The incidence of consecutive manifestations in Von Hippel-Lindau disease.
Adolescent
Adult
Age Factors
Aged
Central Nervous System Neoplasms
/ etiology
Disease Progression
Female
Hemangioblastoma
/ etiology
Heterozygote
Humans
Kaplan-Meier Estimate
Kidney Neoplasms
/ etiology
Male
Middle Aged
Pancreatic Neoplasms
/ etiology
Retinal Neoplasms
/ etiology
Retrospective Studies
Time Factors
Young Adult
von Hippel-Lindau Disease
/ complications
Disease progression
Surveillance
VHL-related manifestations
Von Hippel-Lindau disease
Journal
Familial cancer
ISSN: 1573-7292
Titre abrégé: Fam Cancer
Pays: Netherlands
ID NLM: 100898211
Informations de publication
Date de publication:
07 2019
07 2019
Historique:
pubmed:
16
5
2019
medline:
4
12
2019
entrez:
16
5
2019
Statut:
ppublish
Résumé
Von Hippel-Lindau (VHL) disease is an autosomal dominant rare tumor syndrome characterized by high penetrance. VHL mutation carriers develop numerous manifestations in multiple organs during life. The natural course of development of new and growth of existing VHL-related manifestations is still unclear. In this study we aimed to gain insight into the development of subsequent manifestations in VHL disease. We retrospectively scored each new VHL-related manifestation as detected by standard follow-up (retina, central nervous system, kidneys and pancreas, excluding adrenal and endolymfatic sac manifestations) in 75 VHL mutation carriers. The Kaplan-Meier method was used to plot the cumulative proportions of all consecutive manifestations in each organ against age. The cumulative average number of manifestations in all organs during life was calculated by summating these cumulative proportions. Poisson model parameters were used to calculate average time to the detection of consecutive VHL manifestations in each organ. Consecutive VHL-related kidney and retina manifestations during life occur linearly according to Poisson distribution model. The total number of VHL manifestations rises linearly, with an average of seven VHL-related lesions at age 60 years. The incidence of consecutive VHL-related manifestations is constant during life in VHL mutation carriers. Our data is consistent with the notion that somatic inactivation of the remaining allele (Knudson's "two-hit" hypothesis) is the determining factor in developing new VHL-related manifestations.
Identifiants
pubmed: 31087189
doi: 10.1007/s10689-019-00131-x
pii: 10.1007/s10689-019-00131-x
pmc: PMC6560011
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
369-376Références
Int J Oncol. 2007 Feb;30(2):341-8
pubmed: 17203215
Endocr Relat Cancer. 2013 Dec 20;21(1):63-71
pubmed: 24132471
J Med Genet. 1996 Feb;33(2):120-7
pubmed: 8929948
Hum Mutat. 2010 May;31(5):521-37
pubmed: 20151405
Genet Med. 2016 Jan;18(1):89-97
pubmed: 25834951
Nat Rev Cancer. 2001 Nov;1(2):157-62
pubmed: 11905807
Proc Natl Acad Sci U S A. 1971 Apr;68(4):820-3
pubmed: 5279523
Nat Genet. 2017 Jan 31;49(2):170-174
pubmed: 28138153
Genet Med. 2011 Jun;13(6):519-27
pubmed: 21415761
Genome Biol. 2014 Aug 27;15(8):433
pubmed: 25159823
J Neurosurg. 2014 May;120(5):1055-62
pubmed: 24579662
Ann Neurol. 2006 Jan;59(1):105-10
pubmed: 16261628
Eur J Hum Genet. 2017 Feb;25(3):301-307
pubmed: 27966541
Neurology. 2015 Oct 27;85(17):1500-3
pubmed: 26408493
Eur J Hum Genet. 2011 Jun;19(6):617-23
pubmed: 21386872
BMC Genomics. 2016 Jan 14;17:56
pubmed: 26768750
Proc Natl Acad Sci U S A. 1978 May;75(5):2453-7
pubmed: 276883
Nature. 2013 Sep 19;501(7467):346-54
pubmed: 24048067
Urol Int. 2012;88(1):71-8
pubmed: 22156657
Lancet. 2003 Jun 14;361(9374):2059-67
pubmed: 12814730
J Neurosurg. 2003 Jan;98(1):82-94
pubmed: 12546356
J Neurosurg. 2012 Nov;117(5):818-24
pubmed: 22937928
Ann Neurol. 2004 May;55(5):721-8
pubmed: 15122713
Neurology. 2012 Aug 21;79(8):793-6
pubmed: 22875085
J Neurosurg. 2006 Aug;105(2):248-55
pubmed: 17219830
J Med Genet. 1990 May;27(5):311-4
pubmed: 2352258
Fam Cancer. 2012 Jun;11(2):209-14
pubmed: 22203439