[Function of p16 gene and correlation of p16 with human cancer].
CDKN2/p16 inactivation and p16 immunohistochemistry in astrocytic gliomas.
Hypermethylation of the p16 gene and lack of p16 expression in hepatoblastoma.
p16 loves me, p16 loves me not.
IKKbeta specifically binds to P16 and phosphorylates Ser8 of P16.
The most important of these is p16/CDKN2A.
Mutations of the p16 gene in gliomas.
p16 gene in uncultured tumours.
Inactivation of p16 gene in leukemia.
CDKN2A/p16 in ependymomas.
p16 expression was determined by immunohistochemistry.
The changes of p16 expression is prominent.
[Expression and regulation of p16 in osteosarcoma].
Methylation and p16: suppressing the suppressor.
P16 expression in odontogenic tumors.
Expression of p16 was searched by immunohistochemistry.
The staining pattern was divided into the following four groups: L1-/p16-, L1+/p16-, L1+/p16+, L1-/p16+.
[Study of p16 gene in mesothelioma].
p16 in HPV-associated cancers.
Immunohistochemistry for p16(INK4a) was performed.
Forty-five of the tumors were p16 positive (p16+), 27 were p16 negative (p16-), and 41 had unknown p16 status.
To test the contribution of both of these transcripts in carcinogenesis, full-length cDNA of p16 and p16 beta were cloned in separate vector constructs and then transfected into HNSCC cell lines ...
This alteration in these tumors is not associated with p16 mutation or frequent homozygous p16 gene loss.
Sequence analysis revealed no p16 mutations in the tumors with hemizygous loss of p16.
It was abolished by mutations that abrogate p16 function, as shown by transfection of a Pro81Leu p16 variant.
These cell lines lacked expression of p16 mRNA without deletions of the p16 gene.
The lone p16-resistant line expresses endogenous p16 but lacks functional pRB.
p16 hypermethylation, regarded as an indication of p16 inactivation, was evident in 24 (28.6%) of the tumors.
Frequent deregulation of p16 and the p16/G1 cell cycle-regulatory pathway in neuroblastoma.
p16, p53, and the p16/p53 combination all increased apoptosis in the cells.
Neither deglycosylation of p16 by endoglycosidases nor binding of lectin to p16 was detectable.
Tumorigenicity of the A549-p16 and H460-p16 cells in nude mice was greatly inhibited.
The growth rate of NEC transfected with p16 gene (NEC-p16) was markedly suppressed.
[A study on the inactivation of p16 genes and the expression of P16 protein in primary hepatocellular carcinomas].
The p16 gene (P16, MTS1, CDKN2) encodes a negative regulator of the cell cycle.
5' CpG island methylation of p16 is associated with absence of p16 expression in glioblastomas.
One biphenotypic case, with Rb+p16- and Rb-p16+ areas, was identified as well.
Correlation of p16 hypermethylation with p16 protein loss in sporadic gastric carcinomas.
To investigate the methylation of p16(INK4a) and RB gene, and the expression of p16(INK4a) in meningiomas.
The methylation of p16 gene may cause the inactivation of p16 gene.
The expression of p16 mRNA and p16 protein was detected by RT-PCR and Western blot.
Additionally, SMMC7721-p16 cell growth was not inhibited by exogenous p16 gene.
Loss of p16 expression is seen in all cases with alterations of the p16 gene.
The effect of flavopiridol on the growth of p16+ and p16- melanoma cell lines.
The aim of this study was to compare expression of p16 INK4A (p16) in these two tumour types.
Interaction of expression of p16 and CDK4 plays an important role in the Rb/p16 pathway.
The methylated rates of p16 correlated positively to the lacking rates of p16 protein.
This inhibition was not observed with p16 and no synergy could be obtained between p53 and p16.
p16 expression is repressed epigenetically by Polycomb, but how p16 is induced is not known.
Nine patients with p16- tumors and 28 patients with p16+ tumors received chemotherapy.