Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0005684 (bladder cancer)
 16,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the roll of c-myc protooncogene in human bladder cancer, c-myc gene was transfected into T-24 human bladder cancer cells and the changes of cell characteristics were studied. C-myc gene transfection was performed, using the electroporation method described previously (J.J. Urology, 80, 1989). After electroporation, c-myc gene was transfected and neo cells were cloned in a neomycin containing medium. One typical cloned cell (myc-cl3) was obtained. And this cell clone was shown to contain more than 3 extra-copies of c-myc gene by Southern blotting analysis. Morphology and growth speed of the myc-cl3 cells were not significantly different from those of original T-24 cells. However, they easily made overlapped cell-layers in the confluent growth phase. In the soft-agarose semi-solid medium, myc-cl3 cells formed about 35 times more numerous colonies than T-24 cells. Myc-cl3 cells also formed tumors on nude-mice at a significantly higher rate than T-24 cells did. These results suggest that c-myc gene plays a key roll in clonal growth and tumor formation in human bladder cancer.
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PMID:[Study of c-myc gene transfected T-24 human bladder cancer cells]. 205 96

Expression of the c-myc gene product in urinary bladder cancer was investigated by immunohistochemical staining with anti-c-myc monoclonal antibody (mAb) MYC-1. Positive staining was observed in the cytoplasm, but not in the nucleus in tissues fixed with 10% formalin. On the other hand, positive staining was localized in the nucleus in cryopreserved tissues. Of 34 cryopreserved specimens examined, positive staining with MYC-1 mAb was observed in 1 of 12 (8.3%) of grade 1 (G1), 12 of 15 (80%) of G2 and 6 of 7 (86%) of G3. Positive staining with Ki-67 mAb was observed in 2 of 12 (17%) of G1, 12 of 15 (80%) of G2, and 6 of 7 (86%) of G3. These results suggest that tumors with higher nuclear pleomorphism contain more proliferating cells.
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PMID:Detection of the c-myc gene product in urinary bladder cancer. 212 87

The protein coded by the oncogene c-myc, p62c-myc, was measured using monoclonal antibodies and flow cytometry in nuclei derived from paraffin-wax sections of transitional cell carcinomas of the human bladder. Superficial disease (stages pTa and pT1) which did not recur within 5 years of diagnosis had significantly higher oncoprotein levels than those which did recur or were muscle-invasive (stage pT2 or greater) at presentation (P less than 0.01). These preliminary findings indicate that oncoprotein levels might have prognostic significance for bladder cancer.
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PMID:c-myc oncoprotein levels in bladder cancer. 305 54

When Chinese hamster lung (CHL) cells were cultured in medium containing 25 microM cadmium chloride, resistant cells appeared at a frequency of 0.04%. When one of three tumor promoters, 12-O-tetradecanoylphorbol-13-acetate (TPA), aplysiatoxin and dihydroteleocidin B, was added during selection with cadmium chloride, the frequency of appearance of resistant cells increased more than 50-fold. Two of the resistant clones obtained were characterized. Both clones produced much higher levels of metallothionein I mRNA than the parental CHL cells. Southern blot analysis showed that in these resistant cells, metallothionein I genes were amplified approximately 5-fold. Therefore, it seems that tumor promoters can enhance the frequency of gene amplification. One possible mechanism of the action of tumor promoters in oncogenesis is amplification of activated c-onc genes. Consistent with this idea, it has been reported that c-onc genes are amplified in various cancer cells. We also found that the c-Ha-ras and c-myc genes were amplified in a bladder cancer removed surgically and in a transplanted rat hepatocellular carcinoma, Morris hepatoma 7794A, respectively.
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PMID:Increase in frequency of appearance of cadmium-resistant cells induced by various tumor promoters; evidence for the induction of gene amplification. 668 Jul 25

Archival biopsy specimens from transitional cell bladder tumours (n = 185) were analysed immunohistochemically for expression of c-myc protein. The results were compared with histopathological and clinical parameters and survival. Forty-three per cent of the tumours were negative for c-myc protein and weak, moderate, or strong cytoplasmic expression was found in 34, 14, and 9 per cent of cases, respectively. Nuclear positivity for c-myc protein was detected in 35 per cent of tumours and nuclear positivity was related to overexpression of c-erb B-2 (P = 0.01) and a high proportion of nuclei were also positive for p53 oncoprotein (p < 0.05). Cytoplasmic expression of c-myc protein was related to histological grade (P = 0.005), papillary status (P = 0.007), the S-phase fraction (P = 0.008), the mitotic index (P = 0.021), overexpression of epidermal growth factor receptor (P = 0.045), and c-erb B-2 (P = 0.17). Expression of c-myc protein was not significantly related to the progression of tumours and it had no prognostic value in survival analysis. Independent predictors were the T-category (P < 0.001), papillary status. (P = 0.001), and S-phase fraction (P = 0.061). The results show that while c-myc gene product participates in growth regulation of human bladder cancer cells, it has no independent prognostic significance.
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PMID:Expression of c-myc protein is related to cell proliferation and expression of growth factor receptors in transitional cell bladder cancer. 773 16

Amplification and overexpression of c-myc have been suggested as prognostic markers in human cancer. To assess the role of c-myc gene copy number alterations in bladder cancer, 87 bladder tumors were examined for c-myc aberrations by fluorescence in situ hybridization. Dual labeling hybridization with a repetitive pericentromeric probe specific for chromosome 8 and a probe for the c-myc locus (at 8q24) was performed to analyze c-myc copy number in relation to chromosome 8 copy number on a cell by cell basis. A clear-cut c-myc amplification (up to 40 to 150 copies per cell) was found in 3 tumors. There was a low level c-myc copy number increase in 32 of the remaining 84 tumors. There was no association of low level c-myc copy number increase with c-myc protein overexpression. This suggests that a c-myc gene copy number gain as detected by fluorescence in situ hybridization does not necessarily reflect a disturbed c-myc gene function but may indicate a structural chromosome 8 abnormality including gain of distal 8q. The strong association of low level c-myc (8q) gains with tumor grade (P < 0.0001), stage (P < 0.0001), chromosome polysomy (P < 0.0001), p53 protein expression (P = 0.0019), p53 deletion (P = 0.0403), and tumor cell proliferation (Ki67 labeling index; P = 0.0021) is consistent with a role of chromosome 8 alterations in bladder cancer progression.
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PMID:c-myc copy number gains in bladder cancer detected by fluorescence in situ hybridization. 774 7

The controls determining the initial response of cells to DNA damage probably determine whether a cancer will ultimately occur. Efficient repair or apoptosis represents extremes of control mechanisms. Misrepair can lead to fixation of damage. The changes in oncoprotein expression of three genes involved in the regulation of repair of DNA damage and postdamage proliferation of cells were measured in cultures of normal urothelium from 55 patients without any malignancy. The aim was to obtain information on interperson variation in response to carcinogens in the human population. The group included 10 pediatric patients < 2 years old. Two different carcinogenic agents, ionizing radiation and N-nitrosodiethanolamine, which represent widely different DNA-damaging pathways, were used. Both of these cause bladder cancer in humans. Cells from explanted tissue were examined after carcinogen exposure for levels of p53, c-myc, and bcl-2 proteins. Both carcinogens led to increased levels of cytoplasmic p53 protein expression, although there was significant interpatient variation. bcl-2 showed a very significant increase in expression after radiation exposure. c-myc was high and variable pre- and postexposure. Individual patient culture changes in the expression of the three oncoproteins did not correlate significantly with each other or with cell growth, suggesting that the controls are complex. Pediatric samples had lower mean control values of p53 and bcl-2 than did adult samples. This was due to the absence in this group of high controls seen in some adult cultures. The result suggest that an early breakdown in control mechanisms of growth arrest and apoptosis may occur in urothelium after carcinogen exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Variation in the expression of p53, c-myc, and bcl-2 oncoproteins in individual patient cultures of normal urothelium exposed to cobalt 60 gamma-rays and N-nitrosodiethanolamine. 854 28

Recent investigations have demonstrated p53 and Rb alterations in a subset of transitional cell carcinoma (TCC). Further genetic changes during tumor progression include overexpression of the c-myc gene in a significant number of mainly invasive bladder tumors. To study the possible interactions between these genes in TCC, urothelial cancer cell lines were chosen as an in vitro model. Expression and mutation of p53 was studied in 15 bladder cancer cell lines by immunocytochemistry, Western blot, polymerase chain reaction single-strand conformation polymorphism (PCR-SSCP) analysis and direct sequencing of double stranded PCR products of exons 4, 5, 7 and 8 of genomic DNA. C-myc expression and gene structure were studied using Northern and Southern blot techniques Rb protein expression was analyzed by Western blot. Twelve of 15 cell lines showed either p53 mutations or abnormal protein expression. Consistent with previous studies, five cell lines did not express Rb protein. None of the cell lines studied retained both tumor suppressor genes in a functional form. The c-myc gene appeared to be intact in all cell lines and copy numbers were close to normal. Northern analysis demonstrated that all cell lines expressed c-myc mRNA but evidence for altered regulation was found in at least two cell lines. Our data suggest that amplification or translocation are not the underlying mechanism for c-myc overexpression in urothelial tumors. No correlation between loss of Rb protein and c-myc expression was observed. The results presented here for the cell lines match well those obtained in vivo. Thus, these cell lines may provide a suitable model for further analysis of molecular alterations in urothelial cancer.
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PMID:Inactivation of tumor suppressor genes and deregulation of the c-myc gene in urothelial cancer cell lines. 883 85

To date, very few reports of the establishment of gall-bladder cancer cell lines have appeared, although many cancer cell lines of various kinds have been established. On the other hand, no reports could be found on signet ring cell carcinoma cell lines derived from the gall-bladder and only five cell lines from the stomach. A human gall-bladder cancer cell line (FU-GBC-2) was established in tissue culture from the ascitic fluid of a 69-year-old Japanese female patient. The tumor cells growing in tissue culture exhibited the morphological characteristics of signet ring cells in phase contrast and electron microscopy. The population doubling time was 43 hours. Heterotransplantation was succeeded by inoculation into the dermis of BALB/c nude mice. An immunocytochemical study showed that most of the cultured cells were positive for carcinoembryonic antigen, CA19-9 and epithelial membrane antigen, but negative for vimentin. The modal chromosome number was 120 with a range of 100-124. Flow cytometry showed an aneuploidy pattern in the cultured cells at passage 30. Markedly amplified c-myc oncogene was observed by Southern blot analysis. This cell line may be useful in the study of the morphological and biological characteristics of signet ring cell carcinoma and gall-bladder adenocarcinoma.
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PMID:A human gall-bladder signet ring cell carcinoma cell line. 921 24

The effects of two antisense oligodeoxynucleotide on expression of c-Ha-ras, c-myc proto-oncogene and the growth of human bladder cancer cell line were observed. Synthetic 15-mer directed at the region of the translational initiation site of c-Ha-ras, c-myc proto-oncogene (ASO-r, ASO-m) greatly inhibited the proliferation and DNA synthesis of T24 cell line, inhibited the expression of rasp21, mycp62 protein. The power of tumorigenesis of cell line treated with ASO was decreased. The results implicate the potential value in bladder cancer gene therapy.
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PMID:[Inhibitory effects of malignant phenotype of human bladder cancer cell line by c-Ha-ras, c-myc antisense oligodeoxynucleotide]. 927 77


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