Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
The frequency of mutations and deletions detected differs markedly between cell lines (44%) and primary tumors (10%) suggesting that while p16/CDKN2 may play a role in tumorigenesis in some head and neck squamous cell carcinomas, inactivation of p16/CDKN2 probably occurs more frequently in cell lines as a result of adaptation to cell culture.
|
7923115 |
1994 |
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
In this aspect, the potential role of the CDKN2 gene at 9p21-p22 in ovarian carcinogenesis was assessed in an extended panel of ovarian tumors, 11 human ovarian carcinoma cell lines, and 1 cervical tumor cell line.
|
7743516 |
1995 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Our results suggest that a putative tumor suppressor gene on 9p, possibly CDKN2, may contribute to squamous cell carcinoma tumorigenesis.
|
7658499 |
1995 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Whereas RB defects eliminate the checkpoint completely, aberrations of the upstream components, such as cyclin D1 and p16INK4/CDKN2, can cooperate in multistep tumorigenesis.
|
7585513 |
1995 |
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
From these data we conclude that the occurrence of CDKN2 (p16/MTS1) mutation in primary breast cancer is a rare event and is not likely to be involved in human breast tumour carcinogenesis and progression.
|
7547249 |
1995 |
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
Our results suggest that the CDKN2 alterations contribute in tumorigenesis in some patients with B-NHL.
|
7670111 |
1995 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
These results suggest that CDKN2 plays an important role during tumorigenesis or tumor progression in a significant proportion of pancreatic adenocarcinomas.
|
8589035 |
1995 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
This suggests that CDKN2 is not involved in ovarian tumorigenesis and that another gene(s) may be the target of the frequent 9p allelic losses observed.
|
7591208 |
1995 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Our results suggest that the concurrent amplification of cyclin E and CDK2 genes may play a role in colorectal carcinogenesis.
|
7601562 |
1995 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
To investigate whether CDKN2B and CDKN2 are involved in esophageal tumorigenesis, we studied homozygous deletion, intragenic mutation, and messenger RNA (mRNA) expression of CDKN2 and CDKN2B in nine esophageal squamous cancer cell lines.
|
7547637 |
1995 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
To assess the role of CDKN2 in endometrial tumorigenesis, 34 tumor samples were examined for loss of heterozygosity at 9p21 and mutation in CDKN2.
|
7646759 |
1995 |
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
To define the involvement of p16/CDKN2 and p15/MTS2 inactivation in ovarian tumorigenesis and the association of these inactivation events with histological types and clinical stages of ovarian tumors, we analyzed homozygous deletion and somatic mutation of p16/CDKN2 and p15/MTS2 genes, as well as hypermethylation of the 5'-CpG island of the p16/CDKN2 gene, in 49 primary ovarian tumors and 6 ovarian carcinoma cell lines.
|
8980248 |
1996 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
The p16Ink4/CDKN2, D-type cyclins, their partners Cdk4/Cdk6, and pRb constitute a G1 regulatory pathway commonly targeted in tumorigenesis.
|
8968104 |
1996 |
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
We observed a marked decrease in CDC2 and CDK2 kinase activity associated with a corresponding decrease in the amount of CDC2 but not CDK2 protein; a decreased growth potential of Adp21WAF1/CIP1-infected cells demonstrated by diminished [3H]thymidine incorporation, increased cell doubling time and G1-arrested cell cycle; an association between Adp21WAF1/CIP1-infected cells and inhibition of aneuploid cell accumulation; and an alteration of the malignant phenotype of cells was evidenced by the loss of anchorage-independent growth in soft agar and the failure to induce tumorigenesis in both peripheral and intracerebral xenograft models, including the prevention of tumor formation Adp21WAF1/CIP1 infection 2 days post tumor cell implantation.Adp21WAF1/CIP1.
|
8875977 |
1996 |
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
From the data, it can be argued that p16/CDKN2 and p53 mutations are relatively late occurrences in human oral tumorigenesis and that genetic alterations of the ras genes may not play a significant role in squamous neoplasia.
|
8835820 |
1996 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
As reported previously, the mutational spectrum of CDKN2 in melanomas differs from that of internal malignancies and supports the involvement of UV in melanoma tumorigenesis.
|
8834170 |
1996 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
CDKN2 is not deleted with high frequency in primary breast carcinomas, and the p16 gene does not play a role in breast carcinogenesis via this mechanism.
|
9259969 |
1997 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
The CDKN2 gene appears to be the major tumor suppressor gene on chromosome 9p21, and it is thought to be involved in the tumorigenesis of various lymphoid malignancies.
|
9086436 |
1997 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
To explore the involvement of CDKN2 in prostate carcinogenesis, alterations of CDKN2 were examined in 116 human prostate tissues and cell lines and xenografts.
|
9815578 |
1997 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
The results of deletion mapping also suggest that another TSG(s) may reside at the 9p21-22 area particularly at the D9S162 loci and that co-deletion of this putative gene with CDKN2/p16(INK4A) may play a role in breast carcinogenesis.
|
9990866 |
1998 |
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Our results are in agreement with earlier studies demonstrating CDKN2/p16 inactivation during tumorigenesis of astrocytic tumors.
|
10359140 |
1999 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Although the observed homozygous deletions strengthen the hypotheses that CDKN2 and DBCCR1 are important tumor suppressor genes, there is no evidence that either is a more critical or an earlier target for oncogenesis.
|
11410506 |
2001 |
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Because up-regulation of the cyclin D2/CDK4 complex and down-regulation of cyclin E/CDK2 complex were found in seminomas as well as in non-seminomas and in all tumor stages, these findings seem to be early events during tumorigenesis of testicular GCTS: Together with previous findings that retinoblastoma mRNA and protein expression is strongly decreased in these tumors, these data suggest an unusual deregulated G(1)-S checkpoint as a decisive event for germ cell tumors.
|
11358847 |
2001 |
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Further investigation into the regulatory mechanisms governing CDK2 expression may lead to a better understanding of vestibular schwannoma tumorigenesis.
|
12352662 |
2002 |
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
These results suggested that mutation of the p16/CDKN2 gene was a common factor in the development of human MMMs and ACCs, while this gene may be correlated with development and/or progression of a subtype and play a role in the oncogenesis of these cancers.
|
17912431 |
2007 |