Human Molecular Genetics, Vol 8, 1461-1472, Copyright © 1999 by Oxford University Press
DJ Marsh, JB Kum, KL Lunetta, MJ Bennett, RJ Gorlin, SF Ahmed, J Bodurtha, C Crowe, MA Curtis, M Dasouki, T Dunn, H Feit, MT Geraghty, JM Graham Jr, SV Hodgson, A Hunter, BR Korf, D Manchester, S Miesfeldt, VA Murday, KL Nathanson, M Parisi, B Pober, C Romano and C Eng
Germline mutations in the tumour suppressor gene PTEN have been implicated
in two hamartoma syndromes that exhibit some clinical overlap, Cowden
syndrome (CS) and Bannayan-Riley-Ruvalcaba syndrome (BRR). PTEN maps to
10q23 and encodes a dual specificity phosphatase, a substrate of which is
phosphatidylinositol 3,4,5-triphosphate, a phospholipid in the
phosphatidylinositol 3-kinase pathway. CS is characterized by multiple
hamartomas and an increased risk of benign and malignant disease of the
breast, thyroid and central nervous system, whilst the presence of cancer
has not been formally documented in BRR. The partial clinical overlap in
these two syndromes is exemplified by the hallmark features of BRR:
macrocephaly and multiple lipomas, the latter of which occur in a minority
of individuals with CS. Additional features observed in BRR, which may also
occur in a minority of CS patients, include Hashimoto's thyroiditis,
vascular malformations and mental retardation. Pigmented macules of the
glans penis, delayed motor development and neonatal or infant onset are
noted only in BRR. In this study, constitutive DNA samples from 43 BRR
individuals comprising 16 sporadic and 27 familial cases, 11 of which were
families with both CS and BRR, were screened for PTEN mutations. Mutations
were identified in 26 of 43 (60%) BRR cases. Genotype- phenotype analyses
within the BRR group suggested a number of correlations, including the
association of PTEN mutation and cancer or breast fibroadenoma in any given
CS, BRR or BRR/CS overlap family ( P = 0.014), and, in particular,
truncating mutations were associated with the presence of cancer and breast
fibroadenoma in a given family ( P = 0.024). Additionally, the presence of
lipomas was correlated with the presence of PTEN mutation in BRR patients (
P = 0.028). In contrast to a prior report, no significant difference in
mutation status was found in familial versus sporadic cases of BRR ( P =
0.113). Comparisons between BRR and a previously studied group of 37 CS
families suggested an increased likelihood of identifying a germline PTEN
mutation in families with either CS alone or both CS and BRR when compared
with BRR alone ( P = 0.002). Among CS, BRR and BRR/CS overlap families that
are PTEN mutation positive, the mutation spectra appear similar. Thus, PTEN
mutation-positive CS and BRR may be different presentations of a single
syndrome and, hence, both should receive equal attention with respect to
cancer surveillance.
ARTICLES
PTEN mutation spectrum and genotype-phenotype correlations in Bannayan- Riley-Ruvalcaba syndrome suggest a single entity with Cowden syndrome
Clinical Cancer Genetics and Human Cancer Genetics Programs, Ohio State University Comprehensive Cancer Center, 690C Medical Research Facility, 420 West 12th Avenue, Columbus, OH 43210, USA.
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L.-P. Weng, J. L. Brown, and C. Eng PTEN coordinates G1 arrest by down-regulating cyclin D1 via its protein phosphatase activity and up-regulating p27 via its lipid phosphatase activity in a breast cancer model Hum. Mol. Genet., March 1, 2001; 10(6): 599 - 604. [Abstract] [Full Text] [PDF]
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L.-P. Weng, W. M. Smith, J. L. Brown, and C. Eng PTEN inhibits insulin-stimulated MEK/MAPK activation and cell growth by blocking IRS-1 phosphorylation and IRS-1/Grb-2/Sos complex formation in a breast cancer model Hum. Mol. Genet., March 1, 2001; 10(6): 605 - 616. [Abstract] [Full Text] [PDF]
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J. D Fackenthal, D. J Marsh, A.-L. Richardson, S. A Cummings, C. Eng, B. G Robinson, and O. I Olopade Male breast cancer in Cowden syndrome patients with germline PTEN mutations J. Med. Genet., March 1, 2001; 38(3): 159 - 164. [Abstract] [Full Text]
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L.-P. Weng, J. L. Brown, and C. Eng PTEN induces apoptosis and cell cycle arrest through phosphoinositol-3-kinase/Akt-dependent and -independent pathways Hum. Mol. Genet., February 1, 2001; 10(3): 237 - 242. [Abstract] [Full Text] [PDF]
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L.-P. Weng, O. Gimm, J. B. Kum, W. M. Smith, X.-P. Zhou, D. Wynford-Thomas, G. Leone, and C. Eng Transient ectopic expression of PTEN in thyroid cancer cell lines induces cell cycle arrest and cell type-dependent cell death Hum. Mol. Genet., February 1, 2001; 10(3): 251 - 258. [Abstract] [Full Text] [PDF]
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M. A PARISI, M. B. DINULOS, K. A LEPPIG, V. P SYBERT, C. ENG, and L. HUDGINS The spectrum and evolution of phenotypic findings in PTEN mutation positive cases of Bannayan-Riley-Ruvalcaba syndrome J. Med. Genet., January 1, 2001; 38(1): 52 - 58. [Full Text]
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C. Eng Will the real Cowden syndrome please stand up: revised diagnostic criteria J. Med. Genet., November 1, 2000; 37(11): 828 - 830. [Full Text]
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A. Perren, P. Komminoth, P. Saremaslani, C. Matter, S. Feurer, J. A. Lees, P. U. Heitz, and C. Eng Mutation and Expression Analyses Reveal Differential Subcellular Compartmentalization of PTEN in Endocrine Pancreatic Tumors Compared to Normal Islet Cells Am. J. Pathol., October 1, 2000; 157(4): 1097 - 1103. [Abstract] [Full Text] [PDF]
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X.-P. Zhou, O. Gimm, H. Hampel, T. Niemann, M. J. Walker, and C. Eng Epigenetic PTEN Silencing in Malignant Melanomas without PTEN Mutation Am. J. Pathol., October 1, 2000; 157(4): 1123 - 1128. [Abstract] [Full Text] [PDF]
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P. M DAHIA, O. GIMM, H. CHI, D. J MARSH, P. R REYNOLDS, and C. ENG Absence of germline mutations in MINPP1, a phosphatase encoding gene centromeric of PTEN, in patients with Cowden and Bannayan-Riley- Ruvalcaba syndrome without germline PTEN mutations J. Med. Genet., September 1, 2000; 37(9): 715 - 717. [Full Text]
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 F. Vazquez, S. Ramaswamy, N. Nakamura, and W. R. Sellers Phosphorylation of the PTEN Tail Regulates Protein Stability and Function Mol. Cell. Biol., July 15, 2000; 20(14): 5010 - 5018. [Abstract] [Full Text]
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O. Gimm, T. Attie-Bitach, J. A. Lees, M. Vekemans, and C. Eng Expression of the PTEN tumour suppressor protein during human development Hum. Mol. Genet., July 1, 2000; 9(11): 1633 - 1639. [Abstract] [Full Text] [PDF]
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V. Stambolic, M.-S. Tsao, D. Macpherson, A. Suzuki, W. B. Chapman, and T. W. Mak High Incidence of Breast and Endometrial Neoplasia Resembling Human Cowden Syndrome in pten+/- Mice Cancer Res., July 1, 2000; 60(13): 3605 - 3611. [Abstract] [Full Text]
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X.-P. Zhou, D. J. Marsh, H. Hampel, J. B. Mulliken, O. Gimm, and C. Eng Germline and germline mosaic PTEN mutations associated with a Proteus-like syndrome of hemihypertrophy, lower limb asymmetry, arteriovenous malformations and lipomatosis Hum. Mol. Genet., March 22, 2000; 9(5): 765 - 768. [Abstract] [Full Text] [PDF]
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G. Guanti, N. Resta, C. Simone, F. Cariola, I. Demma, P. Fiorente, and M. Gentile Involvement of PTEN mutations in the genetic pathways of colorectal cancerogenesis Hum. Mol. Genet., January 22, 2000; 9(2): 283 - 287. [Abstract] [Full Text] [PDF]
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Balanced Translocation of 10q and 13q, Including the PTENGene, in a Boy with a Human Chorionic Gonadotropin-Secreting Tumor and the Bannayan-Riley-Ruvalcaba Syndrome J. Clin. Endocrinol. Metab., December 1, 1999; 84(12): 4665 - 4670. [Full Text]
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