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)

The histogenesis of malignant fibrous histiocytoma (MFH) is controversial. To elucidate the cellular origin and characteristics of this neoplasm, the authors analyzed cell lines grown from 17 patients (15 soft tissue MFH and 2 bone MFH) by using light and electron microscopy, immunocytochemistry, enzyme cytochemistry, and functional tests for receptors for the Fc portion of immunoglobulin (Fc receptors) and immunophagocytosis. Each culture exhibited a storiform/pleomorphic pattern with mixed cellular populations consisting of spindle cells, polygonal cells, and bizarre giant cells; these morphologic features corresponded to the histologic characteristics of the primary tumors. The cells in each MFH line displayed histiocytic functional markers such as lysosomal enzymes, Fc receptors and immunophagocytosis. However, these cells differed from monocyte-derived macrophages (histiocytes) in immunoreactivity; the MFH cells expressed a mesenchymal antigen (FU3) distributed among perivascular cells and fibroblasts but demonstrated no positive reactions with Leu-M1 (CD15) and Leu-M3 (CD14), which recognize the cells of the monocyte-macrophage lineage. In conclusion, these findings suggest that MFH is not a tumor of true histiocytes but of facultative histiocytes showing mesenchymal differentiation in vitro. Chromosomal analysis performed in one MFH line demonstrated abnormal karyotypes; the modal chromosome number was 58, with 5 marker chromosomes.
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PMID:Malignant fibrous histiocytoma. A tumor of facultative histiocytes showing mesenchymal differentiation in cultured cell lines. 130 33

Small cell (endocrine cell) carcinoma of the gallbladder in a 62-year-old woman is reported. The palliative cholecystectomy specimen revealed a submucosally invading tumor with extensive hemorrhagic necrosis. At autopsy, performed five months after surgery, a huge tumor measuring 14 x 12 x 8 cm was located at the liver hilus. No signs or symptoms related to overproduction of hormones were recorded throughout her illness. Neither lung lesions nor gall stones were identified. Histologically, diffuse proliferation of small, spindle-shaped atypical tumor cells with numerous mitoses was evident. Intraepithelial tumor cell proliferation in the gallbladder mucosa was seen focally. The neuroendocrine nature of the tumor cells was confirmed by the histologic pattern of growth with pseudo-rosette formation, positive reaction for Grimelius' argyrophilia, neuron-specific enolase and Leu 7, and ultrastructural demonstration of neuroendocrine-type granules. Immunostaining for a variety of hormones was all negative. Characteristically, foci with squamous and adenocarcinomatous differentiation were identified in the tumor tissue. The glandular components were immunoreactive for carcinoembryonic antigen, secretory component, epithelial membrane antigen and CA19-9. The histogenesis and totipotentiality of the neoplasm were discussed.
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PMID:Small cell (endocrine cell) carcinoma of the gallbladder with squamous and adenocarcinomatous components. 131 6

Marek disease virus (MDV) is a herpesvirus of chickens that induces T lymphomas within 3 weeks of infection. The short latency and polyclonal nature of MDV-induced tumors have suggested that the virus may encode one or more direct-acting oncogenes. To date, however, no MDV-specific tumor antigens or candidate transforming genes have been demonstrated. In this paper, we report the identification of a MDV gene encoding a protein with homology to the leucine-zipper class of nuclear oncogenes. It also contains a proline-rich domain characteristic of another class of transcription factors. This gene, designated meq, maps to the long repeat of MDV and is one of the few genes that are highly expressed in MDV-induced T-cell tumors. To our knowledge, a herpesvirus gene closely related to the fos/jun family of oncogenes has not been reported previously.
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PMID:Marek disease virus encodes a basic-leucine zipper gene resembling the fos/jun oncogenes that is highly expressed in lymphoblastoid tumors. 131 48

Okadaic acid, a protein phosphatase inhibitor, is a strong tumor promoter which activates protein phosphorylation. Because another activator of protein phosphorylation, phorbol esters, stimulates hematopoietic differentiation, we sought to determine whether okadaic acid could also induce the differentiation of the human leukemic cell line U937. Differentiation was assessed by measuring changes in the following: mRNA levels, cell growth, morphology, cell surface markers, and the ability to induce superoxide. We found that okadaic acid treatment of U937 cells induces immediate increases in total cellular levels of both c-jun and c-fos mRNAs. Nuclear run-on experiments demonstrate that initial increases are secondary to increases in transcription, whereas latter changes may be secondary to mRNA stabilization. Like phorbol esters, okadaic acid treatment also activates AP-1 enhancer activity and induces the phosphorylation of c-Jun protein. Approximately 6-12 hours after treatment with okadaic acid, mRNA levels of c-myc, p34cdc2, and p58GTA, two cell cycle regulated protein kinases, decrease. Okadaic acid inhibits the growth of U937 cells, induces changes in nuclear morphology, stimulates increases in Mac-1 and Leu 11 surface antigens, and induces these cells to produce superoxide. These changes, taken together, suggest that U937 cells have been induced by okadaic acid to differentiate towards a more mature cell type.
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PMID:Induction of differentiation and c-jun expression in human leukemic cells by okadaic acid, an inhibitor of protein phosphatases. 131 24

Lymphocytes adhere to cells or extracellular matrices to perform functions relating to cytotoxicity, extravasation and tissue localization, as well as modulation of lymphocyte growth and maturation. This adherence is mainly mediated by 3 families of cell-surface adhesion molecules: integrins, immunoglobulin-related molecules and selectins. Since variations in the degree of adherence may affect the pathophysiology of lymphoproliferative disorders, the expression of a large number of adhesion molecules was analysed on Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines (LCLs), and on EBV-positive or EBV-negative Burkitt's lymphoma (BL) lines, by immunofluorescence flow cytometry and immunoprecipitation with monoclonal antibodies. With regard to the beta 1, beta 2 and beta 3 integrin subfamilies, LCLs strongly expressed CD49d/CD29 (VLA-4), CD11a/CD18 (Leu-CAMa, LFA-1) and CD51/CD61 (vitronectin receptor). These cells also abundantly expressed CD54 (ICAM-1) and CD58 (LFA-3) as well as the "homing receptors" L-selectin (LECAM-1) and CD44. BL lines had considerably lower amounts of VLA-4 than LCLs, and ICAM-1 was expressed only by some of the tumor lines. All other adhesion molecules were absent or minimally expressed in the BL cells.
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PMID:Expression of integrins and other adhesion molecules in Epstein-Barr virus-transformed B lymphoblastoid cells and Burkitt's lymphoma cells. 131 64

The phenotypic expression of Russell bodies (RB) in the tumor cells of two patients with different types of B-cell lymphoma and of one patient with plasma cell myeloma were examined. In both B-cell lymphomas, the RBs reacted consistently with anti-Leu 8 and anti-immunoglobulin M. The RBs in one case also reacted with other monoclonal antibodies, including anti-CD5, CD19, CD22, and CD25. The membranes of most of the tumor cells containing RBs did not stain. In the myeloma, the RBs reacted only with anti-immunoglobulin, and the myeloma cells expressed no surface antigens associated with B lymphocytes. This finding suggests that RBs do not form in cells that can transport glycoproteins to the cell membrane, but rather occur as a result of defective transport or process of certain glycoproteins by plasmacytoid cells.
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PMID:Russell bodies consist of heterogenous glycoproteins in B-cell lymphoma cells. 131 69

As compared with the lymphatic system, the mononuclear phagocyte system (MPS) represents the older defense system in the course of evolution. Organisms with defective or with no lymphocytic function are able to live for a certain time while metazoa cannot develop and exist without cells capable of phagocytosis. It is known that up to 80% of the mass of malignant experimental tumors may consist of macrophages. The biological relevance of these tumor-associated macrophages (TAM), however, is contested to date. Besides well-known tasks in specific and non-specific defense, the cells of the MPS possess nutritive functions. The different functions of TAM have been essentially examined in animal experiments in vivo and in vitro up to now. These studies have shown, e.g., that TAM of different phenotypes to some extent are assigned to different functions and that each tumor or tumor cell line has a specific TAM pattern. The available number of monoclonal antibodies (MAB) able to recognize different groups of human macrophages has only increased in the recent past. This also provided evidence of the phenotypic heterogeneity of macrophages in the human system. On the other hand, there is little knowledge to date of the possible biological cause of the presence of numerous macrophages also in the stroma of malignant tumors in man and on the functional relevance of particular macrophage phenotypes. In the present studies, the phenotypic pattern of tumor-associated cells was examined by immunohistochemistry in the model of human mammary carcinoma, using 18 monoclonal antibodies (Ki-M1-8, Leu-M1-3, Leu-M5, EBM11, CD1, anti-transferrin receptor [TFR], anti-MHC I, anti-MHC II or anti HLA-DR) and one polyclonal antibody (anti protein-S100). The first part of the study contains a semiquantitative evaluation of 216 cases of mammary carcinoma. The analytical results are correlated with established prognostic factors available in the case of malignant tumors in general and in that of mammary carcinomas in particular (age, menopausal status of patients, axillary lymph node and estrogen/progesterone receptor status, size of tumor, tumor type according to WHO, degree of malignancy according to histopathological and nuclear grading). As tumor parameters of absolute biological relevance, proliferating activity (Ki67) and MHC phenotype of tumor cells and amount or types of tumor-associated lymphocytes (TAL) are examined in order to analyze their correlation with prognostic factors and their importance in the tumor-macrophage system.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Human mammary carcinoma. A model for the relationship between tumor proliferation, tumor-associate macrophages, and prognostic factors]. 132 68

A previous report using cervical carcinoma cell lines suggests that the inactivation of two tumor suppressor gene products, p53 and pRB, either by complex formation with the E6 and E7 proteins of oncogenic human papillomaviruses (HPVs) or by mutation, may be an important step in cervical carcinogenesis (M. Scheffner et al., Proc. Natl. Acad. Sci. USA, 88: 5523-5527, 1991). The present study was designed to clarify the association between p53 inactivation and infection with oncogenic HPVs in primary carcinomas of human uterine cervix. We examined 36 primary cervical carcinomas for the presence of HPV DNAs by Southern blot analysis with probes specific for HPV-16, -18, -31, -33, -52, -56, and -58. HPV DNA sequences were detected in 19 of 36 tumors: 10 cases with HPV-16; 3 cases with -18; 3 cases with -58; 2 cases with -56; and one case with -52. The presence of HPV-16 and -18 in cervical carcinomas was further reexamined using polymerase chain reaction. HPV DNA sequences were detected in an additional 10 cases: 9 cases with -16 and one case with -18. The inactivation of the p53 gene by allelic loss or by point mutation was also examined. No allelic loss at the polymorphic site in codon 72 of the p53 gene was detected in any of 10 informative cases. Missense point mutations in the highly conserved regions of the p53 gene were demonstrable as single-stranded conformational polymorphisms of polymerase chain reaction-amplified DNA fragments and subsequently identified by direct DNA sequencing. Point mutations were detected in only two cases: one with an ATG----CTG transversion in codon 133 of exon 5, resulting in a Met----Leu substitution, and another with a CGG----TGG transition in codon 248 of exon 7, resulting in an Arg----Trp substitution. Both tumors with point mutations in p53 genes were among 10 tumors which contained a small copy number of HPV-16 DNA sequences (1 copy of HPV/10(1) to 10(5) cells) detectable by polymerase chain reaction amplification but not by Southern blot analysis of genomic DNAs derived from the tumors. None of 19 tumors with a large copy number of HPV DNA sequences detectable by Southern blot analysis (more than 1 copy of HPV/2 to 10 cells) nor any of 7 tumors with undetectable HPV DNA sequences contained p53 gene mutations in the regions examined.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Alterations of the p53 gene in human primary cervical carcinoma with and without human papillomavirus infection. 132 6

We investigated 9 cases of Ki-1 lymphomas morphologically and immunohistochemically. The lymphoma cells infiltrated in the lymph nodes in 7 cases, in the skin in 6 cases, in both in 4 cases and in the bone marrow in 2 cases. In lymph nodes, the giant tumor cells infiltrated paracortical areas, showing a sheet-like appearance or free cell growth pattern and in the marginal and medullary sinuses as well. In the skin, they formed subcutaneous tumor and infiltrated diffusely also in dermis. All cases were positive for Ber-H2, Ki-1 and HLA-DR and 8 cases revealed some of the T cell phenotypes. But Leu-4 and beta F1 for which all 11 peripheral T cell lymphomas were positive, were only positive in 2 cases, respectively. In the present study, the tumor cells were positive for a few antibodies for T lymphocytes and there were few cases showed positivity for Leu-4 and beta F1. The results suggest that it was questionable whether the tumor cells were derived from T lymphocytes. There may be few cases of Ki-1 lymphomas of distinct T cell lineage.
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PMID:[Morphological and immunohistochemical analysis of Ki-1 lymphoma]. 133 63

A missense mutation at cysteine 706, resulting in a retinoblastoma (RB) protein defective in phosphorylation and oncoprotein binding, has been isolated from a human tumor cell line. Since this residue is conserved in murine RB and in the related p107 protein, we studied the activity of in vitro mutants flanking this position. These experiments demonstrated that the thiol atom at codon 706 does not possess intrinsic functional activity as small polar or nonpolar residues could substitute at either codons 706 or 707, while bulkier R-group changes in these positions interfered with in vitro oncoprotein binding or in vivo protein phosphorylation. A series of missense mutants in an adjacent leucine repeat domain also demonstrated a loss of oncoprotein binding that was proportional to the magnitude of amino acid substitutions. To determine whether the cysteine 706 --> phenylalanine RB mutant retained any protein binding activity, we examined its ability to precipitate MYC, which was recently identified as a potential RB-associated protein. These experiments demonstrated that the mutant RB product is capable of binding in vitro to c-myc and L-myc proteins with comparable affinity as wild-type RB. These findings raise questions about the functional role of the RB:MYC interactions and emphasize important differences in the binding patterns between MYC and the other RB-associated proteins.
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PMID:Functional analysis at the Cys706 residue of the retinoblastoma protein. 133 91


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