FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2016348725> ?p ?o ?g. }

• W2016348725 abstract "Testicular cancer (TC) is the most common cancer in males aged 20-40 years, with a worldwide incidence of 7.5 per 100,000, but the rates vary considerably between countries and ethnic groups and there is evidence also for an increasing incidence in last decades. About 95% of all TCs are represented by testicular germ cell tumors (TGCTs), which include seminoma and non-seminoma histological types. It is generally assumed that the development of TGCT is under endocrine control. In particular, unbalanced androgen/estrogen levels and/or activity are believed to represent the key events for TGCT development and progression. Furthermore, recent evidence has suggested genetic association of TGCT with variations in genes involved in hypothalamic-pituitary-testicular axis and steroidogenic enzymes. This recent evidence expands the current knowledge on the role of genetic contribution in testicular cancer susceptibility, and supports the hypothesis that variations in hormone metabolism genes might change the hormonal environment implicated in testicular carcinogenesis. Therefore, hormonal carcinogenesis is an important and controversial area of current research in TGCT, and further attention is given to genetic factors influencing hormone-related cancer risk. The genetic component to TGCT is in general strong. In fact, although environmental factors clearly contribute to TGCT development (and probably to its increasing incidence in some geographical areas), the proportion of TGCT susceptibility accounted for by the genetic effects is estimated at 25%. TGCT has high familial risks compared with most other cancer types that are generally no more than two-fold: brothers of individuals with TGCT have an 8- to 12-fold increased risk of disease, and sons of affected individuals have a 4- to 6-fold increased risk. Despite this strong familial relative risk, early results from linkage studies identified a limited relationship with genetic factors, suggesting that TGCT is a genetically complex trait. However, more recently, four genome-wide association studies (GWAS) from the UK and USA have reported association of TGCTs with six new loci (KITLG, SPRY4, BAK1, DMRT1, TERT, and ATF7IP). The strongest association for TGCT susceptibility was found for SNPs in KITLG (ligand for the membrane-bound receptor tyrosine kinase KIT) gene with a greater than 2.5-fold increased risk of disease per major allele, which is the highest reported for any cancer to date. These studies are being now replicated by other researches and attention is given to the relationship between these genetic variations, TGCT risk and frequently associated anomalies of the reproductive tract, such as cryptorchidism and infertility. Finally, over the past few decades, TCGT research has focused also on external environmental causes acting mainly as endocrine disrupters of androgen and oestrogen pathways, even during the foetal development of the testis. It is well known that the testicular dysgenesis syndrome (TDS) hypothesis, proposed ten years ago, suggests that disturbed testicular development in fetal life may result in one or more of four disorders postnatally, named cryptorchidism, hypospadias, poor semen quality, and TGCT. These four disorders are therefore considered as one clinical entity and are linked together by epidemiological and pathophysiological relations. The relative contribution of genetics and environment in TGCT development, and the interactions between endocrine disruptors and variations in genes involved in hormonal carcinogenesis is therefore another interesting area of research." @default.
• W2016348725 created "2016-06-24" @default.
• W2016348725 creator A5006015349 @default.
• W2016348725 creator A5014371364 @default.
• W2016348725 date "2014-10-21" @default.
• W2016348725 modified "2023-10-16" @default.
• W2016348725 title "Testis Cancer: Genes, Environment, Hormones" @default.
• W2016348725 cites W1986960957 @default.
• W2016348725 cites W2002061253 @default.
• W2016348725 cites W2013617050 @default.
• W2016348725 cites W2080448648 @default.
• W2016348725 cites W2083160633 @default.
• W2016348725 cites W2108007414 @default.
• W2016348725 cites W2114851504 @default.
• W2016348725 cites W2127067110 @default.
• W2016348725 cites W2127257973 @default.
• W2016348725 cites W2131678625 @default.
• W2016348725 cites W2143540684 @default.
• W2016348725 cites W2157272342 @default.
• W2016348725 cites W2158738973 @default.
• W2016348725 cites W2171423639 @default.
• W2016348725 cites W2171525029 @default.
• W2016348725 cites W4252807807 @default.
• W2016348725 doi "https://doi.org/10.3389/fendo.2014.00172" @default.
• W2016348725 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4204530" @default.
• W2016348725 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25374560" @default.
• W2016348725 hasPublicationYear "2014" @default.
• W2016348725 type Work @default.
• W2016348725 sameAs 2016348725 @default.
• W2016348725 citedByCount "5" @default.
• W2016348725 countsByYear W20163487252016 @default.
• W2016348725 countsByYear W20163487252018 @default.
• W2016348725 countsByYear W20163487252019 @default.
• W2016348725 countsByYear W20163487252020 @default.
• W2016348725 countsByYear W20163487252023 @default.
• W2016348725 crossrefType "journal-article" @default.
• W2016348725 hasAuthorship W2016348725A5006015349 @default.
• W2016348725 hasAuthorship W2016348725A5014371364 @default.
• W2016348725 hasBestOaLocation W20163487251 @default.
• W2016348725 hasConcept C104317684 @default.
• W2016348725 hasConcept C121608353 @default.
• W2016348725 hasConcept C126322002 @default.
• W2016348725 hasConcept C134018914 @default.
• W2016348725 hasConcept C42407357 @default.
• W2016348725 hasConcept C502942594 @default.
• W2016348725 hasConcept C54355233 @default.
• W2016348725 hasConcept C60644358 @default.
• W2016348725 hasConcept C71315377 @default.
• W2016348725 hasConcept C71924100 @default.
• W2016348725 hasConcept C86803240 @default.
• W2016348725 hasConceptScore W2016348725C104317684 @default.
• W2016348725 hasConceptScore W2016348725C121608353 @default.
• W2016348725 hasConceptScore W2016348725C126322002 @default.
• W2016348725 hasConceptScore W2016348725C134018914 @default.
• W2016348725 hasConceptScore W2016348725C42407357 @default.
• W2016348725 hasConceptScore W2016348725C502942594 @default.
• W2016348725 hasConceptScore W2016348725C54355233 @default.
• W2016348725 hasConceptScore W2016348725C60644358 @default.
• W2016348725 hasConceptScore W2016348725C71315377 @default.
• W2016348725 hasConceptScore W2016348725C71924100 @default.
• W2016348725 hasConceptScore W2016348725C86803240 @default.
• W2016348725 hasLocation W20163487251 @default.
• W2016348725 hasLocation W20163487252 @default.
• W2016348725 hasLocation W20163487253 @default.
• W2016348725 hasLocation W20163487254 @default.
• W2016348725 hasOpenAccess W2016348725 @default.
• W2016348725 hasPrimaryLocation W20163487251 @default.
• W2016348725 hasRelatedWork W1997759048 @default.
• W2016348725 hasRelatedWork W2010645160 @default.
• W2016348725 hasRelatedWork W2027210979 @default.
• W2016348725 hasRelatedWork W2042044567 @default.
• W2016348725 hasRelatedWork W2043067495 @default.
• W2016348725 hasRelatedWork W2049266444 @default.
• W2016348725 hasRelatedWork W2069420617 @default.
• W2016348725 hasRelatedWork W2080102149 @default.
• W2016348725 hasRelatedWork W2164661085 @default.
• W2016348725 hasRelatedWork W2171532347 @default.
• W2016348725 hasVolume "5" @default.
• W2016348725 isParatext "false" @default.
• W2016348725 isRetracted "false" @default.
• W2016348725 magId "2016348725" @default.
• W2016348725 workType "article" @default.