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PMS2 mutations in childhood cancer

PMS2 mutations in childhood cancer
PMS2 mutations in childhood cancer
Until recently, the PMS2 DNA mismatch repair gene has only rarely been implicated as a cancer susceptibility locus. New studies have shown, however, that earlier analyses of this gene have had technical limitations and also that the genetic behavior of mutant PMS2 alleles is unusual, in that, unlike MLH1 or MSH2 mutations, PMS2 mutations show low heterozygote penetrance. As a result, a dominantly inherited cancer predisposition has not been a feature reported in families with PMS2 mutations. Such families have instead been ascertained through childhood-onset cancers in homozygotes or through apparently sporadic colorectal cancer in heterozygotes. We present further information on the phenotype associated with homozygous PMS2 deficiency in 13 patients from six families of Pakistani origin living in the United Kingdom. This syndrome is characterized by cafe-au-lait skin pigmentation and a characteristic tumor spectrum, including leukemias, lymphomas, cerebral malignancies (such as supratentorial primitive neuroectodermal tumors, astrocytomas, and glioblastomas), and colorectal neoplasia with an onset in early adult life. We present evidence for a founder effect in five families, all of which carried the same R802-->X mutation (i.e., arginine-802 to stop) in PMS2. This cancer syndrome can be mistaken for neurofibromatosis type 1, with important management implications including the risk of the disorder occurring in siblings and the likelihood of tumor development in affected individuals
astrocytoma, female, syndrome, cafe-au-lait spots, child, humans, phenotype, adult, neoplasms, childhood, dna, founder effect, great britain, adolescent, adenosine triphosphatases, human, research support, risk, dna repair, deficiency, genetic predisposition to disease, proteins, enzymes, patients, dna repair enzymes, epidemiology, skin, precursor cell lymphoblastic leukemia-lymphoma, alleles, pakistan, family, colonic polyps, genetics, dna-binding proteins, lymphoma, b-cell, cancer, research, male, glioma, behavior, second primary, protein, arginine, adenosine, mutation, t-cell, leukemia, heterozygote, pigmentation, homozygote, ethnology
0027-8874
358-361
De Vos, Michel
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Hayward, Bruce E.
be290ab5-b27e-4407-8af8-1eb0f0009482
Charlton, Ruth
87f3d284-53e5-4e22-9cfb-db2ae0fbc28e
Taylor, Graham R.
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Glaser, Adam W.
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Picton, Susan
b99bddd5-6ff8-4e7a-84a6-b48e821b147e
Cole, Trevor R.
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Maher, Eamonn R.
577b8856-f8a8-49c2-9484-288d9f964aed
McKeown, Carol M.E.
7b205e3a-2c8e-4c10-8d3d-688b37489d16
Mann, Jill R.
3b570368-f5a1-4515-941f-ad6191830bbd
Yates, John R.
c527c736-14e5-49ef-b196-da9326491376
Baralle, Diana
faac16e5-7928-4801-9811-8b3a9ea4bb91
Rankin, Julia
e10a0f80-2929-4b47-8fa2-8dee01ce39c6
Bonthron, David T.
2e7a8398-acae-4cc1-992c-0136594bc1ae
Sheridan, Eamonn
5df687dd-6945-4092-a06a-558f05c74176
De Vos, Michel
4437917c-a2b5-4684-9b76-a6dbf1817080
Hayward, Bruce E.
be290ab5-b27e-4407-8af8-1eb0f0009482
Charlton, Ruth
87f3d284-53e5-4e22-9cfb-db2ae0fbc28e
Taylor, Graham R.
e07ffb5e-6d60-431e-8ae7-6c240b0657ce
Glaser, Adam W.
9ce6cbd6-98e5-4dc3-a74c-91a9e45feb1c
Picton, Susan
b99bddd5-6ff8-4e7a-84a6-b48e821b147e
Cole, Trevor R.
01da0bb7-93b9-4cc8-9c03-c0586c1e6c59
Maher, Eamonn R.
577b8856-f8a8-49c2-9484-288d9f964aed
McKeown, Carol M.E.
7b205e3a-2c8e-4c10-8d3d-688b37489d16
Mann, Jill R.
3b570368-f5a1-4515-941f-ad6191830bbd
Yates, John R.
c527c736-14e5-49ef-b196-da9326491376
Baralle, Diana
faac16e5-7928-4801-9811-8b3a9ea4bb91
Rankin, Julia
e10a0f80-2929-4b47-8fa2-8dee01ce39c6
Bonthron, David T.
2e7a8398-acae-4cc1-992c-0136594bc1ae
Sheridan, Eamonn
5df687dd-6945-4092-a06a-558f05c74176

De Vos, Michel, Hayward, Bruce E., Charlton, Ruth, Taylor, Graham R., Glaser, Adam W., Picton, Susan, Cole, Trevor R., Maher, Eamonn R., McKeown, Carol M.E., Mann, Jill R., Yates, John R., Baralle, Diana, Rankin, Julia, Bonthron, David T. and Sheridan, Eamonn (2006) PMS2 mutations in childhood cancer. Journal of the National Cancer Institute, 98 (5), 358-361. (doi:10.1093/jnci/djj073).

Record type: Article

Abstract

Until recently, the PMS2 DNA mismatch repair gene has only rarely been implicated as a cancer susceptibility locus. New studies have shown, however, that earlier analyses of this gene have had technical limitations and also that the genetic behavior of mutant PMS2 alleles is unusual, in that, unlike MLH1 or MSH2 mutations, PMS2 mutations show low heterozygote penetrance. As a result, a dominantly inherited cancer predisposition has not been a feature reported in families with PMS2 mutations. Such families have instead been ascertained through childhood-onset cancers in homozygotes or through apparently sporadic colorectal cancer in heterozygotes. We present further information on the phenotype associated with homozygous PMS2 deficiency in 13 patients from six families of Pakistani origin living in the United Kingdom. This syndrome is characterized by cafe-au-lait skin pigmentation and a characteristic tumor spectrum, including leukemias, lymphomas, cerebral malignancies (such as supratentorial primitive neuroectodermal tumors, astrocytomas, and glioblastomas), and colorectal neoplasia with an onset in early adult life. We present evidence for a founder effect in five families, all of which carried the same R802-->X mutation (i.e., arginine-802 to stop) in PMS2. This cancer syndrome can be mistaken for neurofibromatosis type 1, with important management implications including the risk of the disorder occurring in siblings and the likelihood of tumor development in affected individuals

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More information

Published date: 1 March 2006
Keywords: astrocytoma, female, syndrome, cafe-au-lait spots, child, humans, phenotype, adult, neoplasms, childhood, dna, founder effect, great britain, adolescent, adenosine triphosphatases, human, research support, risk, dna repair, deficiency, genetic predisposition to disease, proteins, enzymes, patients, dna repair enzymes, epidemiology, skin, precursor cell lymphoblastic leukemia-lymphoma, alleles, pakistan, family, colonic polyps, genetics, dna-binding proteins, lymphoma, b-cell, cancer, research, male, glioma, behavior, second primary, protein, arginine, adenosine, mutation, t-cell, leukemia, heterozygote, pigmentation, homozygote, ethnology

Identifiers

Local EPrints ID: 59673
URI: http://eprints.soton.ac.uk/id/eprint/59673
ISSN: 0027-8874
PURE UUID: 8b5596a5-b7c4-40ab-8f44-f81edca348cf
ORCID for Diana Baralle: ORCID iD orcid.org/0000-0003-3217-4833

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Date deposited: 04 Sep 2008
Last modified: 16 Mar 2024 03:57

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Contributors

Author: Michel De Vos
Author: Bruce E. Hayward
Author: Ruth Charlton
Author: Graham R. Taylor
Author: Adam W. Glaser
Author: Susan Picton
Author: Trevor R. Cole
Author: Eamonn R. Maher
Author: Carol M.E. McKeown
Author: Jill R. Mann
Author: John R. Yates
Author: Diana Baralle ORCID iD
Author: Julia Rankin
Author: David T. Bonthron
Author: Eamonn Sheridan

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