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Cancer Causes & Control
Published in: Cancer Causes & Control 10/2009

01-12-2009 | Original paper

Hypothesis: neoplasms in myotonic dystrophy

Authors: Christine M. Mueller, James E. Hilbert, William Martens, Charles A. Thornton, Richard T. Moxley III, Mark H. Greene

Published in: Cancer Causes & Control | Issue 10/2009

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Abstract

Tumorigenesis is a multi-step process due to an accumulation of genetic mutations in multiple genes in diverse pathways which ultimately lead to loss of control over cell growth. It is well known that inheritance of rare germline mutations in genes involved in tumorigenesis pathways confer high lifetime risk of neoplasia in affected individuals. Furthermore, a substantial number of multiple malformation syndromes include cancer susceptibility in their phenotype. Studies of the mechanisms underlying these inherited syndromes have added to the understanding of both normal development and the pathophysiology of carcinogenesis. Myotonic dystrophy (DM) represents a group of autosomal dominant, multisystemic diseases that share the clinical features of myotonia, muscle weakness, and early-onset cataracts. Myotonic dystrophy type 1 (DM1) and myotonic dystrophy type 2 (DM2) result from unstable nucleotide repeat expansions in their respective genes. There have been multiple reports of tumors in individuals with DM, most commonly benign calcifying cutaneous tumors known as pilomatricomas. We provide a summary of the tumors reported in DM and a hypothesis for a possible mechanism of tumorigenesis. We hope to stimulate further study into the potential role of DM genes in tumorigenesis, and help define DM pathogenesis, and facilitate developing novel treatment modalities.
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Metadata
Title
Hypothesis: neoplasms in myotonic dystrophy
Authors
Christine M. Mueller
James E. Hilbert
William Martens
Charles A. Thornton
Richard T. Moxley III
Mark H. Greene
Publication date
01-12-2009
Publisher
Springer Netherlands
Published in
Cancer Causes & Control / Issue 10/2009
Print ISSN: 0957-5243
Electronic ISSN: 1573-7225
DOI
https://doi.org/10.1007/s10552-009-9395-y

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