Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a highly frequent homozygous deletion of the p16/CDKN2 gene in the esophageal cancer cell line and a relatively high frequency of homozygous deletion in gastric cancer cell lines. In contrast, in primary esophageal carcinomas, mutation frequency of the p16/CDKN2 gene has been controversial (0, 21, and 52% previously reported), and no reports are available for the mutation frequency of this gene in surgical specimens of gastric carcinomas. Here we report that four (16%) of 25 primary esophageal squamous cell carcinomas were found to be mutated, one in exon 1 and three in exon 2, and that no mutations were observed in 19 surgical specimens of gastric adenocarcinomas. This is the first report showing the absence or quite low frequency of mutation in surgical specimens of gastric carcinomas.
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PMID:Mutation frequency of the p16/CDKN2 gene in primary cancers in the upper digestive tract. 761 82

To study the involvement of the p16 tumor suppressor gene in esophageal cancer development, we examined homozygous deletion of the p16 gene in 13 human esophageal cancer cell lines and 9 gastric cancer cell lines, in which some of genetic alterations have already been characterized. By Southern blot analysis, homozygous deletion was observed in 12 out of the 13 esophageal cancer cell lines (92%), in 2 out of a total of 9 gastric cancer cell lines (22%). It was also found that the p16 gene loss, cyclin D1 amplification and p53 gene mutations occurred independently in these cell lines. These findings suggest that loss or mutations of the p16 gene are involved in most esophageal cancers and that mutation of this gene plays a critical role in the development of esophageal cancer.
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PMID:Highly frequent homozygous deletion of the p16 gene in esophageal cancer cell lines. 809 26

The investigation of molecular evidence of gastric carcinoma will be contributable to the prevention, gene diagnosis and therapy of human gastric neoplasms. To determine the specific genetic change in human gastric cancer (HGC) and precancerous lesions, we analysized FISH, PCR/SSCP, IHC and DNA sequencing by using multiple probes to detect the gene abnormalities (mutation, deletion, amplification or overexpression of genes) of 67 fresh tumors, 63 endoscopic biopsies including 30 dysplasia (DYS) and 33 intestinal metaplasia (IM, and 4 tumor cell lines from HGC patients. Multiple genetic abnormalities including hypomethylation of H-ras gene, amplification and overexpression of met and erbB2, deletion of APC, mts1/p16, p53 and nm23 gene and point mutation of p53 gene were noted in HGC and precancerous lesion of human gastric mucosa. Among these changes, p53 gene was the highest frequence genetic alteration in 39/67 (54-58%) of gastric carcinoma. These results indicate that overexpression of met and H-ras occurs at early stage in progression of neoplasia, amplification of met, erbB2 and akt2 gene occurs at progressing stage of tumorigenesis, deletion of p53, APC, mts1/p16 and nm23 occurs at advanced stage in the progression of cancer. The abnormalities should be associated with malignant phenotypes: poor differentiation, vascular invasion, lymph nodes metastasis, and low survival time. We detected p53 gene mutation in both cancer and precancerous lesions of IM and DYS. These results suggest that p53 may be a susceptible gene and alteration of p53 gene plays an important role in the development of HGC.
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PMID:[Multiple gene alterations involved in the processor of human gastric carcinogenesis]. 869 90

p16 (MTS-1, multiple tumor suppressor gene 1), a putative tumor suppressor gene, is one of the cyclin-dependent kinase inhibitors (CDI) and it regulates the G1/S transition of the cell cycle. To clarify the role of p16 in primary gastric cancer, we have investigated somatic mutations of this gene by using the polymerase chain reaction/single strand conformation polymorphism (PCR-SSCP) method. In 23 surgical specimens of primary gastric cancer, none were detected in exon1 and exon 2. Among the 6 human gastric cancer cell lines examined, PCR products were not found in 2, MKN28 and MKN45, suggesting the presence of homozygous deletions. No mutation was found in the other 4 cell lines. Furthermore, decreased expression levels were not observed in 13 gastric cancer tissues by reverse transcription PCR (RT-PCR). Considering the above results of PCR-SSCP and RT-PCR, genetic alterations of the p16 gene are rarely implicated in human gastric cancer tumorigenesis.
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PMID:Infrequent alterations of the p16 (MTS-1) gene in human gastric cancer. 922 7

We analyzed p15 and p16 gene alterations in gastric cancer. Only MKN45 showed both homozygous deletions but other cell lines and all of tumor specimens did not show any alterations. Using RT-PCR analysis, decreased or no expression of the p16 gene was found in 1 of 7 cell lines (except MKN45) (14.2%) and in 8 of 20 tumors (40%), whereas no abnormalities of p15 gene expression were found. These results suggest that the p16 gene may correlate with tumorigenesis and tumor expansion due to decrease or loss of gene products in gastric cancer.
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PMID:[Alteration of p15 and p16 gene in gastric cancer]. 926 16

Deletion of mts1/p16 gene was frequently detected in many human tumor cell lines. However, whether alteration of the p16 gene was involved in human gastric carcinogenesis, it is not clear. In order to determine the incidence and correlation of the p16 gene deletion with human gastric cancer, we performed analyses of PCR, Southern and Northern blotting on 85 fresh tumor specimens and 5 tumor cell lines from gastric cancer patients. Homozygous deletion was observed in 1 cell line and down-regulation of expression was observed in 3. High rate of gene deletion was detected by PCR in 14 of 85 fresh tumor tissues. Gene deletion was confirmed by Southern blot analysis with p16 cDNA probe in 6 out of 26 tumor specimens examined.
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PMID:[Deletion and down-regulation of mts1/p16 gene in human gastric cancer]. 938 51

The mRNA level of CDKN2 (p16), retinoblastoma (Rb) and p53 in cancerous and non-cancerous tissue samples were compared using a semi-quantitative reverse-transcription-polymerase chain reaction method. The mean CDKN2 mRNA level of 10 gastric cancer specimens was significantly higher than that of their non-cancerous tissue samples (p=0.039). In contrast, the mRNA levels of Rb and p53 in gastric cancer tissues were both significantly lower than those in their non-cancerous tissue samples. Furthermore, both mRNA ratios of Rb/CDKN2 and p53/CDKN2 were significantly decreased in gastric cancer tissues. Therefore, suppression of both Rb and p53 and overexpression of CDKN2 may be associated with the tumorigenesis of gastric cancer.
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PMID:Quantitative analysis of CDKN2, p53 and retinoblastoma mRNA in human gastric carcinoma. 966 18

Cultured human gastric cancer cell line PAMC82 was studied in vitro to further verify anti-tumor effect sof rare-earth elements and explore their mechanism of tumor inhibition. Inhibitory effects of elements lanthanum and cerium on cell growth, reverse effects of them on reduction of malignancy and effects of them on level of expression of oncogene and cancer suppressor gene were observed. Lanthanum chloride, cerium chloride and mixed rare-earth chloride at levels of 0.5 to 1.5 mmol/L could inhibit obviously growth of cancer cells and change cell morphology and microtubule structure of PAMC82, similar to that of normal cells, their colony-forming ability lowered in soft agar, and expression of tumor suppressor gene p53, p16 and p21 increased and that of gene nm23 lowered.
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PMID:[Effects of lanthanum and cerium on malignant proliferation and expression of tumor-related gene]. 981 84

Aberrant methylation of 5' CpG islands is thought to play an important role in the inactivation of tumor suppressor genes in cancer. In colorectal cancer, a group of tumors is characterized by a hypermethylator phenotype termed CpG island methylator phenotype (CIMP), which includes methylation of such genes as p16 and hMLH1. To study whether CIMP is present in gastric cancer, the methylation status of five newly cloned CpG islands was examined in 56 gastric cancers using bisulfite-PCR. Simultaneous methylation of three loci or more was observed in 23 (41%) of 56 cancers, which suggests that these tumors have the hypermethylator phenotype CIMP. There was a significant concordance between CIMP and the methylation of known genes including p16, and hMLH1; methylation of p16 was detected in 16 (70%) of 23 CIMP+ tumors, 1 (8%) of 12 CIMP intermediate tumors, and 1 (5%) of 21 CIMP- tumors (P<0.0001). Methylation of the hMLH1 gene was detected in three of five tumors that showed microsatellite instability, and all three of the cases were CIMP+. The CIMP phenotype is an early event in gastric cancer, being present in the normal tissue adjacent to cancer in 5 of 56 cases. These results suggest that CIMP may be one of the major pathways that contribute to tumorigenesis in gastric cancers.
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PMID:Aberrant methylation in gastric cancer associated with the CpG island methylator phenotype. 1055 13

p14(ARF), generated through an alternative splicing process that replaces the first exon, 1alpha, of p16(INK4a) with exon 1beta, located >15 kb upstream of exon 1alpha, has been shown to function as a growth suppressor. We examined 11 gastric cancer cell lines for mRNA expression, homozygous deletion, mutation, and promoter methylation of the p14(ARF) gene. No mRNA expression was detected in 5 of the 7 diffuse-type cell lines. All intestinal cell lines displayed normal levels of expression except for one with a low level of expression. Of the 5 cell lines without expression, 3 (MKN45, NUGC-2, and NUGC-4) and 1 (KATO III) displayed homozygous deletion and methylation of the p14(ARF) gene, respectively. No mutation was found in the whole coding region of the p14(ARF) gene in 8 cell lines without homozygous deletion. Our results indicate that the p14(ARF) gene is more frequently inactivated by homozygous deletion or methylation in diffuse-type gastric cancer cell lines (5/7, 71.4%) than in intestinal ones (0/4, P = 0.022). When we also analyzed 62 primary gastric cancers for the methylation status of the p14(ARF) promoter region, the methylation frequency tended to be higher in diffuse-type gastric cancers (15/33, 45.5%) than in intestinal ones (7/28, 25%). Thus, p14(ARF) alterations might be involved in diffuse-type gastric carcinogenesis.
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PMID:Alterations and hypermethylation of the p14(ARF) gene in gastric cancer. 1092 58


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