| Id |
Subject |
Object |
Predicate |
Lexical cue |
| TextSentencer_T1 |
0-96 |
Sentence |
denotes |
CDKN2/p16 or RB alterations occur in the majority of glioblastomas and are inversely correlated. |
| T1 |
0-96 |
Sentence |
denotes |
CDKN2/p16 or RB alterations occur in the majority of glioblastomas and are inversely correlated. |
| TextSentencer_T2 |
97-232 |
Sentence |
denotes |
p16 is involved in a cell cycle regulatory cascade that includes cyclin-dependent kinase 4 (cdk4), cyclin D1, and pRb (retinoblastoma). |
| T2 |
97-232 |
Sentence |
denotes |
p16 is involved in a cell cycle regulatory cascade that includes cyclin-dependent kinase 4 (cdk4), cyclin D1, and pRb (retinoblastoma). |
| TextSentencer_T3 |
233-361 |
Sentence |
denotes |
Alterations of each of these components have been described in primary human glioblastoma multiforme (GBM) or in GBM cell lines. |
| T3 |
233-361 |
Sentence |
denotes |
Alterations of each of these components have been described in primary human glioblastoma multiforme (GBM) or in GBM cell lines. |
| TextSentencer_T4 |
362-655 |
Sentence |
denotes |
Because perturbation of any component in this pathway may have similar oncogenic effects, we studied the relationship between abnormalities of CDKN2/p16 and RB, the two commonly involved tumor suppressor genes, in 55 astrocytic gliomas (42 GBMs, 8 anaplastic astrocytomas, and 5 astrocytomas). |
| T4 |
362-655 |
Sentence |
denotes |
Because perturbation of any component in this pathway may have similar oncogenic effects, we studied the relationship between abnormalities of CDKN2/p16 and RB, the two commonly involved tumor suppressor genes, in 55 astrocytic gliomas (42 GBMs, 8 anaplastic astrocytomas, and 5 astrocytomas). |
| TextSentencer_T5 |
656-799 |
Sentence |
denotes |
By using comparative multiplex PCR, homozygous deletions of the CDKN2/p16 gene were detected in 24 GBMs (57%) and in 2 anaplastic astrocytomas. |
| T5 |
656-799 |
Sentence |
denotes |
By using comparative multiplex PCR, homozygous deletions of the CDKN2/p16 gene were detected in 24 GBMs (57%) and in 2 anaplastic astrocytomas. |
| TextSentencer_T6 |
800-960 |
Sentence |
denotes |
Two additional GBMs and one anaplastic astrocytoma had allelic loss of chromosome 9p, as assessed by microsatellite polymorphisms flanking the CDKN2/p16 region. |
| T6 |
800-960 |
Sentence |
denotes |
Two additional GBMs and one anaplastic astrocytoma had allelic loss of chromosome 9p, as assessed by microsatellite polymorphisms flanking the CDKN2/p16 region. |
| TextSentencer_T7 |
961-1181 |
Sentence |
denotes |
Single-strand conformation polymorphism and DNA sequencing analysis of all three coding exons of CDKN2/p16 revealed a frameshift mutation (four-bp deletion) in one of the three GBMs that had lost the remaining 9p allele. |
| T7 |
961-1181 |
Sentence |
denotes |
Single-strand conformation polymorphism and DNA sequencing analysis of all three coding exons of CDKN2/p16 revealed a frameshift mutation (four-bp deletion) in one of the three GBMs that had lost the remaining 9p allele. |
| TextSentencer_T8 |
1182-1331 |
Sentence |
denotes |
Allelic loss of chromosome 13q at the RB gene, RB gene mutations, or loss of pRb expression was noted in 14 GBMs (33%) and 2 anaplastic astrocytomas. |
| T8 |
1182-1331 |
Sentence |
denotes |
Allelic loss of chromosome 13q at the RB gene, RB gene mutations, or loss of pRb expression was noted in 14 GBMs (33%) and 2 anaplastic astrocytomas. |
| TextSentencer_T9 |
1332-1510 |
Sentence |
denotes |
Thirty-six of 42 GBMs (86%) had alterations of either CDKN2/p16 (n = 22), RB (n = 10), or both (n = 4); these two genetic changes, however, were relatively exclusive (P = 0.003). |
| T9 |
1332-1510 |
Sentence |
denotes |
Thirty-six of 42 GBMs (86%) had alterations of either CDKN2/p16 (n = 22), RB (n = 10), or both (n = 4); these two genetic changes, however, were relatively exclusive (P = 0.003). |
| TextSentencer_T10 |
1511-1628 |
Sentence |
denotes |
Furthermore, of the six GBMs without either CDKN2/p16 or RB gene abnormalities, one case had CDK4 gene amplification. |
| T10 |
1511-1628 |
Sentence |
denotes |
Furthermore, of the six GBMs without either CDKN2/p16 or RB gene abnormalities, one case had CDK4 gene amplification. |
| TextSentencer_T11 |
1629-1745 |
Sentence |
denotes |
These data indicate that the vast majority of GBMs probably have inactivation of the p16-cdk4/cyclin D1-pRb pathway. |
| T11 |
1629-1745 |
Sentence |
denotes |
These data indicate that the vast majority of GBMs probably have inactivation of the p16-cdk4/cyclin D1-pRb pathway. |
| TextSentencer_T12 |
1746-1904 |
Sentence |
denotes |
The findings also provide corroborative evidence that CDKN2/p16 and RB are the critical glioma tumor suppressor genes on chromosomes 9p and 13q, respectively. |
| T12 |
1746-1904 |
Sentence |
denotes |
The findings also provide corroborative evidence that CDKN2/p16 and RB are the critical glioma tumor suppressor genes on chromosomes 9p and 13q, respectively. |