Literature DB >> 19574835

Cerebral cavernous malformations: somatic mutations in vascular endothelial cells.

Judith Gault1, Issam A Awad, Peter Recksiek, Robert Shenkar, Robert Breeze, Michael Handler, Bette K Kleinschmidt-DeMasters.   

Abstract

OBJECTIVE: Germline mutations in 3 genes have been found in familial cases of cerebral cavernous malformations (CCMs). We previously discovered somatic and germline truncating mutations in the KRIT1 gene, supporting the "2-hit" mechanism of CCM lesion formation in a single lesion. The purpose of this study was to screen for somatic, nonheritable mutations in 3 more lesions from different patients and identify the cell type(s) in which somatic mutations occur.
METHODS: Somatic mutations were sought in DNA from 3 surgically excised, fresh-frozen CCM lesions by cloning and screening polymerase chain reaction products generated from KRIT1 or PDCD10 coding regions. Laser capture microdissection was used on isolated endothelial and nonendothelial cells to determine whether somatic mutations were found in endothelial cells.
RESULTS: CCM lesions harbor somatic and germline KRIT1 mutations on different chromosomes and are therefore biallelic. Both mutations are predicted to truncate the protein. The KRIT1 somatic mutations (novel c.1800delG mutation and previously identified 34 nucleotide deletion) in CCMs from 2 different patients were found only in the vascular endothelial cells lining caverns. No obvious somatic mutations were identified in the 2 other lesions; however, the results were inconclusive, possibly owing to the technical limitations or the fact that these specimens had a small proportion of vascular endothelial cells lining pristine caverns.
CONCLUSION: The "2-hit" mechanism occurs in vascular endothelial cells lining CCM caverns from 2 patients with somatic and Hispanic-American KRIT1 germline mutations. Methods for somatic mutation detection should focus on vascular endothelial cells lining pristine caverns.

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Year:  2009        PMID: 19574835      PMCID: PMC2722441          DOI: 10.1227/01.NEU.0000348049.81121.C1

Source DB:  PubMed          Journal:  Neurosurgery        ISSN: 0148-396X            Impact factor:   4.654


  43 in total

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4.  PCR amplification introduces errors into mononucleotide and dinucleotide repeat sequences.

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5.  KRIT1 association with the integrin-binding protein ICAP-1: a new direction in the elucidation of cerebral cavernous malformations (CCM1) pathogenesis.

Authors:  Jon S Zawistowski; Ilya G Serebriiskii; Maximilian F Lee; Erica A Golemis; Douglas A Marchuk
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6.  Mutation and expression analysis of the KRIT1 gene associated with cerebral cavernous malformations (CCM1).

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Review 9.  Pathobiology of human cerebrovascular malformations: basic mechanisms and clinical relevance.

Authors:  Judith Gault; Hemant Sarin; Nabil A Awadallah; Robert Shenkar; Issam A Awad
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10.  Mutations in a gene encoding a novel protein containing a phosphotyrosine-binding domain cause type 2 cerebral cavernous malformations.

Authors:  Christina L Liquori; Michel J Berg; Adrian M Siegel; Elizabeth Huang; Jon S Zawistowski; T'Prien Stoffer; Dominique Verlaan; Fiyinfolu Balogun; Lori Hughes; Tracey P Leedom; Nicholas W Plummer; Milena Cannella; Vittorio Maglione; Ferdinando Squitieri; Eric W Johnson; Guy A Rouleau; Louis Ptacek; Douglas A Marchuk
Journal:  Am J Hum Genet       Date:  2003-11-17       Impact factor: 11.025

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5.  Vascular permeability and iron deposition biomarkers in longitudinal follow-up of cerebral cavernous malformations.

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6.  Strategy for identifying repurposed drugs for the treatment of cerebral cavernous malformation.

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7.  Two-hit mechanism in cerebral cavernous malformation? A case of monozygotic twins with a CCM1/KRIT1 germline mutation.

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8.  Cerebral Cavernous Malformations Develop Through Clonal Expansion of Mutant Endothelial Cells.

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Review 9.  Biology of vascular malformations of the brain.

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10.  KRIT1 regulates the homeostasis of intracellular reactive oxygen species.

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