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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tumors are composed of tumor cells, normal host cells, and an ECM. Tumor growth depends on the balance between tumor cell proliferation and tumor cell loss and is significantly influenced by normal vascular, immune, and glial cells of the host. Furthermore, tumor size and growth regulation are probably influenced by components of the ECM and by edema within and surrounding the tumor. To increase the therapeutic value of treatment regimens, investigators must study normal tissues and attempt to identify tumor-specific vulnerabilities and ways to inhibit toxicity to the host. We are entering an era of increased awareness of the complexities of tumor biology. Although our knowledge of tumor cell biology has had only a limited impact on the treatment for brain tumors, rationally developed approaches based upon new knowledge are bound to result in more effective treatment and improved prognosis for patients with brain tumors.
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PMID:Recent perspectives in brain tumor biology and treatment. 264 96

Thrombin can be formed in the tumor cell microenvironment following activation of the clotting cascade by procoagulants of cancer or host cells. We have tested here the effects of thrombin, either "endogenous" or "exogenous" (see below), on arachidonate mobilization from membrane phospholipids of mouse mammary tumor virus-induced (MMTV) carcinoma cells. These tumor cells exhibit in vitro a tissue type procoagulant activity (130 thromboplastin units/10(4) cells) and are therefore able to induce thrombin formation in a plasmatic milieu. To verify the effect of thrombin formation by tumor cell procoagulant ("endogenous thrombin"), either human or mouse platelet-free plasma (20% in DMEM) was added to the cell layer (prelabelled for 5 hr with a trace amount (0.013 microM) of 3H-arachidonate) and the system was recalcified (15 mM CaCl2). Thin-layer radiochromatography of the culture medium showed a significant release of 3H-labelled arachidonate products PGE2, PGF2 alpha and 6-ketoPGF1 alpha after 1 hr of incubation. To verify the effect of thrombin formation from host sources ("exogenous thrombin"), either bovine or purified human alpha-thrombin (0.1-10 U/ml) was added to the cells for different periods (from 5 min to 20 hr). Exogenous thrombin stimulated arachidonate release and metabolism in a dose-related manner. With short labelling periods (0.013 microM 3H-arachidonate for 30 min-1 hr) thrombin stimulated the release of unmetabolized 3H-arachidonate, but not of 3H-arachidonate metabolites. These processes were inhibited by a specific inhibitor of thrombin enzymatic activity (alpha-NAPAP, 140 microM) and by a cyclo-oxygenase inhibitor (ASA 4mM). Tumor-associated procoagulants may thus contribute not only to fibrin deposition but also to generation of multipotent mediators such as arachidonate metabolites.
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PMID:Thrombin stimulates arachidonate metabolism in murine tumor cells. 310 91

A total of 119 patients with a diagnosis of adenocarcinoma of the prostate (Stage B and C) were treated at St. Joseph Hospital Houston, Texas from 1971 through 1984 using a combination of radioactive gold seed implant and external irradiation. The prognostic significance of tumor grading and pelvic node involvement was analyzed. Five and 10-year survival for Stage B was 100% and 85% respectively; for Stage C it was 68% and 43% respectively. The cumulative 94% local control rate for Stage B and C cases obtained in this report suggests more effectiveness to control the disease locally with acceptable rate of complications, when radioactive gold seed implant is added.
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PMID:Adenocarcinoma of the prostate: radioactive gold seed implant plus external irradiation. 314 92

Dissemination of neoplastic cells within the body involves invasion of blood vessels by tumor cells. Since platelets have been shown to contribute to this process, we studied the interaction in vitro of platelets and malignant cells with the vascular endothelium and its underlying basement membrane-like ECM. A metastatic subline (ESb) of the methylcholanthrene-induced DBA/2 T-lymphoma invaded the vascular endothelium at a higher rate than its parental nonmetastatic (Eb) subline. ESb cells also exhibited a much higher ability to degrade the proteoglycan scaffold of the ECM by means of a specific HS degrading endoglycosidase (heparanase). The interaction of platelets with this ECM was associated with platelet activation, aggregation, and degradation of HS by means of the platelet heparanase. Degradation of ECM-HS was facilitated by proteolytic activity that produced a more accessible substrate for further cleavage by heparanase. A similar enhancement was exerted by plasminogen via the activity of the tumor cells or ECM associated PAs. Heparin and chemically modified heparins that lack anticoagulant activity inhibited degradation of the ECM-HS by heparanase. Interaction of platelets and lymphoma cells with ECM covered with vascular endothelial cells was investigated by SEM and by determination of ECM-HS degradation products. SEM studies demonstrated that platelets may adhere to minor gaps between adjacent endothelial cells and degrade the ECM-HS. Platelets were also shown to recruit lymphoma cells into these interendothelial gaps, suggesting that by binding to ECM and release of heparanase, platelets may play an active role in tumor cell invasion and metastasis. Our observation that nonanticoagulant heparins may interfere with heparanase-mediated degradation of ECM-HS suggests a potential therapeutic use for such heparins in neoplastic disorders.
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PMID:Role of heparanase in platelet and tumor cell interactions with the subendothelial extracellular matrix. 332 38

Specific characters of the osteoma osteoid as a beniGN tumor are well known. We report twelve cases of femoral neck localisation. Delays in diagnosis of six months to one year after the onset of symptoms are quite common. Chronic or recurrent pain is localised in the inguinal area with a projection to the leg and to the knee. The pain was relieved by Aspirin in six cases only. X ray of the pelvis antero-posterior showed the tumor, but did not always show the lucent image with the surrounding sclerotic area that is well observed with tomography. The scintigraphy with technetium 99 is perhaps more sensitive as a way of diagnosis. The lesion is the place of intensive uptake. Although the surgical excision "in block" and the replacing of bone graft and material of osteosynthesis gave positive results, many technical problems are present during the intervention because of the important cortical reaction and bone densification. In six cases, peroperative X Ray and histology did not give diagnosis.
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PMID:[Osteoid osteoma of the femur neck in children and adolescents. Apropos of 12 cases]. 339 36

The mechanism leading to the hypercoagulability in pancreatic carcinoma is unclear. The rapid progress of the disease after its diagnosis and the inaccessibility of the tumor make studies on the mechanism difficult in man. With the successful induction of this malignancy and conversion of it into an ascites tumor in Syrian golden hamsters, interactions between isolated tumor cells and individual hemostatic components can be investigated. In this paper, studies on in vitro tumor cell-platelet interactions and some hemostatic changes in hamsters following intravenous injection of isolated tumor cells are described. Freshly isolated tumor cells and tumor-cell sonicates, but not those that had been kept at 4 or -70 C overnight, induced comparable aggregation of human platelets in both heparinized and citrated platelet-rich plasmas (hPRP and cPRP). The aggregation was not followed by clot formation; a specific synthetic thrombin inhibitor had no effect on the aggregation in either hPRP or cPRP. Washed and gel-filtered platelets, even in the presence of 5% of citrated or heparinized platelet-poor plasma (cPPP or hPPP) failed to be aggregated by tumor cells. Tumor-cell-induced platelet aggregation was accompanied by thromboxane formation and serotonin release, both of which were several orders of magnitude greater in cPPP than in hPRP. Aspirin, apyrase, and PGI2 all inhibited tumor-cell-induced platelet aggregation in both PRPs, but the inhibition by aspirin was minimal. Intravenous infusion of isolated tumor cells into normal hamsters resulted in a 50% reduction of platelet count and a 20-30% decline in antithrombin III and fibrinogen. Platelet aggregates and fibrin strands were seen in the lungs of these animals.
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PMID:Platelet interaction with a pancreatic ascites tumor. 351 May 53

For suppression of primary tumor growth and metastatic spread, aspirin and theophylline, either alone or combined, were given daily to inbred female BN rats after sc implantation of a syngeneic nonimmunogenic tumor. Treatment with 200 mg aspirin/kg (body wt) resulted in a statistically significant regression of tumor growth as well as of the number of metastases in the lungs. Aspirin given in a lower dose (20 mg/kg) did not show significant difference from the vehicle group. Theophylline (75 mg/kg) significantly increased primary tumor growth as well as lung metastases. Inhibition of in vitro platelet aggregation, determined in whole blood taken from non-tumor-bearing animals treated with the same therapeutic regimen, was most pronounced in those groups in which tumor growth and spread were significantly retarded. However, this positive correlation between inhibition of tumor spread and platelet aggregation was not associated with a favorable balance of prostacyclin and thromboxane A2 in these animals.
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PMID:Reductive effect of aspirin treatment on primary tumor growth and metastasis of implanted fibrosarcoma in rats. 351 10

Approximately 1,000 assays for estrogen receptor (ER) in primary human breast tumors have been performed at St. Joseph's Hospital over a period of seven years; 700 of these included assays for progesterone receptor (PR). Based on the method of analysis (dextran-coated charcoal) and criteria for a positive result used for this survey, 80 percent of the primary tumors were ER-positive and 56 percent were PR-positive. In those cases where both assays were performed, 47.4 percent were ER-positive, PR-positive; 19.8 percent were ER-positive, PR-negative; 6.2 percent were ER-negative, PR-positive; and 26.6 percent were ER-negative, PR-negative. The mean concentration of ER increased with the advancing age of the patient; essentially the same relationship was observed for PR. The concentration of ER and PR was not directly dependent upon the degree of cellularity of the tumor. Lobular carcinoma and the mixed types containing ductal and lobular elements had the highest frequency of being positive for both steroid receptors, while medullary and papillary carcinomas were lowest. Three hundred and twenty-two cases had follow-up studies and were examined on the basis of the available information in the files of St. Joseph's Hospital Tumor Registry. A higher survival rate in patients with both ER and PR positivity became evident. In a community hospital setting, our data confirm the usefulness of estrogen and progesterone receptor assays in decisions of clinical management and considerations of prognosis in patients with mammary carcinoma.
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PMID:Assessment of results of estrogen and progesterone receptor assays performed in a community hospital. 374 Jul 95

Recombinant leukocyte type A human interferon and human lymphoblastoid interferon in combination with alpha-difluoromethylornithine (DFMO), an inhibitor of polyamine biosynthesis, have synergistic antiproliferative activity against colony formation in vitro by human tumor cells differing greater than 1000-fold in their intrinsic sensitivity to inhibitory effects of interferon. Interferon and DFMO in combination with doxorubicin have greater antiproliferative activity than is expected on the basis of additive effects based on the activity of doxorubicin alone and the synergistic activity of interferon plus DFMO. The addition of the polyamine putrescine to the cell cultures eliminates the synergistic interactions of interferon and DFMO and does not inhibit the activity of interferon itself. Aspirin and indomethacin at concentrations in vitro greater than those required for anti-inflammatory activity in vivo did not inhibit the antiproliferative activity of interferon alone and did not inhibit the synergistic activity of the combination of interferon and DFMO. Combination regimens including interferon and DFMO merit clinical evaluation for therapeutic activity against advanced cancers. Nonsteroidal anti-inflammatory agents should be studied for their ability to ameliorate symptomatic toxicity from interferon.
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PMID:Enhancement of the antiproliferative activity of human interferon by polyamine depletion. 391 54

Monocytes are thought to play a role in host resistance to tumor cell growth in animals and humans. In addition, platelets are known to be involved in tumor metastases. To investigate the interaction of these two cell types and their effect on tumor cells, human monocytes and platelets were examined using an in vitro monocyte-tumor cell cytotoxicity assay. Monocytes alone resulted in 32% +/- 1.5 (mean +/- SEM) tumor cell kill. When platelets were added to monocytes in a 1:1 ratio, an increase in cytotoxicity to 61% +/- 3.2 was observed. The cytotoxicity noted when platelets were added to a fixed number of monocytes and tumor cells was dependent on the number of platelets added. A decrease in cytotoxicity from 32% +/- 1.5 to 12% +/- 2.3 was observed when contaminating platelets were removed from monocyte preparations. Platelets added to tumor cells in the absence of any monocytes were also toxic, resulting in a maximum kill of 95% at a 4:1 platelet/tumor cell ratio. Secreted products of freshly isolated platelets may be responsible for much of the observed cytotoxicity, since supernatants from the platelets were toxic for tumor cells. Platelets pretreated with a cyclooxygenase inhibitor (ASA) or a lipoxygenase inhibitor had decreased cytotoxicity compared with untreated platelets. Our results indicate that products of platelet arachidonate metabolism are toxic for tumor cell lines. They also suggest that the role of the platelet must be considered when studying monocyte-tumor cell cytotoxicity.
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PMID:Human platelets exert cytotoxic effects on tumor cells. 392 50


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