Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunoreactivity for endocrine peptides (serotonin, gastrin, somatostatin, insulin, corticotropin, calcitonin, neurotensin, vasoactive intestinal peptide, and bombesin), cytoskeletal proteins (high and low molecular weight keratins), and tumor differentiation markers (chromogranin, neuron-specific enolase, carcinoembryonic antigen, S100 protein, and Grimelius stain) was sought on nine cervical and one vaginal poorly differentiated small-cell carcinoids. Dense-core secretory granules were ultrastructurally identified in all cases (seven of ten) in which tissue was available for electron microscopy. Immunoreactivity for endocrine secretory products was rarely noted, and only in a minority cell population (serotonin in two of ten). The majority of the tumors exhibited immunoreactivity for low molecular weight keratin (AE1/AE3 in eight of ten; CAM 5.2 in seven of nine), and three of ten tumors focally expressed high molecular weight keratin. Among the markers of neuroendocrine differentiation, neurospecific enolase was more frequently expressed (ten of ten) than chromogranin (five of ten) or argyrophilia (three of ten). Carcinoembryonic antigen was present in eight of ten tumors. S100 protein was absent in all cases. In summary, poorly differentiated small-cell carcinoids of the lower female genital tract, similarly to other small-cell endocrine tumors, occasionally exhibit focal glandular and squamoid differentiation, and only relatively infrequently or focally express immunohistochemically detectable endocrine secretory products, chromogranin, and argyrophilia.
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PMID:Endocrine and tumor differentiation markers in poorly differentiated small-cell carcinoids of the cervix and vagina. 302 70

A soybean gene (Gmhsp17.5-E) encoding a small heat shock protein was introduced into primary sunflower tumors via T-DNA-mediated transformation. RNA blot hybridizations and S1-nuclease hybrid protection studies indicated that the heat shock gene containing 3.25 kilobases of 5'-flanking sequences was strongly transcribed in a thermoinducible (40 degrees C) manner. Transcriptional induction also occurred to a lesser extent upon treatment of whole tumors with sodium arsenite and CdCl2. Basal (26 degrees C) transcription was not detected in soybean seedlings, but it was quite evident in transformed tumor tissue. A 5' deletion to -1,175 base pairs with respect to the CAP site had no effect on the levels of thermoinducible transcription, but it resulted in a large increase in basal transcription. Further removal of DNA sequences (including the TATA-distal heat shock consensus element) to -95 base pairs reduced thermoinducible transcription by 95% and also greatly decreased basal transcription. The termini of the Gmhsp17.5-E RNA in the tumor were generally the same as those present in soybean RNA, with the exception of several additional 3' termini.
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PMID:Upstream sequences required for efficient expression of a soybean heat shock gene. 302 55

Conditions were established where transient transfection of two marker genes resulted in the expression of one or the other, but not both, in individual cells as assayed by immunofluorescence. Thus, the expression from a single cell reflects the activity of single active transcription templates. Under these conditions, a vector encoding the simian virus 40 large tumor antigen (SV40 T-Ag) driven by the SV40 enhancer and early promoter was transfected into CV-1, L, or HeLa cells yielding, for all three cell types, about 10-30% T-Ag-positive cells as assayed by immunofluorescence. Similar vectors containing either mutated or deleted SV40 enhancers also gave T-Ag-positive cells, but at about 1/100 the frequency. Quantitative analysis showed that T-Ag-positive cells produced about the same amount of T-Ag whether or not an active enhancer was present. Chloramphenicol acetyltransferase-encoding vectors gave the same result. The data are consistent with the hypothesis that at a low, but finite, probability, fully functional transcription complexes can form on a given active template in the absence of enhancer DNA. Enhancers seem to increase the number of active templates. Subcloning experiments suggest that these transcription complexes can be surprisingly stable.
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PMID:Formation of stable transcription complexes as assayed by analysis of individual templates. 304 5

The transformation of a potentially neoplastic cell into an autonomous highly malignant and metastatic tumor cell involves a multifactorial cascade of events. This will eventually lead not only to the emergence of a tumor cell with an unlimited potential of replication, but more important will contribute to its ability to ignore and evade homeostatic immune and non-immune regulatory mechanisms. Specifically, those mechanisms which may restrict and direct its growth, dissemination, patterns of differentiation and interaction with the cellular and humoral factors comprising its environment. However, many different factors may contribute to a highly invasive and malignant phenotype. It is obvious that one should expect that a cardinal role should be assigned to alterations in those factors which contribute to the capacity of the malignant cells with its environment at the cell membrane level, which in turn is dependent on the concerted functional expression of specialized membrane associated components (i.e. receptors, cyto adhesion molecules (CAM's), histocompatibility antigens, GAP junction complexes, extracellular matrix components, etc.). In the present studies, we have investigated the contribution of three major factors, which maybe the cause or result of alterations at the level of the cell membrane: MHC encoded antigen expression, susceptibility to the cytolytic activity of NK cells and enhanced expression of the c-K-ras proto-oncogene, as to their development of metastatic capacity of a malignant cell. To address these questions, we used metastatic (IE7) and non-metastatic (IC9) variants of the murine 3-methylcholanthrene induced T-10 fibrosarcoma. Using this system, the following major conceptually important observations were made: A. The restoration by transfection of the expression of membrane associated H-2K encoded glycoproteins abrogates the metastatic capacity of the highly metastatic tumor cell clone, IE7, irrespective of the degree of susceptibility to NK or c-K-ras oncogene expression. This reduction in metastatic capacity is followed by a significant decrease in its tumorigenicity which is concomitant with its ability to induce in vivo potent H-2K restricted CTL's. These results clearly indicate that H-2K region encoded molecules play no apparent role in determining the susceptibility of tumor cells to NK cells, and yet their loss or aberrant expression is a cardinal event in tumor progression towards metastatic capacity, a fact which is supported by similar observations achieved in other murine models (18).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:NK sensitivity, H-2, c-K-ras proto-oncogene expression and metastases: analysis of the metastatic potential of H-2 gene transfected fibrosarcoma cells. 306 49

Mammary explants or isolated mammary cells from rabbit have been cultured in the presence of insulin, prolactin and cortisol alone or in combination. The cellular content in alpha s1-casein, beta-casein and whey acidic protein (WAP) mRNA have been evaluated using the corresponding cDNA as probes. In all cases alpha s1-casein mRNA was the most abundant and WAP mRNA the least abundant mRNA. The three genes showed essentially similar dependency towards hormones. Prolactin stimulated mRNA accumulation and insulin and cortisol amplified this stimulation. The induction by prolactin was rapid whereas stimulation by insulin was slower. Fragments of rabbit genomic DNA inserted in lambda phage and containing alpha s1-casein, and WAP genes have been cloned. The primary sequence around the CAP site of the three genes has been established. A comparison of the sequences located upstream from the CAP site shows several striking homologies with the corresponding genes from cow, rat and guinea-pig. This suggests that these sequences participate in the transcriptional control of the genes by hormones. The mechanism involved in the transduction of the prolactin message to milk protein genes in unknown. Using mammary explants in culture, several classical mechanisms of transduction have been examined. Phorbol ester, phorbol -12, 13-dibutyrate (PdiBu) inhibited prolactin action. However, another tumor promoter, 12-O-tetradecanoyl phorbol-13-acetate (TPA), did not alter prolactin action. Kinase C inhibitor H7 did not prevent prolactin action and did not overcome the inhibition by PdiBu. Kinase C is therefore not essential for the transduction of the prolactin message to milk protein gene. Neomycin, which inhibits phosphatidylinositol hydrolysis by phosphorylase C, prevented prolactin action, whereas other inhibitors of phosphatidylinositol metabolism remained uneffective. Degradation of phosphatidylinositol is therefore likely not an essential step of prolactin action on milk protein genes. Inhibitors of tyrosine kinase and phosphatase exhibited a poor capacity to modify the prolactin response. Hence, transduction mechanisms using tyrosine kinase activity likely cannot account for prolactin action.
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PMID:Recent data on the structure of rabbit milk protein genes and on the mechanism of the hormonal control of their expression. 307 27

We have previously shown that inhibition of uPA activity of a human tumor-HEp3-results in a drastic reduction of its metastasis in the chick embryo. Using 125IUdR-labeled tumor cells, we have now studied the role of uPA in individual steps of tumor metastasis. We found that, 48 hr after inoculation of tumor cells on the CAM, the organs of the embryos, inoculated with cells in which uPA was inhibited, contained 4-fold less cells than the controls. Neither the initial advance of the tumor mass into the CAM nor the process of extravasation was affected by the inhibition of tumor uPA. However, the infiltration of the CAM mesenchyme by individual tumor cells was blocked when tumor uPA activity or production was inhibited. In addition, indirect evidence implicated uPA as an essential factor in the tumor cell intravasation.
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PMID:Plasminogen activator dependent pathways in the dissemination of human tumor cells in the chick embryo. 312 81

The class II (Ia) major histocompatibility complex antigens are a family of integral membrane proteins whose expression is limited to certain cell types, predominantly B lymphocytes, macrophages, and thymic epithelial cells. In B cells, Ia expression is both developmentally regulated and responsive to external stimuli. The differentiation of early B stem cells to mature B lymphocytes is accompanied by the appearance of cell surface Ia antigens; the transition to plasma cells results in loss of class II gene expression. In Ia-expressing B cells, the T cell-derived lymphokine interleukin-4 (IL-4) increases such expression by an as yet undefined mechanism. Chloramphenicol acetyltransferase gene expression was cis-activated by a region of the Ia A alpha k gene in a B lymphoma line, but not in a myeloma line. A nuclear protein that bound to two sites within this region, upstream from previously described transcription elements, was found in normal spleen cells. This binding activity was also found in spleen extracts from athymic mice, which lack T lymphocytes, and in Ia-positive B lymphocyte tumor cell lines, demonstrating that it is a B cell protein. Further analysis showed the activity to be undetectable in an Ia-negative pre-B cell line and in three plasmacytoma cell lines that are Ia negative. IL-4 treatment of normal and athymic mouse spleen cells greatly increased the binding of this nuclear protein to these two sites, concomitant with increased MHC class II gene transcription. Thus, B cells contain a sequence-specific DNA-binding activity whose level is influenced both by IL-4 and by differentiation signals.
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PMID:A DNA binding protein regulated by IL-4 and by differentiation in B cells. 314 43

In case of chemotherapy against brain tumors, it is most important to choose suitable drugs for brain tumors, since human tumors have different drug sensitivity and growth. Heretofore, human tumor clonogenic assays or human glioma-bearing nude mice models were usually used for predicting the drug sensitivity of brain tumor. Human tumor clonogenic assays are one of the best in vitro tests for anticancer drug activity. However, plating efficiency is low, sometimes preventing evaluation of drug sensitivity, and the slow growth of colonies means that culture time is long. Assays using immunodeficient mice are used for predicting the drug sensitivity of human tumors; usually results reflect the sensitivity of the parent tumor. However, procedure using athymic nude mice are slow and expensive. We took notice of Murphy's system for the chemosensitivity test, in which a human tumor is transplanted into the chorioallantoic membrane (CAM) of a chick embryo, because in this system, various kinds of human tumors could be grafted in high rate. By modifying the conventional Murphy's system, we studied the efficiency of this system in predicting the drug sensitivity of brain tumors. We compared the result of a drug sensitivity test using CAM of a chick embryo with that using nude mice. First, we studied the effect of chemotherapeutic agents such as ACNU, bleomycin. Next, we studied the effect of combination treatment of CAP or CAPF. The tumor reduction rate of the sensitivity test using a chick embryo tended to agree with that using nude mice.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Chemosensitivity test for human gliomas]. 319 94

Five acoustic neurinomas have been operated with hearing preservation as a goal. We monitored intraoperative brainstem auditory evoked potentials (BAEP) in all five cases, electrocochleogram (ECoG) using needle electrode in external auditory meatus in four, and compound action potentials directly recorded from the cochlear nerve (CAP VIII) in three. In all five cases the tumor was totally resected and cochlear nerve was anatomically preserved. However, in only one case useful hearing was preserved with preservation of all wave forms of the BAEP. Another patient with preservation of all wave forms of BAEP and the ECoG showed postoperative severe hearing loss. Other three patients showed postoperative severe hearing loss: only Wave I of BAEP and ECoG were preserved without preservation of the CAP VIII in one whose cochlear nerve was thought to be damaged in cerebellopontine angle cistern; Wave I of BAEP, ECoG and CAP VIII were preserved in one in whom it was suggested cochlear nerve near brainstem or cochlear nucleus was damaged; none of the BAEP, ECoG and CAP VIII was preserved in one in whom it was suggested distal cochlear nerve, or internal auditory artery was damaged. These different patterns of changes suggested that different causes for the hearing loss and difficulties in hearing preservation during acoustic neurinoma surgery. Having identified the putative mechanism of the hearing loss by monitoring those potentials, suggestions are made about how such hearing loss might be avoided. For preservation of the hearing in acoustic neurinoma surgery, all of those potentials including all wave forms of BAEP, ECoG and CAP VIII should be preserved during surgery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Intraoperative electrophysiological monitoring for hearing preservation in acoustic neurinoma surgery]. 322 31

Thirty-four cases of tumor of the renal pelvis or ureter or both have been treated in our department during the past decade. The primary tumor was in the renal pelvis in 11 cases, in the ureter in 21 cases and in the ureter and renal pelvis in 2 cases, a co-existent tumor in the bladder was found in 4 cases. Seventeen patients had a tumor on the right side and 17 on the left side. The most frequent symptom was gross hematuria (70.6%) and flank pain was the presenting symptom in 7 cases (20.6%). On the intravenous pyelography, a filling defect in the renal pelvis or ureter (41.2%) and nonvisualization (53.0%) were frequent findings. Twenty-nine cases had undergone total nephroureterectomy with resection of a bladder cuff, 3 had simple nephrectomy and 2 had open biopsy alone. Postoperative radiation therapy was done in 1 case, chemotherapy in 10 cases, and 6 cases of them were treated by CAP therapy (cis-dichlorodiamine platinum, doxorubicin and cyclophosphamide). Actual and relative 5-year survival rates were 53.8% and 63.5%, and no significant difference was found in survival rate between the patients with renal pelvic tumors and those with ureteral tumors.
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PMID:[A clinical study on 34 cases of urothelial cancer of upper urinary tract]. 344 24


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