| Id |
Subject |
Object |
Predicate |
Lexical cue |
| TextSentencer_T1 |
0-112 |
Sentence |
denotes |
De novo germline mutation in the serine-threonine kinase STK11/LKB1 gene associated with Peutz-Jeghers syndrome. |
| TextSentencer_T2 |
113-263 |
Sentence |
denotes |
Peutz-Jeghers syndrome (PJS) is an autosomal dominant disease, characterized phenotypically by mucocutaneous pigmentation and hamartomatous polyposis. |
| TextSentencer_T3 |
264-361 |
Sentence |
denotes |
Affected patients are at an increased risk of developing gastrointestinal and other malignancies. |
| TextSentencer_T4 |
362-495 |
Sentence |
denotes |
Mutations in the STK11/LKB1 (LKB1) gene, which encodes for a serine-threonine kinase, have been identified as a genetic cause of PJS. |
| TextSentencer_T5 |
496-671 |
Sentence |
denotes |
Molecular analysis of the LKB1 gene in a simplex case of PJS revealed a substitution of cytosine (C) for guanine (G) at codon 246 in exon 6, resulting in the Tyr246X mutation. |
| TextSentencer_T6 |
672-820 |
Sentence |
denotes |
The nucleotide substitution leads to a premature stop codon at the 246 residue, predicting a truncated protein and presumed loss of kinase activity. |
| TextSentencer_T7 |
821-940 |
Sentence |
denotes |
Analysis of DNA from both parents of the PJS patient did not show this mutation, which is therefore a de novo mutation. |
| TextSentencer_T8 |
941-1221 |
Sentence |
denotes |
We isolated DNA from microdissected gastrointestinal hamartomatous polyps in the PJS patient and investigated the loss of heterozygosity (LOH) at the LKB1 locus by real-time fluorescence polymerase chain reaction genotyping using a fluorescent resonance energy transfer technique. |
| TextSentencer_T9 |
1222-1314 |
Sentence |
denotes |
The results suggest a different mechanism from LOH in the formation of hamartomatous polyps. |
| T1 |
0-112 |
Sentence |
denotes |
De novo germline mutation in the serine-threonine kinase STK11/LKB1 gene associated with Peutz-Jeghers syndrome. |
| T2 |
113-263 |
Sentence |
denotes |
Peutz-Jeghers syndrome (PJS) is an autosomal dominant disease, characterized phenotypically by mucocutaneous pigmentation and hamartomatous polyposis. |
| T3 |
264-361 |
Sentence |
denotes |
Affected patients are at an increased risk of developing gastrointestinal and other malignancies. |
| T4 |
362-495 |
Sentence |
denotes |
Mutations in the STK11/LKB1 (LKB1) gene, which encodes for a serine-threonine kinase, have been identified as a genetic cause of PJS. |
| T5 |
496-671 |
Sentence |
denotes |
Molecular analysis of the LKB1 gene in a simplex case of PJS revealed a substitution of cytosine (C) for guanine (G) at codon 246 in exon 6, resulting in the Tyr246X mutation. |
| T6 |
672-820 |
Sentence |
denotes |
The nucleotide substitution leads to a premature stop codon at the 246 residue, predicting a truncated protein and presumed loss of kinase activity. |
| T7 |
821-940 |
Sentence |
denotes |
Analysis of DNA from both parents of the PJS patient did not show this mutation, which is therefore a de novo mutation. |
| T8 |
941-1221 |
Sentence |
denotes |
We isolated DNA from microdissected gastrointestinal hamartomatous polyps in the PJS patient and investigated the loss of heterozygosity (LOH) at the LKB1 locus by real-time fluorescence polymerase chain reaction genotyping using a fluorescent resonance energy transfer technique. |
| T9 |
1222-1314 |
Sentence |
denotes |
The results suggest a different mechanism from LOH in the formation of hamartomatous polyps. |