Neurofibroma historical perspective: Difference between revisions
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==Overview== | ==Overview== | ||
In 2006, Yang et al demonstrated a critical neurofibroma microenvironment interaction that includes SCF-stimulated Nf1+/− mast cells potentiating Nf1+/− fibroblast functions. | [[NF-1|NF1]]-like [[cutaneous]] [[tumor]] [[syndromes]] appeared in the [[Literature review|literature]] in 1880s, when Friedrich [[Von Recklinghausen's Disease|von Recklinghausen]] published seminal [[Observation|observations]] detailing [[cutaneous]] [[tumors]] comprised of both [[Neuron|neuronal]] and [[Fibroblast|fibroblastic tissue]] finally termed as [[Neurofibroma|neurofibromas]]. In 2006, Yang et al demonstrated a critical [[neurofibroma]] microenvironment [[interaction]] that includes [[SCF-complex|SCF]]-[[Stimulated emission|stimulated]] [[NF-1|Nf1]]+/− [[mast cells]] [[Potentiator|potentiating]] [[NF-1|Nf1]]+/− [[fibroblast]] [[Function (biology)|functions]]. | ||
== | ==Historical Perspective== | ||
*In 18th century, NF1-like cutaneous tumor syndromes appeared in the literature | *In 18th century, [[NF1]]-like [[cutaneous]] [[tumor]] [[syndromes]] appeared in the [[Literature review|literature]].<ref name="pmid10190829">{{cite journal| author=Morse RP| title=Neurofibromatosis type 1. | journal=Arch Neurol | year= 1999 | volume= 56 | issue= 3 | pages= 364-5 | pmid=10190829 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10190829 }} </ref> | ||
*In 1880s, Friedrich von Recklinghausen published seminal observations detailing cutaneous tumors comprised of both neuronal and fibroblastic tissue finally termed as | *In 1880s, Friedrich [[Von Recklinghausen's Disease|von Recklinghausen]] published seminal [[Observation|observations]] [[Detailed balance|detailing]] [[cutaneous]] [[tumors]] comprised of both [[Neuron|neuronal]] and [[Fibroblast|fibroblastic tissue]] finally termed as [[Neurofibroma|neurofibromas]]. | ||
*In 2006, Yang et al demonstrated a critical neurofibroma microenvironment interaction that includes SCF-stimulated Nf1+/− mast cells potentiating Nf1+/− fibroblast functions.<ref> | *In 2006, Yang et al demonstrated a critical [[neurofibroma]] microenvironment [[interaction]] that includes [[SCF complex|SCF]]-[[Stimulated emission|stimulated]] [[NF-1|Nf1]]+/− [[mast cells]] [[Potentiator|potentiating]] [[NF-1|Nf1]]+/− [[fibroblast]] [[Function (biology)|functions]].<ref name="StaserYang2010">{{cite journal|last1=Staser|first1=Karl|last2=Yang|first2=Feng-Chun|last3=Clapp|first3=D. Wade|title=Mast cells and the neurofibroma microenvironment|journal=Blood|volume=116|issue=2|year=2010|pages=157–164|issn=0006-4971|doi=10.1182/blood-2009-09-242875}}</ref> | ||
==References== | ==References== |
Latest revision as of 15:40, 1 November 2019
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Mohsin, M.D.[2]
Overview
NF1-like cutaneous tumor syndromes appeared in the literature in 1880s, when Friedrich von Recklinghausen published seminal observations detailing cutaneous tumors comprised of both neuronal and fibroblastic tissue finally termed as neurofibromas. In 2006, Yang et al demonstrated a critical neurofibroma microenvironment interaction that includes SCF-stimulated Nf1+/− mast cells potentiating Nf1+/− fibroblast functions.
Historical Perspective
- In 18th century, NF1-like cutaneous tumor syndromes appeared in the literature.[1]
- In 1880s, Friedrich von Recklinghausen published seminal observations detailing cutaneous tumors comprised of both neuronal and fibroblastic tissue finally termed as neurofibromas.
- In 2006, Yang et al demonstrated a critical neurofibroma microenvironment interaction that includes SCF-stimulated Nf1+/− mast cells potentiating Nf1+/− fibroblast functions.[2]
References
- ↑ Morse RP (1999). "Neurofibromatosis type 1". Arch Neurol. 56 (3): 364–5. PMID 10190829.
- ↑ Staser, Karl; Yang, Feng-Chun; Clapp, D. Wade (2010). "Mast cells and the neurofibroma microenvironment". Blood. 116 (2): 157–164. doi:10.1182/blood-2009-09-242875. ISSN 0006-4971.