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Cancer Detection and Prognosis
Published in Attila Lorincz, Nucleic Acid Testing for Human Disease, 2016
Santiago Ropero, Manel Esteller
Increasing numbers of molecular genetic technologies lend themselves to the study of chromosomal aberrations, such as chromosome banding, high-throughput analysis of LOH, comparative genome hybridization (CGH), fluorescence in situ hybridization (FISH), restriction landmark genomic scanning (RLGS), and representational difference analysis (RDA).
Spotlight on ocular Kaposi’s sarcoma: an update on the presentation, diagnosis, and management options
Published in Expert Review of Ophthalmology, 2021
Nandini Venkateswaran, Juan C. Ramos, Adam K. Cohen, Osmel P. Alvarez, Noah K. Cohen, Anat Galor, Carol L. Karp
KS is a low-grade tumor of the vascular or lymphatic endothelial cells that is caused by the oncogenic virus HHV8 [16]. HHV8, also known as the KS associated herpesvirus (KSHV), has an estimated prevalence of 1–5% in the United States, more commonly in men who have sex with men, but is more widespread globally, with a prevalence of 10–20% in certain Mediterranean countries and 30–50% in parts of sub-Saharan Africa [17–19]. In 1994, Drs. Yuan Chang and Patrick S. Moore discovered that HHV8 caused KS lesions using representational difference analysis, a subtraction technique for identifying differences between genomes that is highly useful for researching the genetics of cancers such as KS [16,20].
Thymosin β4 and the vasculature: multiple roles in development, repair and protection against disease
Published in Expert Opinion on Biological Therapy, 2018
The suggestion that Tβ4 may promote mural cell differentiation via the TGFβ pathway is consistent with a mechanism proposed for differentiation of the yolk sac vasculature. Tβ4 was identified by representational difference analysis [47], and confirmed by chromatin immunoprecipitation and transcriptional assays [4], to be a downstream target of the basic helix-loop-helix transcription factor, Hand1. Hand1-null embryoid bodies revealed vascular differentiation defects and Hand1-null embryos displayed defective yolk sac vasculogenesis [4]. Exogenous administration of TB4 rescued expression of EC and SMC markers in Hand1-null embryoid body cultures and, moreover, rescued Hand1-null embryos to prolong survival. In contrast to control embryos, which developed within a yolk sac with an organized capillary plexus, null embryos lacked yolk sac vascular plexus formation and arrested in development by embryonic day (E)8.5. Injection of pregnant female mice with TB4 was sufficient to rescue Hand1-null embryos, which were recovered at E8.5 with an appropriately formed yolk sac capillary network and in which the embryos had developed beyond the arrested stage of the mutants. Mechanistically, genes of the TGFβ and Notch signaling pathways, which were found to be dysregulated in Hand1 mutant yolk sacs, were rescued to control levels with TB4 treatment [4]. It is not known whether Hand1 also regulates Tβ4 expression at later embryonic stages, perhaps at the time points when Tβ4 is required for systemic or coronary vasculogenesis, nor is it fully understood how Tβ4 impacts on the key vasculogenic signaling pathways, those that regulate EC proliferation, migration, and differentiation, that include, but may not be limited to, TGFβ and Notch1.