anemia proteins. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2016-08-21 Xavier Renaudin,Leticia Koch Lerner,Carlos Frederico Martins Menck,Filippo Rosselli
Fanconi anaemia (FA) is a hereditary disorder characterized by bone marrow failure, developmental defects, predisposition to cancer and chromosomal abnormalities. FA is caused by biallelic mutations that inactivate genes encoding proteins involved in replication stress-associated DNA damage responses. The 20 FANC proteins identified to date constitute the FANC pathway. A key event in this pathway involves
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DNA repair mechanisms and their clinical impact in glioblastoma. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2016-08-21 Hélène Erasimus,Matthieu Gobin,Simone Niclou,Eric Van Dyck
Despite surgical resection and genotoxic treatment with ionizing radiation and the DNA alkylating agent temozolomide, glioblastoma remains one of the most lethal cancers, due in great part to the action of DNA repair mechanisms that drive resistance and tumor relapse. Understanding the molecular details of these mechanisms and identifying potential pharmacological targets have emerged as vital tasks
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Functional Implications of the spectrum of BCL2 mutations in Lymphoma. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2016-08-21 Khushboo Singh,James M Briggs
Mutations in the translocated BCL2 gene are often detected in diffuse large B-cell lymphomas (DLBCLs), indicating both their significance and pervasiveness. Large series genome sequencing of more than 200 DLBCLs has identified frequent BCL2 mutations clustered in the exons coding for the BH4 domain and the folded loop domain (FLD) of the protein. However, BCL2 mutations are mostly contemplated to represent
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Role of nucleotide excision repair proteins in response to DNA damage induced by topoisomerase II inhibitors. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2016-05-29 Jaqueline C Rocha,Franciele F Busatto,Temenouga N Guecheva,Jenifer Saffi
In cancer treatment, chemotherapy is one of the main strategies used. The knowledge of the cellular and molecular characteristics of tumors allows the use of more specific drugs, making the removal of tumors more efficient. Among the drugs of choice in these treatments, topoisomerase inhibitors are widely used against different types of tumors. Topoisomerases are enzymes responsible for maintaining
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Y chromosome b2/b3 deletions and male infertility: A comprehensive meta-analysis, trial sequential analysis and systematic review. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2016-05-29 Sandeep Kumar Bansal,Gopal Gupta,Singh Rajender
The correlation of Y-chromosome b2/b3 partial deletions with spermatogenic failure remains dubious. We undertook a systematic review of the literature followed by meta-analyses and trial sequential analyses in order to compare the frequency of b2/b3 deletions between oligo/azoospermic infertile and normozoospermicmen. Out of twenty-four studies reviewed for meta-analysis, twenty reported no correlation
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Mechanisms of mutagenesis: DNA replication in the presence of DNA damage. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2016-05-29 Binyan Liu,Qizhen Xue,Yong Tang,Jia Cao,F Peter Guengerich,Huidong Zhang
Environmental mutagens cause DNA damage that disturbs replication and produces mutations, leading to cancer and other diseases. We discuss mechanisms of mutagenesis resulting from DNA damage, from the level of DNA replication by a single polymerase to the complex DNA replisome of some typical model organisms (including bacteriophage T7, T4, Sulfolobus solfataricus, Escherichia coli, yeast and human)
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Epigenetic alterations induced by genotoxic occupational and environmental human chemical carcinogens: A systematic literature review. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2016-05-29 Grace Chappell,Igor P Pogribny,Kathryn Z Guyton,Ivan Rusyn
Accumulating evidence suggests that epigenetic alterations play an important role in chemically-induced carcinogenesis. Although the epigenome and genome may be equally important in carcinogenicity, the genotoxicity of chemical agents and exposure-related transcriptomic responses have been more thoroughly studied and characterized. To better understand the evidence for epigenetic alterations of human
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The many faces of histone H3K79 methylation. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2016-05-29 Zeenat Farooq,Shahid Banday,Tej K Pandita,Mohammad Altaf
Dot1/DOT1L (disruptor of telomeric silencing-1) is an evolutionarily conserved histone methyltransferase that methylates lysine 79 located within the globular domain of histone H3. Dot1 was initially identified by a genetic screen as a disruptor of telomeric silencing in Saccharomyces cerevisiae; further, it is the only known non-SET domain containing histone methyltransferase. Methylation of H3K79
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Biomonitoring of genotoxic effects for human exposure to nanomaterials: The challenge ahead. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2016-05-29 Laetitia Gonzalez,Micheline Kirsch-Volders
Exposures to nanomaterials (NMs), with their specific physico-chemical characteristics, are likely to increase over the next years, as their production for industrial, consumer and medical applications is steadily rising. Therefore, there is an urgent need for the implementation of human biomonitoring studies of genotoxic effects after NM exposures in order to monitor and assure safety for workers
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Molecular genetics of the COL2A1-related disorders. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2016-05-29 Hao Deng,Xiangjun Huang,Lamei Yuan
Type II collagen, comprised of three identical alpha-1(II) chains, is the major collagen synthesized by chondrocytes, and is found in articular cartilage, vitreous humour, inner ear and nucleus pulposus. Mutations in the collagen type II alpha-1 gene (COL2A1) have been reported to be responsible for a series of abnormalities, known as type II collagenopathies. To date, 16 definite disorders, inherited
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Unraveling the mechanisms of extreme radioresistance in prokaryotes: Lessons from nature. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2016-04-03 Athanasia Pavlopoulou,Giannis D Savva,Maria Louka,Pantelis G Bagos,Constantinos E Vorgias,Ioannis Michalopoulos,Alexandros G Georgakilas
The last 50 years, a variety of archaea and bacteria able to withstand extremely high doses of ionizing radiation, have been discovered. Several lines of evidence suggest a variety of mechanisms explaining the extreme radioresistance of microorganisms found usually in isolated environments on Earth. These findings are discussed thoroughly in this study. Although none of the strategies discussed here
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Contributions of DNA repair and damage response pathways to the non-linear genotoxic responses of alkylating agents. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2016-04-03 Joanna Klapacz,Lynn H Pottenger,Bevin P Engelward,Christopher D Heinen,George E Johnson,Rebecca A Clewell,Paul L Carmichael,Yeyejide Adeleye,Melvin E Andersen
From a risk assessment perspective, DNA-reactive agents are conventionally assumed to have genotoxic risks at all exposure levels, thus applying a linear extrapolation for low-dose responses. New approaches discussed here, including more diverse and sensitive methods for assessing DNA damage and DNA repair, strongly support the existence of measurable regions where genotoxic responses with increasing
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The Comet assay in insects--Status, prospects and benefits for science. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2016-04-03 Maria Augustyniak,Marcin Gladysz,Marta Dziewięcka
The Comet assay has been recently adapted to investigate DNA damage in insects. The first reports of its use in Drosophila melanogaster appeared in 2002. Since then, the interest in the application of the Comet assay to studies of insects has been rapidly increasing. Many authors see substantial potential in the use of the Comet assay in D. melanogaster for medical toxicology studies. This application
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Enigmatic 5-hydroxymethyluracil: Oxidatively modified base, epigenetic mark or both? Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2016-04-03 Ryszard Olinski,Marta Starczak,Daniel Gackowski
The aim of this review is to describe the reactions which lead to generation of 5-hydroxymethyluracil, as well as the repair processes involved in its removal from DNA, and its level in various cells and urine. 5-hydroxymethyluracil may be formed during the course of the two processes: oxidation/hydroxylation of thymine with resultant formation of 5-hydroxymethyluracil paired with adenine (produced
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The importance of de novo mutations for pediatric neurological disease--It is not all in utero or birth trauma. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2016-04-03 Robert P Erickson
The advent of next generation sequencing (NGS, which consists of massively parallel sequencing to perform TGS (total genome sequencing) or WES (whole exome sequencing)) has abundantly discovered many causative mutations in patients with pediatric neurological disease. A surprisingly high number of these are de novo mutations which have not been inherited from either parent. For epilepsy, autism spectrum
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Genome defense against exogenous nucleic acids in eukaryotes by non-coding DNA occurs through CRISPR-like mechanisms in the cytosol and the bodyguard protection in the nucleus. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2016-04-03 Guo-Hua Qiu
In this review, the protective function of the abundant non-coding DNA in the eukaryotic genome is discussed from the perspective of genome defense against exogenous nucleic acids. Peripheral non-coding DNA has been proposed to act as a bodyguard that protects the genome and the central protein-coding sequences from ionizing radiation-induced DNA damage. In the proposed mechanism of protection, the
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The comet assay: Reflections on its development, evolution and applications. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2016-04-03 Narendra P Singh
The study of DNA damage and its repair is critical to our understanding of human aging and cancer. This review reflects on the development of a simple technique, now known as the comet assay, to study the accumulation of DNA damage and its repair. It describes my journey into aging research and the need for a method that sensitively quantifies DNA damage on a cell-by-cell basis and on a day-by-day
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How Trypanosoma cruzi deals with oxidative stress: Antioxidant defence and DNA repair pathways. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2016-04-03 Alice Machado-Silva,Paula Gonçalves Cerqueira,Viviane Grazielle-Silva,Fernanda Ramos Gadelha,Eduardo de Figueiredo Peloso,Santuza Maria Ribeiro Teixeira,Carlos Renato Machado
Trypanosoma cruzi, the causative agent of Chagas disease, is an obligatory intracellular parasite with a digenetic life cycle. Due to the variety of host environments, it faces several sources of oxidative stress. In addition to reactive oxygen species (ROS) produced by its own metabolism, T. cruzi must deal with high ROS levels generated as part of the host's immune responses. Hence, the conclusion
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Genotoxic sensitivity of the developing hematopoietic system. Mutat. Res. Rev. Mutat. Res. (IF 5.803) Pub Date : 2016-04-03 Ion Udroiu,Antonella Sgura
Genotoxic sensitivity seems to vary during ontogenetic development. Animal studies have shown that the spontaneous mutation rate is higher during pregnancy and infancy than in adulthood. Human and animal studies have found higher levels of DNA damage and mutations induced by mutagens in fetuses/newborns than in adults. This greater susceptibility could be due to reduced DNA repair capacity. In fact