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Hypermethylation of the p16 Gene and Lack of p16 Expression in Hepatoblastoma [PDF]

open access: yesModern Pathology, 2003
Hepatoblastoma is the most frequent pediatric liver tumor that develops mostly in young children. Abnormal regulation of cell cycle regulatory genes including p16 has been described, displaying no p16 mRNA and p16 protein in hepatoblastomas. The inactivation of p16, leading to the disruption of cell cycle control is involved in many types of human ...
Eunsil Yu, Ja June Jang, Jung Sun Kim
exaly   +3 more sources
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Study on P16 gene in acute leukemia

Current Medical Science, 2000
To study the change of suppressing cancer gene P16 in acute leukemia, the P16 antigen expression of leukemia cell surfaces in 61 cases were investigated with ABC assay and gene structural defects in 51 cases of acute leukemia were examined with multiple comparative PCR method.
Y, Chen, H, Zhang, B, Yue, H, Li
openaire   +2 more sources

Alterations of the p15, p16, and p18 genes in osteosarcoma

Cancer Genetics and Cytogenetics, 1996
Activation of cyclin-dependent kinases (CDKs) by interaction with cyclins regulates progression through cell cycle checkpoints. This process is counterbalanced by CDK inhibitors (CDKIs), which can inhibit progression through the cell cycle. Because CDKI expression acts to inhibit cellular proliferation, CDKIs may have a role as tumor suppressors.
C W, Miller   +5 more
openaire   +2 more sources

Adenovirus p16 gene therapy for prostate cancer

World Journal of Urology, 2000
Surgery, radiation, or hormone deprivation alone does not adequately affect local control of clinical or pathologic stage T3 prostate cancer. Lack of local cancer control ultimately leads to a higher incidence of morbidity, distant metastasis, and decreased survival, with patients having disease-specific mortality exceeding 75%.
J A, Allay   +5 more
openaire   +2 more sources

p16 gene overexpression in mouse bladder carcinomas

Cancer Letters, 1998
Deletion of 9p21 has frequently been observed in human bladder carcinomas. A candidate target suppressor gene, p16, was recently identified within this deleted region. In this study, we therefore investigated the loss of heterozygosity (LOH) of the p16 gene which is located on mouse chromosome 4, as well as its expression in mouse bladder carcinomas ...
M, Asamoto   +6 more
openaire   +2 more sources

Decreased expression of p16 gene in gastric cancer

International Journal of Oncology, 1996
We analyzed gastric cancers for p16 gene alterations. Homozygous deletion of the p16 gene was found in 1 of 8 gastric cancer cell lines and none of 20 primary gastric cancers. Mutations of the p16 gene were not detected in exon 1-3. Reverse transcription-polymerase chain reaction (RT-PCR) analysis showed decreased or no expression of the p16 gene in 1 ...
S, Fushida   +5 more
openaire   +2 more sources

Mutational analysis of the p16 gene in human neuroblastomas

Molecular Carcinogenesis, 1997
Neuroblastoma is one of the most frequent tumors in infancy. We analyzed 26 neuroblastomas, two ganglioneuromas, and a neuroblastoma metastasis for mutations and homozygous deletions of the p16 (or MTS1 or CDKN2) gene by means of the polymerase chain reaction (PCR) in combination with the single-strand conformation polymorphism (SSCP) technique and by ...
J S, Castresana   +4 more
openaire   +2 more sources

Changes of the p16 gene but not the p53 gene in human chondrosarcoma tissues

International Journal of Cancer, 2000
The role of two important tumour suppressor genes, p16 and p53, was evaluated in cartilaginous tumour tissues. Genomic DNA from 22 chondrosarcomas, 5 benign chondroid tumours, 1 sample of reactive proliferative cartilage and 2 samples of normal cartilage were analysed using polymerase chain reaction, single strand conformational polymorphism, DNA ...
J, Asp   +6 more
openaire   +2 more sources

Inactivation of the p16 Tumor Suppressor Gene in Adrenocortical Tumors

Journal of Clinical Endocrinology & Metabolism, 1999
The mechanisms of adrenocortical tumorigenesis are still unknown. Evidence that the majority of adrenocortical tumors are monoclonal in origin suggests that a progressive accumulation of genetic aberrations, due to activation of protooncogenes and/or inactivation of tumor suppressor genes, leads to abnormal cell proliferation through a multistep ...
PILON C   +6 more
openaire   +3 more sources

Hypermethylation of the p16 gene in nasopharyngeal carcinoma.

Cancer research, 1996
We have recently reported that inactivation of the p16 gene by mutation and deletion is common in nasopharyngeal carcinoma (NPC). The present study demonstrates that hypermethylation of the 5' CpG island can serve as an alternative mechanism for inactivation of the p16 gene in this tumor.
Chung, YF   +9 more
openaire   +2 more sources

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