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| http://dx.doi.org/10.1016/j.jdcr.2018.05.019 | DOI Listing |
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A new species of Cis Latreille (Coleoptera: Ciidae) widespread in Brazil but with similarities to the African fauna.
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Cis caramelo sp. nov. is described based on specimens collected in the North, Northeast, and Southeast Regions of Brazil.
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The genetic landscape of urologic cancers has evolved with the identification of actionable mutations that impact diagnosis, prognosis, and therapeutic strategies. This narrative review consolidates existing literature on genetic mutations across key urologic cancers, including bladder, renal, prostate, upper tract urothelial, testicular, and penile. The review highlights mutations in DNA damage repair genes, such as BRCA1/2 and PTEN, as well as pathway alterations like FGFR and PD-L1 overexpression.
View Article and Find Full Text PDFSurgical treatment of hypospadias with lichen sclerosus: Long-term outcomes from a single center.
Andrology
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Department of Pediatric Surgery, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
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The role of HR-HPV integration in the progression of premalignant lesions into different cancer types.
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August 2024
Research in Cytopathology and Histochemical Laboratory, Faculty of Chemical and Biological Sciences, Autonomous University of Guerrero, Chilpancingo, Guerrero, 39089, Mexico.
High-risk human papillomavirus (HR-HPV) is associated with the development of different types of cancer, such as cervical, head and neck (including oral, laryngeal, and oropharyngeal), vulvar, vaginal, penile, and anal cancers. The progression of premalignant lesions to cancer depends on factors associated with the host cell and the different epithelia infected by HPV, such as basal cells of the flat epithelium and the cells of the squamocolumnar transformation zone (STZ) found in the uterine cervix and the anal canal, which is rich in heparan sulfate proteoglycans and integrin-like receptors. On the other hand, factors associated with the viral genotype, infection with multiple viruses, viral load, viral persistence, and type of integration determine the viral breakage pattern and the sites at which the virus integrates into the host cell genome (introns, exons, intergenic regions), inducing the loss of function of tumor suppressor genes and increasing oncogene expression.
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