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Query: UMLS:C0178874 (tumor progression)
 40,807 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathological and cytogenetic features of an extrarenal malignant rhabdoid tumor (MRT) arising from the paravertebral region in an infant were investigated. The patient died 4 months after diagnosis, due to aggressive tumor progression. The tumor was composed of medium-sized round cells with cytoplasm containing eosinophilic inclusions, which ultrastructurally were composed of densely packed whorled intermediate filaments. Flow-cytometric analysis of the tumor cells revealed a diploid pattern. Amplification of the N-myc oncogene was not identified. Immunohistologically, the inclusion bodies showed a positive reaction with antiserum against vimentin. The tumor cells were not reactive with antiserum against epithelial membrane antigen, anti-keratin (polyclonal) or cytokeratin (monoclonal, CK1), but did react with 5H10, an antiserum established from human sarcomatous Wilms' tumor. This case is discussed with reference to the literature on extrarenal MRT, placing stress on the histogenesis of this tumor.
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PMID:Cytogenetic characteristics of a malignant rhabdoid tumor arising from the paravertebral region. A case report. 150 7

The expression of cytokeratin (CK) polypeptides was studied in 59 transitional cell carcinomas (TCC) of the urinary tract of different grade and stage. Using a panel of 14 polypeptide-specific monoclonal CK-antibodies we identified immunohistochemically 8 different CKs separately, ie, CKs 4, 7, 8, 10, 13, 14, 18, and 19, while in immunoblotting studies CK5 expression was detected indirectly by using the antibody RCK102, recognizing CK5 + 8. In low-grade TCCs (G1-G2), the CK distribution was comparable to that in normal urothelium, however with a variable expression of CK13 in the different tumors and a uniform distribution of CK7. In higher-grade TCCs (G3), a decrease in CK13 expression was observed, particularly in the areas of muscle invasion. Furthermore, the appearance and increasing expression of CK14 (not present in normal urothelium or G1 TCCs) with higher grade and stage was striking. With tumor progression changes in epitope configurations of CK8 and CK18 were detected, as concluded from immunohistochemical assays with the panel of monoclonal antibodies for each of these two CKs. In extreme cases this resulted in differential staining patterns of the invasive and noninvasive components within one tumor. In 7 of 32 G3 TCCs, some of which showed areas with evident squamous differentiation, a decrease in the expression of CK7 and/or CK8 was seen. We conclude that tumor progression in TCCs is associated with discrete changes of CK expression, which can be detected using monoclonal antibodies.
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PMID:Distribution of cytokeratin polypeptides in human transitional cell carcinomas, with special emphasis on changing expression patterns during tumor progression. 168 41

Immunohistochemical study of cervical carcinoma used EE21-06d monoclonal antibodies which identify five cytokeratin polypeptides inherent in the squamous epithelium. PAP-method and reaction of immunofluorescence were employed. Initial stages of squamous cell carcinoma invasion were characterized by bleaching or complete cell discoloring of most tumor cells. However, in deeply invading tumors, the share of intensively stained cells was markedly increased. The results point to expression of different cytokeratins or cell clones replacement with tumor progression. The peculiarities of cytokeratin distribution may serve to determine the degree of invasion and differentiation of tumor cells.
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PMID:[Immunohistochemical study of cells of invasive cancer of the vaginal part of the cervix uteri]. 169 88

Immunohistochemical characterization is an accepted method of human cell typing and tumor diagnosis. The differentiation of undifferentiated carcinoma from amelanotic melanoma is usually achieved by demonstration of cytokeratin (CK) intermediate filaments in carcinoma but not in melanoma. In examination of 100 melanomas fixed in formalin or methacarn and frozen tissue sections, we have found CK-immunoreactivity in 2, 8, and 21% of cases, respectively, with multiple anticytokeratin antibodies displaying overlapping antigenic specificities. In addition, we have confirmed the anomalous expression of low molecular weight CK proteins by one- and two-dimensional gel electrophoresis and immunoblotting of extracts of an immunohistochemically positive case. This latter finding indicates that CK staining in melanomas reflects the presence of authentic CK peptides and is not an artefact induced by fixation or cross-reacting antibodies. These observations have direct implications for the application of immunohistochemistry to the present practice of diagnostic surgical pathology. The anomalous CK expression by melanoma limits the diagnostic reliability of immunohistochemically demonstrated CK alone to indicate a diagnosis of carcinoma, without the concomitant detection of additional tumor-associated antigens. The finding of anomalous CK expression only in metastatic or recurrent melanomas raises an interesting question of possible association with tumor progression.
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PMID:Anomalous cytokeratin expression in malignant melanoma: one- and two-dimensional western blot analysis and immunohistochemical survey of 100 melanomas. 169 24

The cellular origin of estrogen-induced kidney tumors in male Syrian hamsters has been repeatedly the subject of controversy. Several authors have proposed that the tumors arise from proximal tubules, from a combination of tubular and interstitial stromal cells, or solely from interstitial cells. Because of the model character of this tumor for hormone-associated cancer, it was further investigated in this study with respect to morphology, enzyme and intermediate filament pattern, the expression of alpha-smooth muscle actin and the extracellular matrix proteins fibronectin and tenascin. These analyses were carried out with early and late tumors as well as metastases to determine possible changes in expression of biochemical parameters during the development and progression of this neoplasm. The enzyme histochemical and intermediate filament patterns were usually the same as those described previously for proliferative foci and early tumors, i.e. highly elevated activities of glucose-6-phosphate dehydrogenase, adenylate cyclase and alkaline phosphatase, a lack of glucose-6-phosphatase and gamma-glutamyltransferase and coexpression of vimentin and desmin, alpha-smooth muscle actin could not be detected in early lesions. In five of 24 advanced tumors inclusions of kidney tubules were found which showed various degrees of alteration in their morphology and enzyme histochemical pattern, but were often directly connected with tubular segments of normal appearance outside the tumor. Like the normal tubules, the enclosed tubular segments were strongly positive for cytokeratin but never expressed vimentin or desmin. Among the 24 tumors studied, two contained cysts which expressed cytokeratin and sometimes also vimentin but not desmin. The enzyme histochemistry of the cells lining the cysts was similar to that of the surrounding tumor mass, except adenylate cyclase was lacking and alkaline phosphatase was not uniformly distributed. In tumors containing cytokeratin-positive cysts, there often were cytokeratin-positive, vimentin-negative and desmin-negative tumor formations in close contact to these cysts. With the exception of cyst formation, the pattern of metastases were identical to that of the primary tumors. All large tumors and the main component of the metastases expressed vimentin, desmin and fibronectin. Mesothelia surrounding metastatic tumor complexes were positive for vimentin, desmin, alpha-smooth muscle actin, fibronectin, cytokeratin and tenascin. It was concluded from these and previous observations on early stages of tumor development that the estrogen-induced hamster kidney tumor originates from mesenchymal interstitial cells (probably pericytes) which may rarely acquire an epithelial phenotype by metaplastic transformation during tumor progression.
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PMID:Changes in the cellular phenotype and extracellular matrix during progression of estrogen-induced mesenchymal kidney tumors in Syrian hamsters. 171 81

Malignant breast cancers appear to metastasize first via the lymphatics to colonize regional lymph nodes, and then via the blood circulation to colonize distant organs. Using a rat mammary tumor model based on the 13762NF adenocarcinoma, evidence is presented that malignant cell subpopulations spread lymphatically to regional lymph nodes, then become blood-borne and metastasize to lungs. Using chromosome and cytokeratin markers to identify specific tumor cell subpopulations, tumor progression in this system appears to be associated with the appearance of a highly specialized, metastatic cell subpopulation. This highly malignant cell subpopulation is completely uncoupled by gap junctions when examined for gap-junctional communication, in contrast with less malignant subpopulations that show varying degrees of cell communication through gap junctions. Loss of cell-cell communication may be one of the epigenetic events that leads to the generation of tumor cell diversification and heterogeneity. In concert with host selective pressures, this could result in the evolution of highly malignant cell subpopulations with unique characteristics.
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PMID:Cytoskeletal and junctional heterogeneity in mammary tumor cells and their possible significance in tumor progression. 322 82

We established trophoblast cell cultures with extended lifespans by introducing into first trimester human trophoblasts the gene encoding simian virus 40 large T antigen. The transfected trophoblasts were characterized according to their expression of various morphological and functional markers. Both parental (HTR-8) and transfected (HTR-8/SVneo) lines were morphologically similar and positive for cytokeratin, confirming their epithelial (trophoblastic) identity. Whereas the parental cells senesced after 12-14 passages, the transfectants have been in culture for over 32 passages. Human chorionic gonadotrophin was detected only in the HTR-8/SVneo cells and not in the parental cells. Both lines required at least 5% serum in order to sustain growth in vitro and responded to transforming growth factor-beta (TGF-beta) with reduced [3H]-thymidine incorporation in a dose-dependent manner. Treatment with TGF-beta also resulted in decreased secretion of plasminogen activators (PAs) and reduced PA activity by both lines. Both cell lines secreted mostly 72-kDa type IV collagenase as determined by substrate gel zymography, but the level of secretion of this enzyme was not significantly affected by TGF-beta in either line. Even though both lines exhibited similar in vitro invasive abilities, only the invasiveness of the parental cells was reduced by TGF-beta. Neither parental or transfected cells were capable of growth in soft agar and no sign of tumor formation was evident more than 5 months after subcutaneous inoculation of the transfected cells into nude mice. These results indicate that apart from their ability to sustain prolonged growth in culture, the transfected HTR-8/SVneo cells share a number of phenotypic properties with the parental trophoblast cells. For this reason, these transfected trophoblasts may prove to be an important tool for the study of placental function and/or tumor progression.
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PMID:Establishment and characterization of first trimester human trophoblast cells with extended lifespan. 768 92

The DNA of human papillomavirus (HPV) types found in cervical carcinomas can immortalize primary human keratinocytes. However, in analogy to tumor progression in vivo, HPV-immortalized keratinocytes require secondary events for malignant conversion. Here, we report on an HPV16-immortalized keratinocyte cell line (HPKIA) which after gamma-irradiation and long term culturing in vitro has acquired the ability to form squamous cell carcinomas in nude mice. The HPV16 integration locus and the viral transcript pattern of HPKIA cells at different passages have remained unaltered. A difference in cytokeratin expression was noted for HPKIA-induced cysts and HPKIA-induced carcinomas. In addition to the expression of suprabasal markers such as cytokeratin 10 and involucrin, carcinomas also express cytokeratin 8 and 18. The latter cytokeratin pair is often expressed in high-grade cervical neoplasia and cervical squamous cell carcinomas. Extensive cytogenetic analyses of nontumorigenic HPKIA cells and their tumorigenic segregants has revealed no single chromosomal abnormality which is confined to all tumorigenic cells. A consistent net loss of chromosomes 3, 5, 9, 12, and 22 was evident for all malignant cells. HPKIA cells represent all stages of transformation and are thus useful for defining secondary genetic events that potentially mark malignant progression in human cells in vivo.
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PMID:Malignant progression of an HPV16-immortalized human keratinocyte cell line (HPKIA) in vitro. 854 32

Minimal residual disease in patients with operable esophageal cancer is frequently missed by current noninvasive tumor staging. Here we applied an immunocytochemical cytokeratin assay that allows identification of individual esophageal carcinoma cells disseminated to bone marrow. Prior to therapy, bone marrow was aspirated from the upper iliac crest of 71 patients with esophageal cancer at various disease stages as well as an age-matched control group of 20 noncarcinoma patients. Tumor cells in cytologic bone marrow preparations were detected with monoclonal antibodies (mAbs) CK2, KL1, and A45-B/B3 to epithelial cytokeratins (CKs) using the alkaline phosphatase antialkaline phosphatase method. CK-positive cells were found in 14 (36.8%) of 38 cancer patients treated with curative intent and 16 (48.5%) of 33 patients with extended disease. The overall frequency of these cells was 1 per 4 x 10(5) to 82 per 4 x 10(5) mononuclear cells with no significant differences between patients at different tumor stages. After a short median follow-up of 9.5 months (3-24 months), 7 of 11 patients who underwent complete surgical resection but had tumor cells in bone marrow presented with tumor relapse compared to 2 of 19 corresponding patients without such cells (p < 0.01). It was concluded that although bone marrow is not a preferential site of overt metastasis of esophageal cancer, the frequent occurrence of isolated tumor cells at this distant site indicates that hematogenous dissemination of viable malignant cells occurs early in tumor progression.
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PMID:Disseminated epithelial tumor cells in bone marrow of patients with esophageal cancer: detection and prognostic significance. 866 32

Matrix metalloproteinase (MMP) family members have been associated with advanced-stage cancer and contribute to tumor progression, invasion, and metastasis as determined by inhibitor studies. In situ hybridization was performed to analyze the expression and localization of all known MMPs in a series of human breast cancer biopsy specimens. Most MMPs were localized to tumor stroma, and all MMPs had very distinct expression patterns. Matrilysin was expressed by morphologically normal epithelial ducts within tumors and in tissue from reduction mammoplasties, and by epithelial-derived tumor cells. Many family members, including stromelysin-3, gelatinase A, MT-MMP, interstitial collagenase, and stromelysin-1 were localized to fibroblasts of tumor stroma of invasive cancers but in quite distinct, and generally widespread, patterns. Gelatinase B, collagenase-3, and metalloelastase expression were more focal; gelatinase B was primarily localized to endothelial cells, collagenase-3 to isolated tumor cells, and metalloelastase to cytokeratin-negative, macrophage-like cells. The MMP inhibitor, TIMP-1, was expressed in both stromal and tumor components in most tumors, and neither stromelysin-2 nor neutrophil collagenase were detected in any of the tumors. These results indicate that there is very tight and complex regulation in the expression of MMP family members in breast cancer that generally represents a host response to the tumor and emphasize the need to further evaluate differential functions for MMP family members in breast tumor progression.
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PMID:Expression of most matrix metalloproteinase family members in breast cancer represents a tumor-induced host response. 868 51


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