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1 is related to the number and distribution of hamartomatous brain growths (cortical tubers) that chara
3 ulin (FLCN) cause Birt-Hogg-Dube syndrome, a hamartomatous disease marked by mitochondria-rich kidney
4 tuberous sclerosis complex (TSC), a dominant hamartomatous disorder that often presents with mental r
5 , Lhermitte-Duclos disease (LDD) caused by a hamartomatous enlargement of the cerebellum, ataxia, sei
12 ps the region for Cowden disease, a distinct hamartomatous intestinal polyposis syndrome with increas
13 sphatase and tensin homolog (PTEN) generates hamartomatous intestinal polyps with epithelial and stro
15 on of TSC2 can be critical in development of hamartomatous lesions in TSC and cancer pathogenesis.
16 lly been regarded as nonneoplastic, possibly hamartomatous lesions, but the pathogenesis of FGPs in b
17 ltisystem growth of benign tumours and other hamartomatous lesions, which leads to diverse and debili
19 lyps, 1 or more of which was hyperplastic or hamartomatous (N = 397), were prospectively recruited.
20 tionally have been regarded as nondysplastic hamartomatous or hyperplastic lesions, but their pathoge
23 an-Riley-Ruvalcaba syndrome (BRRS) is a rare hamartomatous polyposis condition with features of macro
26 0) is an autosomal dominant gastrointestinal hamartomatous polyposis syndrome in which patients are a
27 nile polyposis (JP) is an autosomal dominant hamartomatous polyposis syndrome where affected individu
30 rectal cancer (HNPCC) or Lynch syndrome, the hamartomatous polyposis syndromes, and certain other rar
32 testinal features that are classic for other hamartomatous polyposis syndromes, such as Bannayan-Rile
33 otein phosphatase and a protein kinase cause hamartomatous polyposis syndromes, which are characteris
34 We sought to determine the prevalence of hamartomatous polyposis-associated mutations in the susc
36 ile polyposis syndrome (JPS) is an inherited hamartomatous-polyposis syndrome with a risk for colon c
37 shared clinical features of gastrointestinal hamartomatous polyps among the three syndromes and the c
38 aim of this review is to categorize gastric hamartomatous polyps and aid in the identification of hi
41 d disorder characterized by gastrointestinal hamartomatous polyps and mucocutaneous melanin pigmentat
45 e characterized by multiple gastrointestinal hamartomatous polyps in the absence of the extraintestin
47 autosomal-dominant disorder characterized by hamartomatous polyps in the gastrointestinal tract and b
50 utosomal dominant condition characterized by hamartomatous polyps of the gastrointestinal tract and a
51 with incomplete penetrance characterized by hamartomatous polyps of the gastrointestinal tract and a
52 er which is characterized by the presence of hamartomatous polyps throughout the gastrointestinal tra
53 n disorder in which individuals have typical hamartomatous polyps within the gastrointestinal tract.
54 minant condition characterized by intestinal hamartomatous polyps, mucocutaneous melanin deposition,
57 ologic characteristics of their polyps, each hamartomatous syndrome carries an elevated risk for canc
60 ith tuberous sclerosis complex (TSC) develop hamartomatous tumors showing loss of function of the tum
61 disease tuberous sclerosis, characterized by hamartomatous tumors, results from mutations in either T
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