Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0007097 (carcinoma)
 152,788 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 111 thyroid cancer patients consisting of 89 papillary carcinomas, 17 follicular carcinomas, 2 medullary carcinomas, 1 squamous cell carcinoma and 2 malignant lymphomas, the levels of 12 tumor markers, including thyroglobulin (Tg), were measured in the serum by radioimmunoassay and radioimmunoassay related methods. Serum levels of Tg were elevated in 58.6%, those of CA-M26 in 15.7%, CA 19-9 in 5.3%, CT in 3.6%, NSE in 3.6%, CA 15-3 in 2.6%, CA 125 in 2.6%, CEA in 0.9%, CA-M 29 in 0%, ferritin in 0%, SCC in 0% and AFP in 0% of cases. Among the patients, there was a case of thyroid carcinoma secreting thyroglobulin and CA 19-9, both of whose titer decreased after surgery. Immunohistochemical studies were carried out on 57 of the above mentioned patients plus 6 anaplastic carcinomas, 15 adenomas, 5 adenomatous goiters, 6 Hashimoto's thyroiditis, 15 Graves' disease and 15 normal subjects. CA 19-9 was positive in 58% of the papillary carcinomas, EGF in 73% of papillary carcinomas, 67% of anaplastic carcinomas, and 33% of follicular carcinomas, while EGF-R was found in 73% of the papillary carcinomas, and 33% of the follicular carcinomas. Enhanced expression of ras p 21 oncogene and (c-myc oncogene) was demonstrated in 100% (100%) of anaplastic carcinomas, in 100% (67%) of follicular carcinomas and in 63% (90%) of papillary carcinomas. Our results indicate that a better tumor marker is required and more extensive molecular oncology research should be pursued.
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PMID:Tumor markers and oncogene expression in thyroid cancer using biochemical and immunohistochemical studies. 169 52

Diagnosis- and/or prognosis-related alterations of (proto) oncogenes may be detected in neuroblastoma (N-myc), carcinoma of breast and ovary (HER2/neu), NHL (c-myc, bcl-2), CML (c-abl/bcr), and some other neoplasias. A wide variety of methods for the detection of gene alterations can be applied. The methods of detection have to be chosen according to the expected mechanisms of oncogene activation, the availability of adequately prepared tissue, and the technical standard of the laboratory. The sensitivity, specificity, and quantitation of morphological techniques (immunohistochemistry and in situ hybridization) is restricted and their results have to be interpreted most carefully. Whenever possible, at least two different techniques should be used, preferably on two different levels, i.e. RNA/DNA and protein. Furthermore, the combination of morphological and non morphological methods should be aspired.
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PMID:[Oncogenes and oncogene products--possibilities and significance of their detection]. 170 8

We established a human carcinoma cell line (KHC 287) from a patient with large-cell-typing lung carcinoma associated with marked leukocytosis. The culture supernatant of KHC 287 cells promoted granulocytic colony formation of human bone-marrow cells in semi-solid culture. Colony formation was almost completely suppressed by treatment of the supernatant with a monoclonal anti-granulocyte colony-stimulating factor (G-CSF) antibody. Not only G-CSF but also interleukin-1 alpha (IL-I alpha), IL-I beta and IL-6 were detected in the culture supernatant by an ELISA method. Northern blot analysis of KHC 287 cells revealed distinct expression of these cytokine genes. Southern blot hybridization of KHC 287 DNA showed 20- and 40-fold co-amplification of c-myc and c-ki-ras, respectively. The chloramphenicol acetyl transferase (CAT) activity was distinctly enhanced in the KHC 287 cells which were transfected with the 360 bp upstream region of G-CSF gene inserted into pSV00CAT, but not in non-G-CSF-producing tumor cell lines. These results suggest that overproduction of the transactivating factor(s) which binds to the 360 bp of the G-CSF upstream region is responsible for the abnormal expression of G-CSF gene in KHC 287 cell line.
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PMID:Analysis of abnormal expression of g-csf gene in a novel tumor cell line (KHC 287) elaborating G-CSF, IL-1 and IL-6 with co-amplification of c-myc and c-ki-ras. 171 Feb 8

Experiments have been designed to investigate hormonal effects on the human prostatic carcinoma cell line LNCaP in the presence of complete foetal calf serum. At physiological concentrations (3.3 x 10(-9)M), several derivatives of 17 alpha-methyl-testosterone led to a significant reduction of cell proliferation, inhibition of colony formation in soft agar, change of morphology, induction of a prostate specific mRNA and down-regulation of c-myc RNA. Two different antiandrogens, hydroxyflutamide and cyproterone acetate, were capable of reversing the effects exerted by the synthetic androgens on growth properties. The proliferation rate of control cells devoid of androgen receptor was not inhibited by synthetic androgens. Our results indicate that the cellular androgen response mechanism of LNCaP cells is intact and that synthetic androgens elicit androgen receptor mediated suppression of the transformed phenotype. Rare cases of remission of prostatic cancer on androgen treatment have been reported. LNCaP cells may be a model of an uncommon class of prostatic cancer which responds favourably to androgen treatment.
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PMID:Synthetic androgens suppress the transformed phenotype in the human prostate carcinoma cell line LNCaP. 171 53

Nine cases of prostatic carcinoma and 5 cases of benign prostatic hyperplasia (BPH) were examined for the in vivo expression of mRNA by an in situ hybridization technique for cellular proto-oncogenes, c-myc, c-fos, and c-sis. The latter of which encodes the B-chain of the platelet-derived growth factor (PDGF). High levels of c-myc and c-sis mRNAs were demonstrated in one highly differentiated prostatic carcinoma. Signals were localized in epithelial cells, both in packed cancer cells and in benign hyperplastic cells with glandular differentiation. A lower level of c-fos mRNA was also detected in the same areas. Four other carcinoma specimens showed c-sis mRNA, three of which also expressed c-fos mRNA. One other carcinoma expressed only c-myc mRNA. Three BPH specimens also contained c-sis and c-fos mRNA with one also exhibiting c-myc mRNA in the glandular epithelial cells. The results support the possibility that local production of growth factors, i.e. PDGF, may play a role in proliferation of prostatic epithelial cells.
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PMID:In situ expression of mRNA for proto-oncogenes in benign prostatic hyperplasia and in prostatic carcinoma. 171 28

A poly(ADP-ribose) polymerase inhibitor, benzamide (BA), was found to induce flat revertants of NIH 3T3 cells that had been transformed by human Ha-ras, rat Ki-ras, rat c-raf, and human ret-II. These genes had been amplified in original transformants, but they were completely eliminated by BA. Contrary to this, endogenous activated Ha-ras in a human bladder carcinoma cell line, T24, was not eliminated by BA. The gene loss seemed to be restricted to exogenous and/or amplified sequences. BA also eliminated the amplified c-myc gene in HL-60 cells, concomitant with differentiation into granulocytes. We demonstrated that the amplified c-myc gene was not present as episomes. It is probably present as double minutes or a homogeneously staining region. Dimethylsulfoxide also induced differentiation at a concentration that did not inhibit poly(ADP-ribose) polymerase. The cell lost the c-myc gene in association with this differentiation. The amplified c-myc gene in a colon adenocarcinoma cell line, COLO 320HSR, and the amplified mdr-1 gene in an adriamycin-resistant myelogenous leukemia cell line, K562/ADM, were not eliminated by BA. Various poly(ADP-ribose) polymerase inhibitors also eliminated human Ha-ras in the NIH 3T3 transformant and the c-myc gene in HL-60 cells.
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PMID:Loss of amplified genes by poly(ADP-ribose) polymerase inhibitors. 177 88

In breast tumor cell lines, c-myc amplification is frequently associated with estrogen unresponsiveness. We, however, succeeded in characterizing an estrogen-responsive cell line VHB1 derived from a duct cell carcinoma, which exhibits c-myc amplification and overexpression. We therefore studied the effects of estrogen and antiestrogen on c-myc expression in this particular cell line. We also investigated these effects on the expression of c-mil and c-myb oncogenes, also expressed but not amplified in VHB1 cells. Short-(1 h) and long-(72 h) term stimulations were performed. Our experiments showed that estradiol (E2 10(-8) M) was still able to stimulate c-myc expression equally either after short or long-term treatment. In the same way, the antiestrogen 4-hydroxytamoxifen equally decreased c-myc expression but the reversal effect of E2 after long-term antiestrogen treatment was more pronounced than after short-term treatment. The effects of E2 and 4-OH Tam on the expression of the not-amplified c-mil and c-myb oncogenes were stronger than those observed on c-myc expression; however, the E2 reversal effect was identical either after short or long-term antiestrogen treatment. Our results may enlighten some aspects of the complex action of some of the early- and late-growth regulated genes in breast cancer.
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PMID:C-myc overexpression, c-mil, c-myb expression in a breast tumor cell line. Effects of estrogen and antiestrogen. 177 59

To understand the possible role of oncogenes in the development of human esophageal cancer, the expression of c-myc and HER-1 genes was studied by in situ hybridization. The results showed that: (a) The c-myc and HER-1 protooncogenes were transcriptionally activated (b) Activation of c-myc gene was observed in hyperplastic cells and carcinoma cells. (c) The degree of pathological changes of the esophageal epithelium was related to the level of c-myc transcription, the highest level of c-myc expression was seen in invasive carcinoma cells. (d) Expression of HER-1 gene in carcinoma cells is higher than that in normal and adjacent non-tumor cells, but its frequency is lower than that of c-myc gene.
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PMID:[Expression of c-myc and HER-1 genes in the development of human esophageal cancer]. 178 50

The effects of three hormonal agents with a different mechanism of action (tamoxifen [TAM], medroxyprogesterone acetate [MPA] and estradiol [E2]) on tumor growth, differentiation and oncogene expression were evaluated using the estrogen-receptor positive human breast carcinoma cell line MCF-7 transplanted into nude mice. In MCF-7 tumors treated with E2, tumor incidence, mean weight of tumors, 3H-thymidine labelling index, differentiation antigen HMFGM (human milk-fat globule membrane) and ras p21, c-myc, neu oncogene products, the level was significantly increased. On the other hand MPA suppressed all of them. TAM increased the level of c-myc expression and HMFGM antigen, but suppressed the others. This evidence indicates that E2 induces both proliferation and differentiation of MCF-7 tumor cells. MPA suppresses both proliferation and differentiation, and TAM induces differentiation and suppresses proliferation.
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PMID:Effects of tamoxifen, medroxyprogesterone acetate and estradiol on tumor growth and oncogene expression in MCF-7 breast cancer cell line transplanted into nude mice. 183 73

In this paper a number of anticancer agents of natural origin will be presented. Hydroxycamptothecin (HCPT) was found to produce a strong inhibitory action on a variety of animal tumors. It is also effective for treatment of patients with gastric carcinoma, liver carcinoma, tumor of head and neck or leukemia. Pharmacologic studies showed that it could depress S phase of tumor cells significantly and cause formation of cellular chromatid breaks. By means of alkaline elution and nick translation methods it has been proved that HCPT induced DNA single strand breaks remarkably. Homoharringtonine (HHRT) was shown to be effective against acute leukemia. Recent experiments in tumor-bearing mice indicated that (HHRT) could diminish tumor metastasis. Using molecular hybridization technique it was demonstrated that (HHRT) decreased the content of c-myc RNA in the cytoplasm but not in the nuclei. Lycobetaine (LBT) possessed strong inhibitory effects on a number of ascites tumors. In clinical trials it was effective against ovarian and gastric carcinomas. It is able to intercalate into DNA. Oxalysine (OXL) is a new antibiotic and shown to be effective against tumor metastatis. When used in combination with 5-FU, its anticancer action could be enhanced. Other natural compounds such as indirubin, beta-elemene, irisquinone, oridonine, norcantharidin and PSP have been also found to possess antitumor action.
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PMID:Recent advances in pharmacologic study of natural anticancer agents in China. 184 13


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