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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recessive lethal mutations in the fat locus of Drosophila cause hyperplastic, tumor-like overgrowth of larval imaginal discs, defects in differentiation and morphogenesis, and death during the pupal stage. Clones of mutant cells induced by mitotic recombination demonstrate that the overgrowth phenotype is cell autonomous. Here we show that the fat locus encodes a novel member of the cadherin gene superfamily: an enormous transmembrane protein of over 5000 amino acids with a putative signal sequence, 34 tandem cadherin domains, four EGF-like repeats, a transmembrane domain, and a novel cytoplasmic domain. Two recessive lethal alleles contain alterations in the fat coding sequence, and the dominant fat allele, Gull, contains an insertion of a transposable element in the 33rd cadherin domain. Thus, this novel member of the cadherin gene superfamily functions as a tumor suppressor gene and is required for correct morphogenesis.
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PMID:The fat tumor suppressor gene in Drosophila encodes a novel member of the cadherin gene superfamily. 195 33

Tumorigenesis and invasive capacity of tumor cells are affected by the interactions between the tumor cells and the host cells; in particular, they are regulated by growth factors released from host cells. We have studied the effect of growth factors and cytokine on tumorigenesis and invasive capacity of tumor cells by examining a regressor tumor cell line (ER-1) derived from SHR rat mammary adenocarcinoma. The regressor tumor cells grew progressively in immunosuppressed rats, but spontaneously regressed in normal rats. We studied in vitro effect of growth factors on invasive capacity of ER-1 tumor cells into mesothelial cells obtained from SHR rats. As the results, pretreatment with EGF or TGF-beta significantly enhanced invasive capacity of ER-1 cells, whereas TNF-alpha did not show any effect. We pretreated ER-1 cells with EGF or TGF-beta for 24 hours in vitro, and then intraperitoneally transplanted them into SHR rats. The treated regressor tumor cells grew and killed the host. These results suggest that tumorigenesis and invasive capacity of regressor tumor cells are mediated by growth factors which promote growth and invasive abilities of tumor cells.
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PMID:[Enhancement of tumorigenesis and invasive capacity of regressor tumor cell by growth factors]. 195 44

The C-erbB-2 gene was first found in human genomic DNA as a sequence which had homology in nucleotide sequence to the V-erbB by molecular hybridization under relaxed conditions. The product of this gene is a receptor type protein-tyrosine kinase which has a structure highly related to that of epidermal growth factor receptor (EGF-r: C-erbB-1). The proto-neu gene is a rat counterpart of the C-erb B-2 gene. The C-erbB-2 gene is also called as the HER-2 gene. The C-erbB-2 gene acquires the ability to transform NIH 3 T 3 cells by, 1) mutation which alters valine 659 in transmembrane region to glutamic acid as was found in neu gene activation, 2) deletion of c-terminal regulatory domain or 3) gene-amplification or overexpression. C-erbB-2 expresses in human embryos on mucous membranes and glands, but only faintly in adult tissues. High expression or gene amplification in human tumor appeared to be an indication for high risk of metastasis or high degree of malignancy.
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PMID:[Proto-oncogene C-erbB-2 and human cancer]. 196 37

Peptide growth factor-induced signal transduction leads to a long-term adjustment of the genetic programs of responding cells. A point mutation in the transmembrane domain of the neu receptor has been found to activate its tyrosine kinase and oncogenic potential. Our previous studies show that ligand stimulation of a chimeric epidermal growth factor receptor-neu proto-oncogene (EGF-R/neu) induces the neu tyrosine kinase and leads to the programmed activation of cell growth-regulated genes. We have now studied the effect of the neu oncoprotein on the genomic growth factor response in cells expressing the EGF-regulated neu tyrosine kinase. Expression of the neu oncogene in these cells inhibited 75-90% of the EGF-stimulated mRNA induction of the immediate early serum response genes, such as junB encoding a transcription factor, N10 encoding a putative nuclear hormone binding receptor for an as yet undefined ligand, and B10, the protein product of which is still unknown. The relative lack of mRNA induction was not due to a loss of the chimeric EGF-R/neu receptors from the cell surface. Also, the neu oncogene decreased serum- and tumor promoter induction of these genes. Our results suggest that the neu oncogene is capable of deregulating mRNA responses to extracellular signalling, similar to the effects of the c-Ha-ras oncogene. Knowledge of the mechanisms responsible for these changes in gene regulation will help to define oncogenic transformation of cells in molecular terms.
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PMID:Downregulation of the early genomic growth factor response in neu oncogene-transformed cells. 197 91

Expression of the c-erbB-2 gene product and the epidermal growth factor receptor (EGF-R) was investigated in 54 cases of human bladder cancer immunohistologically and by Western blot analysis. For detection of the c-erbB-2 product, two specific antibodies, a rabbit polyclonal antibody directed to the intracellular domain and a murine monoclonal antibody recognizing an epitope in the extracellular domain, were used. Seventeen cases of bladder cancer were stained by the anti-c-erbB-2 polyclonal antibody, while 20 cases were stained by the monoclonal antibody, with good correlation on both stainings (p less than 0.01). There were four c-erbB-2 positive cases in 26 G1 tumors, four in 15 G2 tumors, and nine in 13 G3 tumors. There were also eight erbB-2 positive cases in nine muscle-invasive tumors, nine of 45 superficial tumors, four of five with lymph node metastasis, and seven of 14 without metastasis, as revealed by staining with the polyclonal antibody. Thus, the c-erbB-2 gene product was more frequently expressed in high grade tumors (p less than 0.01), in high stage tumors (p less than 0.01), and nodal metastatic tumors (N.S. by Chi-square test). Twenty-two of the 54 tumors were stained by an anti-EGF-R monoclonal antibody, 528 IgG. The expression of EGF-R was independent of histological grading, tumor stage, and nodal status, and no correlation was observed between expression of the c-erbB-2 product and EGF-R. The c-erbB-2 product may be applicable as a tumor marker for evaluation of malignant potential, invasiveness, and probably metastatic potential of human bladder cancer.
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PMID:Expression of c-erbB-2 gene product in urinary bladder cancer. 198 41

The authors investigated the presence of epidermal growth factor (EGF-R), estrogen (ER), progesterone (PR), and androgen (AR) receptors in 42 laryngeal squamous cell carcinomas and 20 normal laryngeal mucosa specimens. EGF-R were expressed in all tumor specimens analyzed, with significantly higher levels in tumor samples compared with normal mucosa (P less than 0.05). The immunohistochemical study demonstrated the presence of EGF-R in basal and parabasal cells of normal mucosa and in most of the cancer cells. There was no correlation between EGF-R and tumor localization or T classification. On the other hand, the authors did find an interesting correlation between EGF-R levels and grading, EGF-R levels being significantly higher in G3 than in G1-G2 tumors. Moreover, the three patients whose tumors expressed the highest EGF-R levels had disease recur within 8 months. Among tumor specimens, 9.5%, 35.7%, and 9.5% expressed very low but detectable ER, PR, and AR levels, respectively. No statistically significant difference was found between the levels of steroid receptors in the tumor and normal mucosa specimens, and neither was there any correlation of ER, PR, and AR with the pathologic findings. The authors' results suggest that the EGF-R system may play a role in regulating the growth of laryngeal cancer. Additional studies should demonstrate whether, as in other tumor types, EGF-R expression may have prognostic significance in human laryngeal cancer.
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PMID:Receptors for epidermal growth factor and steroid hormones in primary laryngeal tumors. 199 Dec 97

To select human melanoma cells that are highly tumorigenic and metastatic in nude mice we have implanted fragments of a fresh human melanoma metastasis subcutaneously (s.c.) into a nude mouse. After 3 passages in nude mice, part of the xenograft was cultured and a new melanoma cell line, MV3, was established. After intravenous (i.v.) inoculation of 2 x 10(6) MV3 cells, 95% of the nude mice (n = 20) developed lung colonies within 6 weeks. S.c. inoculation of 2 x 10(6) MV3 cells resulted in 95% tumor take, while 90% of the mice (n = 20) showed spontaneous metastases in the lungs within 7 weeks. Histological and immunohistological features of the original tumor of the patient were largely retained in the tumors of the mice and in the cell line in vitro. As shown by Alcian blue staining, MV3 cells contain large quantities of glycosaminoglycans (GAGs) and/or proteoglycanes (PGs), both in vivo and in vitro. The cells showed a marked expression of transferrin receptor, ICAM-1, EGF-receptor, and VLA-2 integrin. As only few human melanoma cell lines are available that frequently show metastasis in nude mice, the highly metastatic MV3 cell line represents a useful tool for studying the expression and regulation of molecules on human melanoma cells involved in the process of metastasis.
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PMID:Establishment and characterization of a human melanoma cell line (MV3) which is highly metastatic in nude mice. 201 61

The epidermal growth factor receptor (EGFR) level in 56 esophageal cancer tissues was measured by 125I-EGF binding assay to elucidate its role in tumor progression. The survival rate of patients with high EGFR level (more than 50 fmol/mg protein) was significantly lower than that of patients with low EGFR level (less than 50 fmol/mg protein, P less than 0.01), although a correlation between EGFR level and the pathologic findings was not observed. The expression of EGF was examined immunohistochemically using anti-EGF monoclonal antibody in 100 esophageal cancer tissues; EGF-positive tumor cells were detected in 92.0%. The immunoreactivity of EGF was classified arbitrarily into four grades according to the number of stained tumor cells. The expression of EGF significantly correlated with the differentiation of esophageal squamous cell carcinoma (P less than 0.01, by chi-square test). The survival rate of patients with high EGF immunoreactivity (Grade 2 or 3) was much lower than in those with lower grade (0 or 1) tumors, (P less than 0.01). Patients with both high EGFR level and EGF immunoreactivity had a much worse prognosis than if both were low. Furthermore, the mitotic index was higher in groups with both high EGFR and EGF than if both were low (16.39 +/- 5.35 versus 6.90 +/- 3.31). These results suggest that EGF and EGFR in the autocrine system may play an important role in tumor progression in esophageal cancer and their expression could be of prognostic significance.
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PMID:Clinical significance of the expression of epidermal growth factor and its receptor in esophageal cancer. 204 34

Primary cultures of non malignant human breast tissues, benign mastopathies and breast carcinoma were performed in defined culture conditions. Epithelial cells from these primary cultures were characterized for mammary epithelial cell specific markers, for in vitro cell proliferation, for steroid receptors and hormone sensitivity (estradiol, progesterone and prolactin) and for EGF sensitivity. We show that although some mastopathies have estradiol and progesterone receptors, they did not respond to hormone treatment. Human prolactin had no effect on the proliferation of one mastopathy but stimulates the cell growth of another fibrocystic mastopathy. EGF was capable of stimulating the three types of primary cultures. As regards growth characteristics, steroid hormone receptors and prolactin sensitivity, phenotypes of mastopathy cells differ from each other; some are similar to non malignant cells, whereas others are comparable to tumor cells.
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PMID:Primary cultures of human benign mastopathies and mammary carcinomas; growth factor requirements. 206 47

Malignant progression in breast cancer represents the processes through which localized, hormone-dependent tumor cells become resistant to endocrine manipulations and metastasize to sites distant from the primary tumor. By selection in ovariectomized athymic nude mice, we have isolated a variant (MIII) of the hormone-dependent, poorly invasive, human breast cancer cell line MCF-7. MIII cells have lost their absolute requirement for estrogen to form proliferating tumors in nude mice. Furthermore, these tumors are significantly more invasive than the parental MCF-7 cell line. MIII cells retain some responsivity to estrogens and antiestrogens, indicating that they have progressed to a hormone-independent but hormone-esponsive phenotype. In an attempt to determine the nature of this process, we have compared the phenotype of MIII cells with that of other MCF-7 variants. These comparisons strongly suggest that the factors contributing to perturbations in antiestrogen sensitivity, hormone-dependent growth, metastatic potential and tumorigenicity are essentially independent of each other and acquired in a random manner. Loss of estrogen receptor expression and overexpression of EGF receptors tend to occur later in the process of malignant progression.
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PMID:The process of malignant progression in human breast cancer. 208 84


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