By Paula E. North, Tara Sander
This e-book comprehensively covers the type, histopathology, pathogenesis, and molecular analysis of vascular tumors and malformations, correlating those with present ways to scientific administration. It deals a brand new multidisciplinary source for clinicians, pathologists, molecular diagnosticians, and scientists within the box of vascular medication and biology, fostering cross-cutting collaboration in scientific perform and learn. basic heritage details on vascular tumors and malformation is supplied, whereas additionally together with the most up-tp-date details to be had on pathogenic mechanisms underlying this heterogenous workforce of problems and the consequences for molecular prognosis and healing intervention.
Written by way of specialists within the box, Vascular Tumors and Developmental Malformations: Pathogenic Mechanisms and Molecular Diagnosis offers the clinical and medical group with an important, sensible source to lead exact analysis, well-targeted treatments, and trained research of particular clinicopathological entities in the spectrum of vascular anomalies.
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Additional resources for Vascular Tumors and Developmental Malformations: Pathogenic Mechanisms and Molecular Diagnosis
This need for a second hit could explain why many inherited VMCM lesions appear in adolescence rather than at birth. In more than half of inherited VMs, the detected TIE2 mutation is an Arg849 to tryptophan (R849W) substitution [149, 151]. More recent studies have also identified somatic TIE2 mutations in 85 % of sporadic VMs, although in these cases the mutation (L914F) leads to substitution of a leucine to a phenylalanine, producing a stronger TIE1-hyperphosphorylation effect than the inherited R849W mutation of VMCM [150, 152].
By MRI, VMs are slow flow lesions, with low vascular resistance and bright hypersignal on T2-weighted spin echo. Superficial lesions enlarge over time due to increased venous pressure (increased by dependency or exertion). Common complications include chronic low-grade consumptive coagulopathy in large/extensive lesions and phleboliths and pain of unclear origin. Histology Endothelia of venous malformations are flattened and mitotically inactive. The vessel walls have no elastic interna and contain a variable amount of well-differentiated smooth muscle (usually scant relative to luminal diameter) (Fig.
Rossi and Fletcher found upon literature review in 2002 only 5 bona fide examples of spontaneous or radiation-induced angiosarcoma arising in benign vascular lesions and added 4 spontaneously arising cases (3 from AVMs and 1 from an intramuscular lesion) . Hepatic angiosarcoma unresponsive to steroids or vincristine occurring coincidently with multiple cutaneous infantile hemangiomas has also been reported . Mechanisms linking chronic lymphedema to development of angiosarcoma remain uncertain, although theories abound.
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