|
Retinoblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
KRAS<sup>G12D</sup> overexpression in these cells activated transforming growth factor-β signaling and expression of CDKN2B, which, along with CDKN2A, led to cellular senescence and protected cells from KRAS-mediated transformation via inhibition of retinoblastoma phosphorylation.
|
28892048 |
2018 |
|
Retinoblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In addition, expression of p15(INK4b) and RB1 was analysed by quantitative real-time PCR.
|
16682076 |
2006 |
|
Retinoblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Both the retinoblastoma and p53 pathways are often genetically altered in human cancers and their complex regulation is in part mediated by the three gene products p16, p14(ARF), and p15 of the INK4 locus on chromosome 9p21.
|
15837753 |
2005 |
|
Retinoblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Smad3 overexpression recapitulated activin-induced p15 expression and repression of cyclin A and Rb phosphorylation.
|
16140969 |
2005 |
|
Retinoblastoma
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
A series of 23 retinoblastoma tissue specimens and 2 retinoblastoma cell lines (Y79 and WERI-Rb1) were subjected to methylation-specific PCR (MSP) analysis of hypermethylated genes identified in human cancers, including p14(ARF), p15(INK4b), p16(INK4a), VHL, and MGMT.
|
11980845 |
2002 |
|
Retinoblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
To test the hypothesis that cell cycle regulatory gene abnormalities are determinants of clinical outcome in adult acute lymphoblastic leukemia (ALL), we screened lymphoblasts from patients on a Southwest Oncology Group protocol for abnormalities of the genes, retinoblastoma (Rb), p53, p15(INK4B), and p16(INK4A).
|
10733508 |
2000 |
|
Retinoblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
It was shown that p14ARF and p16INK4a play active roles in the p53 and Rb tumor suppressive pathways, respectively, and p15INK4b is a mediator of the extracellular growth inhibition signals.
|
10537333 |
1999 |
|
Retinoblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The tumor suppressor genes p53, retinoblastoma (RB), p16, and p15 encode proteins that regulate the cell cycle cooperatively by controlling the transition from G1 to S phase and may play an important role in cell growth and differentiation.
|
9058294 |
1997 |
|
Retinoblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In the present study, we analyzed human ovarian carcinoma cell lines for abnormalities in the tumor suppressor gene Rb (retinoblastoma) and in cyclin-dependent kinase 4 (CDK4) inhibitor genes (p16INK4 and p15INK4B) using molecular biology techniques.
|
9194486 |
1997 |
|
Retinoblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
However, among these negative regulators in cell cycle control, only 4 have been shown to be consistently involved in the development of human cancers as tumor suppressors: Rb (Retinoblastoma susceptibility protein), p53, and two recently identified cyclin-dependent kinase inhibitors, p16INK4A/MTS1 and p15INK4B/MTS2.
|
8652807 |
1996 |
|
Retinoblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Alterations of the RB, p53, p16(CDKN2), and p15 genes in human astrocytomas were screened by single strand conformation polymorphism analysis of polymerase chain reaction products (PCR-SSCP analysis) and then confirmed by dideoxy sequencing.
|
8674005 |
1996 |