Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0178874 (tumor progression)
 40,807 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Our study reports 6 patients with advanced adenocarcinoma of the fallopian tube, with elevated levels of serum CA 125 (greater than 35 U/ml). In two patients the serum CA 125 values were followed during treatment. In one of them the CA 125 values decreased during clinical remission and increased at the time of tumor progression. In the second patient we observed increasing levels of CA 125 preceding clinical evidence of recurrent disease. The possible usefulness of CA 125 for monitoring patients with tubal cancer is discussed.
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PMID:Levels of CA 125 in patients with recurrent carcinoma of the fallopian tube: two case histories. 347 Feb 29

Host factors that might be associated with the variable response of tumors to effective chemotherapy were studied in B6C3F1 mice bearing transplanted mammary adenocarcinoma 16/C tumors and treated with melphalan. Tumor response ranged from regression to an unpalpable size to growth under treatment. That biochemical resistance of the cell population was not primarily responsible for the variability was demonstrated by passage of responsive and nonresponsive tumors into new hosts followed by treatment with melphalan. When the implanted subcutaneous tumor weighed 1.0 g or less (usually 12 to 13 days postimplant), both the plasma levels of melphalan and the variability in plasma levels were similar to those observed in tumor-free mice. With tumor progression beyond 1.0 g, an increase in mean plasma levels and in variability, but not in plasma half-life, was observed. A correlation between the dose of melphalan administered, the schedule, and the percentage of tumor responses was found. There was no correlation between the plasma levels in individual mice following a given dose of melphalan and subsequent tumor response. Also, there was no correlation between the plasma levels of melphalan in individual mice following the second, third or fourth treatment in a multiple-dose treatment schedule and the response of the tumor in that mouse to previous treatments. Prior therapy (1, 2 or 3 doses administered 4 days apart) either prevented the increase in plasma levels that occurred in mice bearing untreated advanced tumors or reduced the plasma level (and the variability) to approximately that found in tumor-free mice. Whether this was a direct result of the effects of melphalan on the host or an indirect result of tumor inhibition is not known. A similar study in tumor-free mice indicated that prior treatment had only minimal effects on subsequent plasma levels. These studies indicate that heterogeneity of the host was not a major factor in variable tumor response if therapy was initiated when the tumors weighed 1.0 g or less.
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PMID:Variability of tumor response to chemotherapy. I. Contribution of host heterogeneity. 369 Aug 3

We have isolated clonal cell lines from a transplanted adenocarcinoma induced by the RIII strain of mouse mammary tumor virus in a BALB/c mouse. Three major morphological cell types of these lines are developmentally linked; polygonal cells give rise to cuboidal and then to elongated cells. All cell lines expressed markers that are characteristic of mammary basal cells. In addition, the polygonal lines contained cells that have cell markers and ultrastructural features of epithelial cells; in these lines an occasional cell was found with myoepithelial features. The cuboidal and elongated lines lacked many epithelial differentiation characteristics and showed no myoepithelial differentiation. The cell lines contained variable numbers of acquired mouse mammary tumor virus and ecotropic murine leukemia virus proviruses. The various subclones derived from the original cell lines contained, in addition to the acquired proviruses of the parental line, one or more unique proviruses of either mouse mammary tumor virus or ecotropic murine leukemia virus origin. These unique insertions were used as genotypic markers to demonstrate the clonal relationship of the cell lines. Both polygonal and elongated cells are tumorigenic and give rise to adenocarcinomas and sarcoma-like tumors, respectively. In contrast, the cuboidal cells are poorly tumorigenic. Since cuboidal cells are derived from the polygonal cells, this suggests that tumor progression in this system proceeds via intermediates that are either poorly or nontumorigenic.
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PMID:In vitro differentiation and progression of mouse mammary tumor cells. 375 29

DU-PAN-2 is a high molecular weight glycoprotein defined by a murine monoclonal antibody elicited to a pancreatic ductal adenocarcinoma cell line. This monoclonal antibody recognizes an oncofetal antigen present on the surface of pancreatic tumor cells. The antigen has also been detected in the sera of patients with adenocarcinoma of the pancreas by a competition radioimmunoassay (RIA). Ninety-four per cent (31/33) of patients with pancreatic adenocarcinoma in this study had DU-PAN-2 serum antigen levels greater than 300 units/ml by RIA, whereas sera from normal adults had serum levels less than 300 units/ml. Serial studies of DU-PAN-2 serum antigen in pancreatic cancer patients with elevated DU-PAN-2 serum levels (mean: 2873 units/ml) and surgically resectable neoplasms demonstrated a return to the normal range within 1 to 3 weeks after surgery in five of six patients. Five patients in clinical remission had normal DU-PAN-2 serum levels (mean: 110 units/ml). With tumor progression, however, the DU-PAN-2 level increased in all patients (mean: 2835 units/ml) an average of 2 months before evidence of progressive disease by clinical parameters. Serial DU-PAN-2 determinations are sensitive monitors of the progression of pancreatic cancer and may be useful as early indicators of response to therapy.
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PMID:Carcinoma of the pancreas. Therapeutic efficacy as defined by a serodiagnostic test utilizing a monoclonal antibody. 405 97

The presence of dopamine receptors in normal colonic cells has been postulated from physiological studies. The existence of such receptors in human colonic tumor cells and their role in tumor progression are still unknown. The aim of the present work was to characterize the dopaminergic receptors in a human colonic adenocarcinoma cell line (HT29) and to evaluate the effect of dopamine on cAMP, protein and DNA synthesis. The binding characteristics of 3H-dopamine on the tumor cells were rapid, reversible, specific, saturable and stereospecific. The first site characterized corresponds to a D3 subtype:KD 3.09 nM, insensitive to sulpiride, unrelated to adenylate cyclase. Competitive inhibitions of 3H-dopamine binding by different drugs showed the existence of a second binding site, D1, with an apparent affinity for dopamine of 6,700 nM. The rank order of potency of inhibitors of 3H-dopamine binding was: haloperidol greater than dopamine greater than cis flupenthixol greater than (+) butaclamol greater than (-) butaclamol greater than trans flupenthixol greater than isoproterenol greater than clonidine greater than prazosin. D3 binding sites are modulated with age, Bmax was 116 fmol/10(6) cells on the 5th day and decreased to 8.2 fmol/10(6) cells on the 15th day of culture. Cell culture in serum-deprived medium allowed an increase in the number of high-affinity receptor sites. D1 sites are coupled to adenylate cyclase as shown by a dose-dependent cAMP accumulation from 10(-8) M to 10(-5) M dopamine concentrations. Interacting with D1 sites, dopamine evokes an increase in protein synthesis with no modification of 3H thymidine incorporation. The present results indicate that the human colonic cancer cell line HT29 exhibits dopamine receptors and that stimulation may induce metabolic modifications in the tumor cells.
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PMID:Dopamine receptors in a human colonic cancer cell line (HT29). Some receptor-related biological effects of dopamine. 609 66

Fiberoptic bronchoscopy was performed before and during administration of chemotherapy in 32 patients with unresectable non-small cell carconoma of the lung. Pretreatment findings varied with the histologic cell type. Direct visual and/or pathologic evidence of cancer was obtained in 11 of 11 patients with epidermoid, in 5 of 7 with large cell, and in 9 of 14 with adenocarcinoma. In 5 of the 32 patients, intrathoracic tumor was documented at bronchoscopy but not by chest x-ray. During chemotherapy, one of five episodes of response and eight of 21 episodes of chest tumor progression were detected solely by bronchoscopy, while in an additional two objective responses and six progressions, bronchoscopic and radiographic findings simultaneously improved or deteriorated. The likelihood of documenting disease progression by bronchoscopy also depended upon the histologic type of cancer. Enlarging chest tumor found solely by chest x-ray occurred exclusively in patients with large cell carcinoma and adenocarcinoma. During chemotherapeutic treatment of our pateints, addition of serial bronchoscopic examinations to standard means of assessing tumor response frequently allowed the earlier discontinuation of an ineffective drug regimen.
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PMID:Evaluation of response to chemotherapy with fiberoptic bronchoscopy in non-small cell lung cancer. 624 82

In order to explore whether immune complex (IC) formation and immunoglobulin M-class rheumatoid factor (RF) synthesis are related to tumor progression, solid-phase enzyme immunoassays were used to test for ICs and RF in rats bearing three different syngeneic mammary adenocarcinomas. The mammary adenocarcinoma cell lines used produced either extensive metastasis (13762), metastasis in only a proportion of the animals given injections (R3230AC), or no metastasis (DMBA8). DMBA8 and 13762 tumor-bearing rats developed only low levels of circulating ICs. Of 18 animals bearing R3230AC tumors, four developed palpable lymph node metastasis (macrometastasis), while another five showed evidence of metastasis only upon histological examination (micrometastasis). R3230AC tumor-bearing animals which did not develop metastasis were found to have significantly higher IC levels than those rats with metastasis. Several sera from rats bearing R3230AC tumors were fractionated by molecular sieve chromatography. Most of the ICs in these sera were 7S to 19S in size. Significant RF synthesis occurred only in rats bearing R3230AC tumors and only during terminal tumor growth. These results show that IC formation and RF synthesis varies in animals bearing different mammary adenocarcinomas.
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PMID:Circulating immune complexes and immunoglobulin M-class rheumatoid factor in rats bearing mammary adenocarcinomas which vary in ability to metastasize. 684 60

Seven consecutive ascitic tumors were obtained over a 9-month period from a patient with serous adenocarcinoma of the ovary. The tumor cell populations were analyzed for cellular proliferation (labeling index, agar clonogenicity, and self-renewal capacity), for cell differentiation (cell surface expression of carcinoembryonic antigen and histochemical stain for fat accumulation), and for karyotypic changes. Evidence is presented of increased aggressiveness of proliferative features together with a decreasing proportion of cells with differentiated features. Parallel temporal changes were documented in density-volume characteristics of the tumor cell population, from small, high-density to large, low-density cells. The only karyotypic change identified over this period was the loss of one X-chromosome and the increased frequency of cells containing double minute bodies. The progressive characteristics described in this human tumor are not, therefore, associated with gross chromosomal changes. The accumulation of double minute chromosome bodies may be associated with a low-dose methotrexate exposure or with the tumor progression.
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PMID:Tumor progression studied by analysis of cellular features of serial ascitic ovarian carcinoma tumors. 684 99

The regression or progression of the T1699 murine mammary adenocarcinoma was analyzed with histologic an immunohistologic techniques to determine the tissue distribution of both macrophages and anti-tumor antibody. Changes in integrity of tumor blood vessels were apparent during tumor growth and regression. Tumors at early stages of growth were invaded in the capsule by multiple vascular branches which later permeated tha tumor. Following the appearance of anti-tumor in the serum, these vessels often showed immune complex deposition which preceded vessel leakage, destruction and hemorrhage. After these changes, tumor cells appeared coated with antibody. Macrophages appeared predominantly in the tumor capsule during early stages of tumor growth, while at later stage they were observed within tumors most prominently near the edge of growing hemorrhagic and necrotic areas. As tumors regressed, connective tissue septation lined by macrophages became apparent. Phagocytosis of seemingly intact tumor cells was common and appeared to account for much of the loss in tumor cell numbers. In immunosuppressed animals (ATXBM,450R) in which tumor progression always occurred, the above features were markedly diminished or absent. This model emphasizes the interplay of many factors in tumor regression. These include immune complex deposition, blood vessel destruction, macrophage infiltration and connective tissue development, all of which are associated with tumor regression and seem to be infrequent and/or inconsequential during progressive tumor growth.
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PMID:Immunohistologic evidence for the role of antibody and macrophages in regression of the murine T1699 mammary adenocarcinoma. 703 46

The structure, size and number of uterine endometrial surface epithelial cells and specialized structures, cilia and microvilli were analyzed by light microscopy, transmission and scanning electron microscopy. The purpose was to further our understanding of the biological, morphological and prognostical implications of change in hormonal status and neoplastic progression. The results of this study showed that the quantitative and qualitative alterations followed a similar pattern: the cilia and microvilli were minimally developed in atrophic endometrium, and gradually progressed in size and number in relation to oped in atrophic endometrium, and gradually progressed in size and number in relation to the hormonal cycle and hyperplastic endometrium, unless associated with cellular atypia. Lesions with atypical adenomatous hyperplasia showed irregular and disorganized surface structure, progressively more apparent in specimens from adenocarcinomas. Decreasing degree of differentiation of the tumor and radiation treatment caused a reduction in number and size, as well as derangement in the structure of cilia and microvilli. The results showed the sensitivity of the uterine lining to hormonal changes, the distinction between different types of edometrial hyperplasia and the close interrelationship between atypical adenomatous hyperplasia and early adenocarcinoma, as well as the extent and severity of different clinical entities, including radiation treatment.
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PMID:Surface ultrastructure of human endometrium. Effect of hormonal status and neoplastic progression. 719 57


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