Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0677930 (primary tumor)
 20,210 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pretreatment serum levels of the tumor-associated antigens CA-125, tissue polypeptide antigen (TPA), carcinoembryonic antigen (CEA), and placental alkaline phosphatase (PLAP) were analyzed in 142 patients with epithelial ovarian carcinoma, and related to clinical and histopathological parameters. In a linear multiple regression model CA-125 serum levels were profoundly influenced by the type of tumor, i.e., mucinous or nonmucinous. Clinical stage also had significant impact, whereas grade of differentiation did not, when the other two factors were taken into account. CEA levels were also dependent mainly on histological type. Mucinous tumor cases had high levels. Only clinical stage or tumor burden had a significant impact on TPA levels. PLAP levels were significantly influenced by histological type of tumor and by grade of differentiation but not by clinical stage. The dependence of CA-125 levels upon clinical stage was evident only in nonmucinous tumors. Furthermore, size of the primary tumor was not important for the CA-125 value, in contrast to FIGO stage. Thus CA-125 is primarily a sensitive indicator of disseminated disease in ovarian carcinoma patients. On the basis of the CA-125 level it was possible to predict the extent of disease with an overall accuracy of 55%. If TPA and CEA levels were also considered, the predictive accuracy was 63%.
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PMID:Pretreatment serum levels of CA-125, carcinoembryonic antigen, tissue polypeptide antigen, and placental alkaline phosphatase in patients with ovarian carcinoma: influence of histological type, grade of differentiation, and clinical stage of disease. 222 70

A case of metastatic spermatocytic seminoma with metastases to homolateral retroperitoneal paraaortic lymph nodes in a 50-year-old man is described. The metastases were detected 18 months after orchiectomy. A retroperitoneal biopsy with cytoreductive lymphadenectomy was performed followed by radiotherapy and consecutively by combination chemotherapy. The patient died 25 months after orchiectomy of complications arising after a second course of chemotherapy. No signs of further tumor spread were observed. Autopsy was not performed. The tissue of the metastases fulfilled the light microscopic criteria for spermatocytic seminoma and ultrastructurally showed intercellular communications with typical intercellular bridges. The absence of placental alkaline phosphatase in tumor cells is also consistent with this diagnosis. The metastases differed from the primary tumor in the presence of focal lymphocytic infiltration and granulomatous reaction. This patient represents the first fully documented case of a metastasizing spermatocytic seminoma.
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PMID:Metastatic spermatocytic seminoma. A case report with light microscopic, ultrastructural, and immunohistochemical findings. 245 27

Using continuous human ovarian cancer cell lines, i.p. xenografts were successfully established in nude mice from four of four attempts. When primary tumor material was used, xenografts grew in 8 of 10 attempts. From these eight, three passageable xenograft cell lines have been established. To our knowledge, this is the first report published of such xenografts. I.p. xenografts closely mimic the clinical behavior of human ovarian cancer, and those developed from primary tumor material maintain close morphological similarity to the parent primary tumor. When expression of placental alkaline phosphatase and the tumor associated antigens defined by the monoclonal antibodies HMFG1, HMFG2, AUA1, and F36/22 by these models was determined, those i.p. xenografts derived from primary tumor material exactly matched the original tumor, while none of the xenografts derived from the cell lines expressed these antigens. These models will be useful for investigating the biology and treatment of ovarian cancer.
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PMID:Intraperitoneal xenografts of human epithelial ovarian cancer in nude mice. 356 97

Factors that influence early events of primary tumor development have been cumbersome to evaluate because of the need to either wait for tumor palpability after experimental manipulation or use of radiolabel to evaluate cell clearance. To facilitate these and similar analyses of cells in vivo, new methods are described that utilize histochemical marker genes to quantitate tumor cell number in a target tissue through the use of luminescent, enzymatic assays for these gene products. 3T3 Cells transfected with either human placental alkaline phosphatase or bacterial lacZ genes were injected subcutaneously into athymic nude mice. Using luminescent substrates designed for marker gene enzymes, extracts from homogenized tumor cell-bearing skins were assayed for the corresponding marker enzyme activities, which were optimized for recovery from skin extracts and correlated to cell number. The homogenization buffer used for these assays was designed to accommodate the optimal and simultaneous recovery of cytosolic beta-galactosidase and membrane-linked alkaline phosphatase from the skin, as well as from cultured cells. These assays provide an inexpensive, sensitive method for quantitatively monitoring the fate of cells genetically tagged with marker genes in various in vivo environments.
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PMID:Quantitation of two histochemical markers in the same extract using chemiluminescent substrates. 781 4

To facilitate detection of tumor cells at the highest resolution in any organ in athymic nude mouse model systems, a histochemical marker gene [bacterial lacZ or human placental alkaline phosphatase (ALP)] was transfected into specified transformed/tumor cells (fibrosarcoma or neuroblastoma). The fates of tumor cells were followed qualitatively and quantitatively by histochemical staining of whole organs or organ sections. Primary tumors developed initially via formation of "curly-haired" complexes of cells in the subcutis or dermis, followed by division of a large fraction of cells. When two tumor classes were mixed before injection, outgrowth occurred in regional concentrations of the primary tumor. Blood microvessels were detectable within 72 hr of injection, growing into tumor regions. iv injection routinely yielded multicellular foci in the lungs within minutes as precursors of experimental metastases. Micrometastasis was further resolved with cells "inactivated" by different treatments and by co-injection of two different tagged cell types. These approaches using different histochemical marker genes to "tag" different tumor cell classes, along with more advanced molecular biological approaches, permit us to characterize gene expression and its reversibility during the earliest stages of primary tumor formation and micrometastasis to virtually any organ in the recipient animal.
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PMID:Earliest steps in primary tumor formation and micrometastasis resolved with histochemical markers of gene-tagged tumor cells. 956 66

Mouse fibrosarcoma (3T3 cells transfected with different oncogenes), human neuroblastoma, or human prostate carcinoma cells have been genetically-tagged with different histochemical marker genes (E. coli lacZ, placental alkaline phosphatase, or Drosophila alcohol dehydrogenase). Injection into athymic nude mice permits their tracking at all stages of primary tumor formation and micrometastasis to various organs at the single-cell level. Two different tumor classes, tagged with different marker genes, can be tracked together. Primary tumors display regional dominance of one tumor class with exclusion of other classes. During micrometastasis, tumor cells are detected binding to the endothelium of lung blood vessels, followed by establishment of multiple-cell micrometastases. Micrometastases in some organs are transient while in other organs there is differential expansion into overt metastases. Tagged tumors also reveal the timing of angiogenesis of developing primary tumors and overt metastases. In all three tumor systems, there are three classes of genetic stability of marker gene expression in clonal populations-high stability, intermediate stability, and high instability. Instability in marker gene expression in one tagged prostate carcinoma system does not depend on a hypermethylation mechanism, suggesting a genetic basis for loss of activity. Use of histochemical marker genes, combined with laser-capture microdissection and various PCR methods, can now be used to evaluate gene activities in single or multiple tumor cells in virtually any organ and primary tumor of the animal model system.
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PMID:Tumor progression, micrometastasis, and genetic instability tracked with histochemical marker genes. 1031 77

We describe the clinicopathologic findings in a so far unrecognized thymic tumor. The tumor occurred in a 70-year-old woman with respiratory distress but neither myasthenia gravis nor other symptoms. Metastases or another primary tumor were absent. The well-circumscribed neoplasm was located in the thymic region, measured 18 x 12 x 8 cm, and showed a homogeneous, tan-colored, soft cut surface. By histology, the tumor lacked a true capsule and a lobular growth pattern, was almost devoid of stroma, and infiltrated among remnant thymus lobules. The polygonal tumor cells formed solid sheets, trabeculae, or occurred as single cells that resembled hepatocytes. Proliferative activity was low. Portal structures, sinuses, and bile were absent as were areas of conventional thymoma, adenocarcinoma, or germ cell tumor. The tumor expressed cytokeratins 7 and 19, alpha1-antitrypsin, alpha1-antichymotrypsin, and hep-Par-1. Alpha-fetoprotein (AFP), human beta-chorionic gonadotropin (beta-HCG), placental alkaline phosphatase, CD5, CD30, CD31, CD34, CD45, CD68, CD99, S-100, HMB45, desmin, actin, or neuroendocrine markers were not expressed, and intratumorous CD1a+ or TdT+ immature T cells were absent. AFP was repeatedly undetectable in the blood. Mediastinal tumor recurrence was detected 6 months after surgery. Following radiochemotherapy, the patient has remained free of disease for 26 months. We conclude that this tumor is a thymic carcinoma (WHO type C thymoma). A diagnosis of hepatoid yolk sack tumor appears unlikely considering absence of a bona fide germ cell component, lack of AFP expression, and the patient's female gender. Because of its morphologic and immunohistochemical features, we propose the term "hepatoid thymic carcinoma" for this new type of thymic carcinoma.
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PMID:Hepatoid thymic carcinoma: report of a case. 1504 16