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)

Correlation between the expression of growth factor/receptor systems or the alterations of tumor suppressor genes and biological malignancy of gastric cancer was described. Overexpression of many growth factors/receptors, such as EGF, TGF alpha, EGF receptor and ERBB2, and reduction of type I receptor for TGF beta may be linked with new prognostic factors of gastric carcinomas. The expression of cripto, a novel gene of EGF family, shows a tendency to correlate with tumor staging of well differentiated gastric adenocarcinomas. p53 gene abnormalities take place in 60% of gastric carcinomas including early stage carcinoma. Loss of heterozygosity on chromosomes 1q, 7p and 7q is frequently observed in advanced gastric carcinomas of well differentiated type. Molecules which regulate tumor invasion and metastasis such as nm23, tissue inhibitor of metalloproteinase (TIMP) and endogenous galactoside-binding lectin may provide for prognostic factors of gastric cancer.
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PMID:[New prognostic factors in human gastric carcinomas]. 134 86

K-SAM gene was originally isolated as an amplified gene in a stomach cancer cell line by in-gel DNA renaturation method. K-SAM encodes a membrane receptor with tyrosine kinase and is often amplified in poorly differentiated type of stomach cancer, while c-ERBB-2 is often amplified in well differentiated type of stomach cancer. There are several forms of K-SAM mRNAs which are generated by alternative splicing, and two types of K-SAM protein without transmembrane region. The ligand of K-SAM is considered to be growth factor(s) belonging to fibroblast growth factor (FGF) or heparin binding growth factor (HBFG) family. We have also frequently found amplification of HST-1 or HSTF1 gene in esophageal cancer. HST-1 gene, originally found as a transforming gene, is located on human chromosome 11q13, and it locates 35 kbp apart from its related gene, INT-2. Neither of the genes was expressed even in cancer cells with the co-amplification. By cosmid walking, we have identified at least two genes, designated tentatively as EXP1 and EXP2, on the same amplicon as HST-1 and INT-2, and the mRNAs for EXP1 and EXP2 genes were increased in amounts proportional to the degree of amplification.
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PMID:Biological significance of gene amplification in carcinogenesis. 184 51

Molecular mechanism of development and progression of gastric cancer which could be a base of molecular diagnosis was described. Amplification and point mutation of oncogenes are less common in gastric carcinomas, even though it is valuable for diagnosis. Amplification of ERBB2 seems to be an indicator for metastatic ability of gastric carcinoma. Overexpression of EGF/receptor system is a biologic marker for high malignancy. Diagnostic significance for scirrhous gastric carcinomas is found in over-expression of TGF beta, IGF and PDGF. Loss of heterozygosity on chromosomes 5q and 17p frequently occurs commonly in well differentiated type gastric cancer. More accumulation of molecular alterations in the development and progression of gastric cancer should make the molecular diagnosis more valuable in clinical field.
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PMID:[Molecular diagnosis of gastric cancer]. 198 3

Hematopoietic growth factors have recently been well characterized by complementary DNA cloning. For human epidermal growth factor, granulocyte-macrophage colony-stimulating factor recombinant proteins have been expressed in Escherichia coli. To reduce the toxic side effects of chemotherapy on the bone marrow, recombinant human granulocyte-macrophage colony-stimulating factor and recombinant human interleukin 3 were applied to patients suffering of gastrointestinal cancers. To determine the influence of recombinant human granulocyte-macrophage colony-stimulating factor and recombinant human interleukin 3 on human pancreas and gastric cancer cell cells in vitro, a sensitive microculture test system was established that allows precise quantification of proliferation. A more than twofold enhancement of proliferation was observed by interleukin 3 and granulocyte-macrophage colony-stimulating factor in two of two cell cultures derived from gastric carcinoma cells, while two of nine cultures from pancreas carcinoma cells have shown enhanced cell growth in the presence of recombinant human interleukin 3 or recombinant human granulocyte-macrophage colony-stimulating factor. In comparison, recombinant human epidermal growth factor increased cell growth in two of two gastric and in five of nine pancreas carcinoma cultures. In general, 1-10 ng/mL of the growth factors yielded the highest growth rate, but even 1-pg amounts produced increased cell growth. Expression of messenger RNA for granulocyte-macrophage colony-stimulating factor, interleukin 3, and the oncogene HER2/neu remained undetectable in all of the tested cell lines, while the various abundance of messenger RNA for the epidermal growth factor receptor was different in each cell line. The reported results imply that the hematopoietic growth factors interleukin 3 and granulocyte-macrophage colony-stimulating factor influence cellular growth of pancreas and gastric carcinoma cells by a paracrine mechanism and may possess a more general regulatory function than originally anticipated.
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PMID:Stimulation of pancreas and gastric carcinoma cell growth by interleukin 3 and granulocyte-macrophage colony-stimulating factor. 201 78

DNA fragments amplified in a stomach cancer-derived cell line, KATO-III, were previously identified by the in-gel DNA renaturation method, and a 0.2-kilobase-pair fragment of the amplified sequence was subsequently cloned. By genomic walking, a portion of the exon of the gene flanking this 0.2-kilobase-pair fragment was cloned, and the gene was designated as K-sam (KATO-III cell-derived stomach cancer amplified gene). The K-sam cDNAs, corresponding to the 3.5-kilobase K-sam mRNA, were cloned from the KATO-III cells. Sequence analysis revealed that this gene coded for 682 amino acid residues that satisfied the characteristics of the receptor tyrosine kinase. The K-sam gene had significant homologies with bek, FLG, and chicken basic fibroblast growth factor receptor gene. The K-sam gene was amplified in KATO-III cells with the major transcript of 3.5-kilobases in size. This gene was also expressed in some other stomach cancer cells, a small cell lung cancer, and germ cell tumors.
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PMID:K-sam, an amplified gene in stomach cancer, is a member of the heparin-binding growth factor receptor genes. 237 25

All of 13 human esophageal cancer cell lines contained mRNAs for both basic fibroblast growth factor (bFGF) and its receptor, FGFR1/N-sam protein, while they did not have mRNAs for keratinocyte growth factor (KGF) despite the presence of mRNAs for the KGF receptor gene, K-sam. The results indicate that in human esophageal cancer, bFGF plays roles in an autocrine manner, while KGF acts as a paracrine mediator. In contrast, only one of seven human gastric cancer cell lines contained bFGF mRNAs, while three out of the seven had mRNAs for FGFR1/N-sam protein. The KGF gene was not expressed in any of the gastric cancer cell lines, while K-sam mRNAs were detected in six out of the seven. The results demonstrate that in most human gastric cancers, bFGF does not act as an autocrine mediator, while KGF acts as a paracrine factor. The mRNAs for the other four members of the fibroblast growth factor (FGF) family, including acidic FGF, int-2 protein, hst-1 protein, FGF5 protein and FGF6/hst-2 protein could not be detected in the esophageal and gastric cancer cell lines.
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PMID:Expression of fibroblast growth factor gene family and its receptor gene family in the human upper gastrointestinal tract. 751 92

The K-sam gene was originally cloned from KATO-III human gastric cancer cells and is identical to the bek or keratinocyte growth factor (KGF) receptor (KGFR) or fibroblast growth factor receptor 2 gene. K-sam generates several variant transcripts by alternative splicing, and the most abundant K-sam transcript in KATO-III cells was cloned as the K-sam-IIC3 cDNA, which has the KGF-binding motif and a short carboxyl terminus lacking a putative phospholipase C-gamma 1 association site, Tyr-769. The K-sam-IIC3 cDNA was distinct from the K-sam-IIC1 cDNA, which was the same as the previously reported KGFR cDNA. The K-sam-IIC1 product contains a long carboxyl terminus with Tyr-769. K-sam-IIC3 showed greater transforming activity in NIH 3T3 cells than did K-sam-IIC1, and in gastric cancer cell lines in general, the level of K-sam-IIC3 mRNA was greater than that of K-sam-IIC1 mRNA. Here we report that the K-sam-IIC3 product was less autophosphorylated than the K-sam-IIC1 product in NIH 3T3 transfectants. K-sam-IIC3-transfected keratinocytes showed a stronger mitogenic response to KGF than did K-sam-IIC1 transfectants. Moreover, K-sam-IIC3-transfected L6 myoblast cells hardly differentiated when cultured in differentiation-inducing medium and growth was not significantly affected, while K-sam-IIC1 transfectants showed a differentiated phenotype with a reduced growth rate. These data indicate the difference in the signal transduction mediated by two KGFR-type K-sam variants generated by alternative splicing which might be involved in certain differentiation and carcinogenesis scenarios.
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PMID:A truncated K-sam product lacking the distal carboxyl-terminal portion provides a reduced level of autophosphorylation and greater resistance against induction of differentiation. 779 73

We found that the expression of human platelet-activating factor receptor (PAFR) gene is differentially regulated by estrogen and TGF-beta 1. Primer extension analysis revealed that the levels of the PAFR transcript 2 were increased by estrogen, but decreased by TGF-beta 1 in the human stomach cancer cell line (JR-St cells) which expressed both functional endogenous PAFR transcript 1 (leukocyte-type) and transcript 2 (tissue-type). Both ligands did not affect the expression of intrinsic PAFR transcript 1. Furthermore, the response elements to estrogen and TGF-beta 1 in the PAFR promoter 2 were delineated by a transient expression assay using the chloramphenicol acetyltransferase (CAT) gene as a reporter in this cell line. A negative response element for TGF-beta 1 was mapped on the sequence from -90 bp to -81 bp, which has consensus sequence for TIE (TGF-beta 1 inhibitory element). Although consensus estrogen response element (AGGTCAnnnTGACCT) is not present in this promoter, the entire sequence comprising two AGGTCA half motifs spaced by 153 bp (from -257 bp to -93 bp) conferred weak but significant estrogen responsiveness. Thus, through these elements in the PAFR promoter 2, estrogen and TGF-beta 1 may regulate the PAFR gene to achieve a tissue-specific expression.
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PMID:Positive and negative regulations of human platelet-activating factor receptor transcript 2 (tissue-type) by estrogen and TGF-beta 1. 780 41

The ERK gene has been isolated as a genomic DNA encoding a part of the receptor protein-tyrosine kinase which belongs to the EPH subfamily. We previously identified a partial complementary DNA (cDNA) encompassing the catalytic domain of ERK from the expression library of human gastric cancer with an antiphosphotyrosine antibody. Using this cDNA as a probe, the cDNAs encoding mature ERK protein were isolated. The putative mature ERK protein, a total of 967 deduced amino acid residues, showed high homology with chicken Cek5 (92.5%) and mouse Nuk (99.1%). Chromosomal in situ hybridization revealed that human ERK cDNA is localized to chromosome 1p34-35. In Northern blot analysis of normal human tissues, the ERK gene was ubiquitously expressed mainly in cells of epithelial origin but not in the brain. Studies on RNAs from 76 human tumor tissues and cell lines showed that ERK is expressed at higher levels in various tumors of epithelial origin than in corresponding normal tissues, most frequently in gastric cancers (12 of 16, 75.0%). Overexpression of ERK was also detected in one osteosarcoma cell line. These findings suggest that ERK plays some significant role in carcinogenesis in the stomach and other tissues.
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PMID:Overexpression of ERK, an EPH family receptor protein tyrosine kinase, in various human tumors. 803 77

K-SAM/FGFR2 gene encodes a receptor tyrosine kinase which belongs to the fibroblast growth factor receptor family and is amplified and overexpressed in KATO-III gastric cancer cells. To characterize K-sam proteins in cancer cells, anti-K-sam rabbit polyclonal antibody PK1-2 was raised and used for the immunoprecipitation analysis. 135, 125, and 110-kDa transmembrane proteins were detected in KATO-III cell lysate, while a soluble truncated 85-kDa K-sam protein was found in the conditioned medium. The molecular size of the soluble K-sam protein does not match with those predicted from the secreted forms of the K-sam cDNA which have been cloned so far. The soluble K-sam protein was highly N-glycosylated like the transmembrane versions, and N-glycosylation appeared to be necessary for its release.
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PMID:A soluble form of K-sam/FGFR2 protein in the culture medium of human gastric cancer cells. 806 Mar 18


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