Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Natural killer (NK) cell activity was studied together with tumor marker serotests (PSA, PAP) and blood testosterone, estradiol, cortisol, and prolactin concentrations in treated prostate cancer patients. NK cell activity data were correlated with tumor stage (stage D0 + D1 versus stage D2) and showed statistically insignificant differences. Both tumor progression and stabilization of metastatic disease, triggered by the application of more appropriate therapy in progressive subjects, yielded low NK activity data. By contrast, normal NK activity was found during both partial remission of stage D2 tumor and stabilization of the same disease, after an initial period of tumor remission. Differences between NK activity data from the aforementioned two groups are statistically significant (P less than 0.01). In subjects examined, the application of NK activity assay to those with advanced disease reflected changes in the outcome of the treatment more closely than it did routine tumor marker assessment. The activity of NK cells seems unaffected by changes in basal blood estradiol, cortisol, testosterone, and prolactin concentrations that occur during therapy with pharmacological agents (estradiol, cyproterone acetate, diethylstilbestrol, and flutamide) and during surgical castration. The reported NK activity recordings in treated prostate cancer patients might be indicative of the presence of tumor cells in the circulation. If this holds true, the measurement of NK activity would appear to furnish urological oncology with a new tool for early, rapid recognition of progressive metastatic tumors.
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PMID:NK cell activity in treated prostate cancer patients as a probe for circulating tumor cells: hormone regulatory effects in vivo. 138 13

In searching an animal model to study metastasis formation we used cultured cells of experimental rhabdomyosarcomas and their inoculation tumors in adult nude mice. Supplementing earlier observations (Katenkamp et al. 1987) we found that long-term cultured sarcoma cells induce tumors in adult nude mice which do not metastasize spontaneously but produce lung metastases after repeated incomplete tumor removal. Possible factors and mechanisms responsible for metastasis emergence are discussed. The metastasis model introduced may be apt to study cellular changes at cytogenetic and molecular biological level that occur during tumor progression and metastatic dissemination.
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PMID:Metastasis induction by incomplete tumor resection. A new metastasis model using inoculation sarcomas in adult nude mice after long-term cultivation of sarcoma cells. 139 12

Recently we reported that human dermal fibroblasts, or conditioned media obtained from such cells, affect the growth of human melanoma cells as a direct function of tumor progression: melanoma cells obtained from early-stage (metastatically incompetent) primary lesions were growth inhibited, whereas cells obtained from more advanced (metastatically competent) primary lesions, or metastases, were growth stimulated. Ion-exchange and gel-filtration chromatography of fibroblast conditioned medium revealed the inhibitor to be a protein of molecular mass between 20 and 30 kDa and distinct from the stimulator. This is the approximate molecular mass of interleukin 6 (IL-6), a ubiquitous multifunctional cytokine known to affect in particular many kinds of hemopoietic and lymphoid cells. Since this cytokine is known to be made by fibroblasts, we attempted to determine if the human fibroblast-derived growth inhibitor (hFDGI) was identical to IL-6. Neutralizing antibodies specific for IL-6 completely eliminated the inhibitory activity of hFDGI. Moreover, exposure to human recombinant IL-6 was found to inhibit the growth of early-stage melanoma cells obtained from radial growth phase (RGP) or early vertical growth phase (VGP) primary lesions in three of four cases. In contrast, melanoma cells from a number of more advanced VGP primary lesions, or from distant metastases, were completely resistant to this IL-6-mediated growth inhibition. Acquisition of an "IL-6-resistant" phenotype by metastatically competent melanoma cell variants may provide such cells with a proliferative advantage within the dermal mesenchyme (a hallmark of melanoma cells that are malignant), helping them eventually to dominate advanced primary lesions and to establish secondary growths elsewhere.
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PMID:Interleukin 6: a fibroblast-derived growth inhibitor of human melanoma cells from early but not advanced stages of tumor progression. 140 27

A volume of data that has accumulated for over a century has suggested that fibrin may facilitate the persistence and progression of malignancy. Techniques that have been developed recently have shown that fibrin is indeed a component of the connective tissue stroma in human malignancy but in only a few tumor types. However, therapeutic intervention studies with drugs that limit thrombin activity or enhance fibrinolysis have shown favorable clinical effects in at least one such tumor type. These favorable findings affirm the concept that cause-and-effect relationships do, in fact, exist between thrombin generation with fibrin formation and tumor progression, and suggest that a rational basis exists for the design of future drug intervention trials that target reactions relevant to specific tumor types. These findings also provide a basis for the design of experiments capable of defining further the role of fibrin in the integrity of these tumor types. Because fibrinogen is found much more commonly than fibrin in the connective tissue of a variety of human malignancies, attention might reassumably be directed to determining the possible contribution of this molecule as well as of fibrin to tumor progression.
Cancer Metastasis Rev 1992 Nov
PMID:The role of fibrin in tumor metastasis. 142 19

Prostaglandins and other eicosanoids have been studied extensively in their physical, biochemical, biophysical and pharmacological aspects. However, studies on their role in tumor progression, especially metastases are relatively recent. Following a brief overview of the history of discovery and metabolism of eicosanoids and other fatty acids, we discuss the functions of these fatty acids (with emphasis on prostacyclin, thromboxane A2, 12-hydroxyeicosatetraenoic acid and 13-hydroxyoctadecadienoic acid) in cell transformation, tumor promotion and particularly in tumor cell metastasis. The relation between these monohydroxy fatty acids and tumor cell metastasis is discussed from three different perspectives, i.e., their effects on tumor cells, on platelets and on endothelial cells. The mechanism of these effects are then addressed at cell adhesion molecule, motility, protease, cell cytoskeleton, protein kinase and eicosanoid receptor levels. Finally, regulation of three key enzymes which generate eicosanoids (phospholipase, prostaglandin endoperoxide synthase and lipoxygenase) is explored.
Cancer Metastasis Rev 1992 Nov
PMID:Fatty acid modulation of tumor cell-platelet-vessel wall interaction. 142 24

Tumors arise as a result of a chain of genetic alterations that impair normal cell functions and lead to invasion and development of metastases. These genetic alterations may result either in qualitative or quantitative changes in genes that play a key role in normal cell function, called proto-oncogenes, or in inactivation of genes that normally inhibit cell growth, called tumor suppressor genes. Whatever the mechanism involved, responses of the cell to changes in the environment become inappropriate. This paper successively reviews the various categories of proto-oncogenes, the mechanisms by which proto-oncogenes can be activated, and several examples of tumor suppressor genes. The various genetic factors involved in cell transformation probably act together to create a network of molecular interactions that results in tumor progression.
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PMID:[Oncogenes and tumor-suppressor genes]. 144 69

Transitional cell carcinoma of the bladder has a high recurrence rate after local treatment. Progression to a higher stage occurs in 10-30% of the recurrent tumors, and early detection of potentially progressive tumors is important. In the current study morphometric, densitometric, and chromatin textural features of nuclei of superficial bladder tumors (pTa-T1) were studied to determine the value of karyometric features in the prediction of tumor progression. Seventy-two histological samples from 36 patients, consisting of both the primary and the first recurrent superficial tumor, were analyzed. Patients were divided into two groups: those with tumor progression, defined as an increase in tumor stage or occurrence of metastatic disease, and those without. Discriminant analysis on four karyometric features resulted in correct prediction of prognosis of 78% and 97% in the primary and recurrent tumors, respectively (P < 0.001). Tumor grade and stage did not offer additional information concerning prognosis. Karyometric analysis of recurrent superficial transitional cell tumors can be useful in selecting patients who need a more aggressive therapy. However, tumor characteristics of recurrent tumors varied and continuous evaluation of the karyometric features is necessary for early detection of an increase in the malignant potential of the tumor.
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PMID:Karyometry in recurrent superficial transitional cell tumors of the bladder. 145 71

Bladder cancer ranks as the third most common malignancy among men and tenth among women. Superficial transitional cell carcinomas (stage Ta, Tis, and T1) account for approximately 70-80% of these tumors, while the remaining 20-30% are invasive (T2, T3, and T4). Approximately 70% of superficial tumors will have one or more recurrences, with 25% of these expressing a higher histologic grade and 10-15% subsequently developing invasive and/or metastatic disease. The detection and prediction of tumor recurrence and/or tumor progression is crucially important if timely and appropriate therapy is to be instituted. Conventional histopathologic evaluation usually provides definitive diagnosis upon which therapeutic planning is based. However, at present there are no more reliable morphologic indicator to identify which individuals will have recurrent disease or who will progress to invasive and/or metastatic cancer. Recent advances in tumor biology have identified markers that are good candidates for clinical applications in early tumor detection, as well as for the stratification of patients with like-appearing morphological lesions with different biological and clinical behavior. The ultimate goal is to develop predictive assays that would segregate patients with high probability of failures versus patients who would be cured by localized modes of therapy.
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PMID:Cell surface differentiation antigens of normal urothelium and bladder tumors. 146

Single-cell DNA cytophotometry was employed to analyze the tumors of 271 patients with locally advanced prostatic carcinoma as to DNA ploidy and heterogeneity and the distribution of the phases of the cell cycle before and during therapy, with the intention of establishing prognostic factors apart from those already known (stage, grade). Follow-up periods ranged from 1 to 9 years. 198 (73%) of the 271 patients had carcinoma stage T3 N0 M0, and 73 (27%) of them had carcinoma stage T3/T4 N+M1. The tumors were evaluated cytologically to establish the grades of malignancy. 11.8% were grade I carcinoma, 64.3% were grade II and 23.9% were grade III carcinoma. Single-cell DNA cytophotometry demonstrated aneuploidy rates of up to 73% and diploidy rates of up to 23.8% for the higher grades of malignancy, whereas the diploidy rate established for grade I carcinoma was 71% and the respective aneuploidy rate was 15.2%. These differences are significant (p < 0.001). There was a significant correlation between the results of DNA cytophotometry and the clinical course of the disease. Patients with diploid tumor cell nuclei developed no metastases and no local tumor progression during the follow-up period of 9 years, whereas patients with aneuploid tumor cell nuclei showed metastases and local tumor progression within 8-22 months, despite changes in therapy. These patients died of carcinoma after an average 18 months following primary diagnosis.
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PMID:Nuclear DNA analysis: DNA heterogeneity in the monitoring of patients with locally advanced prostatic carcinoma. 149 May 8

Tumorigenesis is a multistep process involving mutations of dominantly acting proto-oncogenes and mutations and loss-of-function mutations of tumor suppressor genes. Some of these mutations may be inherited, but most of them are acquired. Models for the sequential steps of the genetic changes involved in tumor development have been proposed for certain cancers, such as colon cancer. In the case of ovarian cancer, relatively little is known about the genetic events associated with the initiation or subsequent progression and metastases of the tumor. Cytogenetic analysis has revealed a high incidence of both structural and numerical chromosome changes, and the extent of these changes seems to increase with tumor progression. Oncogene activations of the proto-oncogenes K-ras, c-myc and c-erbB-2 have been found more frequently in aggressive ovarian tumors and may be associated with poor survival. Tumor-specific allele loss involving putative tumor suppressor genes has been observed for loci at chromosomes 11p, 17p, and 17q,--loci commonly deleted in other cancers too. A relatively high incidence of allelic loss on chromosome 6q appears to be specific to ovarian carcinoma. Familial breast/ovarian cancer has been suggested to map to chromosome 8q. Recently we have found a germ-line mutation in the tumor suppressor gene p53 in a family with breast- and ovarian cancers, indicating that this is the predisposing gene in this family. Genetic changes important for the etiology of ovarian cancers seem to involve both somatic mutations of oncogenes and somatic or germ-line inactivation of tumor suppressor genes.
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PMID:Oncogenesis in ovarian cancer. 150 89


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