UMLS:C0677930 - FACTA Search

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Query: UMLS:C0677930 (primary tumor)
20,210 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 61 year old woman presented with profound hyponatremia and markedly low serum osmolality. Urine osmolality was greater than the serum osmolality, an abnormality that was corrected by water restriction, suggesting inappropriate ADH secretion. Although there were no physical signs of Cushing's syndrome, her serum potassium level was low and markedly elevated levels of plasma and urine corticosteroids were not altered by the administration of large amounts of dexamethasone, suggesting the ectopic ACTH-MSH syndrome. Plasma levels of immunoreactive ACTH and beta-MSH were elevated. At autopsy, a metastastic oat cell carcinoma of the lung, not detected antemortem by chest roentgenograms and bronchoscopy, was found. Immunoreactive ADH, ACTH and beta-MSH were detected in the primary tumor and in metastases to the liver. beta-MSH was also detected in the spleen, in which metastases were observed. This is the first documented case of the simultaneous production of ADH, ACTH and beta-MSH by neoplastic tissue associated with clinical manifestations of the syndrome of inappropriate ADH secretion and the ectopic ACTH-MSH syndrome.
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PMID:Ectopic production of antidiuretic hormone (adh), adrenocorticotrophic hormone (ACTH) and beta-melanocyte stimulating hormone (beta-MSH) by an oat cell carcinoma of the lung. 18 5

A hot water bath was used to heat locally a metastasizing carcinoma in Wistar/Furth rats. Applying heat such that intratumor temperature is maintained at a mean value of 42.3 degrees for two 90-min sessions results in a decreased growth rate of the primary tumor as well as distant metastases. Heating the primary tumor for only one 90-min session or heating the leg contralateral to the tumor-bearing limb has no effect on the growth rate of either the primary tumor or metastases. Heat therapy has no detrimental effect on the spleen cell-mediated tumor immune response of rats as tested by an in vitro lymphocytotoxicity assay 1 day later. However, heating isolated spleen cells to similar temperatures in vitro reduces their capacity for in vitro tumor cell killing.
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PMID:Effects of hyperthermia on primary and metastatic tumor growth and host immune response in rats. 62 54

The effects of two new Ru(III) complexes, [mer-RuCl3(DMSO)2Im] degrees and Na[trans-RuCl4(DMSO)Im], were investigated on primary tumor growth and on the survival time using three solid metastasizing tumors of the mouse: Lewis lung carcinoma, B16 melanoma and MCa mammary carcinoma. Na[trans-RuCl4(DMSO)Im] appears to be the most promising compound, in that: (1) it is soluble in water and therefore easy to handle in comparison with the neutral species [mer-RuCl3(DMSO)2Im]degrees or to the already described BBR2382; (2) similarly to cisplatin, though at a lower level, it reduces tumor growth in its primary site in each tumor model employed; (3) unlike cisplatin, it increases the life span of tumor-bearing hosts in all tumors used, independently of the effects on primary tumor growth; and (4) it is also effective in reducing spontaneous metastasis formation when the effects on primary tumor growth are completely absent. Dimethylsulfoxide (DMSO), used for solubilizing poorly water-soluble compounds (i.e. [mer-RuCl3(DMSO)2Im]degrees) or for stabilizing the compound in the solution before injection (i.e. Na[trans-RuCl4(DMSO)Im]), reduces the anti-tumor potency. Conversely, the antitumor effects of Na[trans-RuCl4(DMSO)Im] are more pronounced in mice hydrated with isotonic saline. We conclude that Na[trans-RuCl4(DMSO)Im] is a good candidate for further investigations aimed at ascertaining the mechanism of the anti-metastatic activity and of the positive effects on survival time of mice bearing solid metastasizing tumors.
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PMID:Effects of the Ru(III) complexes [mer-RuCl3(DMSO)2Im]degrees and Na[trans-RuCl4(DMSO)Im] on solid mouse tumors. 162 12

Recombinant human (rhu) interleukin 2 (IL-2) was evaluated alone and in combination with local hyperthermia (LH) in mice inoculated s.c. with 5 x 10(5) Lewis lung carcinoma cells. Four treatment regimens were begun 6 days postinoculation at a time when the tumor had grown to approximately 8.0 mm in diameter. Treatments were: group 1, saline injected as control; group 2, LH; group 3, rhuIL-2; or group 4, LH combined with rhuIL-2. LH utilized hot water circulation by a Brann Thermomix 1420. The intratumor temperature was maintained at 43 +/- 0.2 degrees C for 30 min each on days 6 and 10 and rhuIL-2 was given s.c. at 5 x 10(4) units twice a day for 5 days. Thirty mice in each group were sacrificed 28 days after tumor inoculation. An additional 20 mice in each group were observed for survival time. The size of primary tumor and the number of lung metastases were reduced and the survival time was prolonged in mice treated by either LH or IL-2. However, a greater antitumor effect in Lewis lung carcinoma tumor-bearing mice was observed using IL-2 therapy combined with LH. Tumor growth was associated with increased splenic granulocyte-macrophage progenitor cells and an abnormal L3T4+/Lyt-2+ lymphocyte subset ratio (less than 1.0). Splenic granulocyte-macrophage progenitor cell numbers and the L3T4+/Lyt-2+ ratio returned to normal in the group treated with combination therapy, the best responder group. The L3T4+/Lyt-2+ ratio did not change in the groups treated with single therapy. These results suggest the efficacy and possible clinical relevance of combined therapy with rhuIL-2 and LH for certain metastatic tumors.
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PMID:Effects of interleukin 2 treatment combined with local hyperthermia in mice inoculated with Lewis lung carcinoma cells. 237 68

Malignant ascites is often refractory to therapy and rapidly deteriorating the nutritional and physical state of the cancer patient. Nevertheless, ascites does not always implicate preterminal state of the cancer process (e.g. ovarian carcinoma). A short review is made of the pathophysiology of ascites in cirrhosis and in malignancy, and different modes of treatment are discussed. The results of medical therapy of malignant ascites (salt and water restriction, diuretics, intraperitoneal cytostatics or radiocolloids) are not convincing. The immunotherapy with OK-432, as worked out by Katano (16-46) has to prove its value. The best and most hopeful results in cases of massive previously resistant ascites, are obtained with a peritoneojugular shunt, improving immediately the nutritional status and life condition, providing excellent palliation. The superiority of the Denver shunt versus the Le Veen shunt has been assessed recently, especially for malignant ascites. Some technical and perioperative details merit more attention, to limit the high risk ratio. Control of the intrathoracic position of the catheter tip, the maintenance of the bloodflow in the jugular vein, the intramuscular tunnelisation of the peritoneal catheter, the discard of 3 or 5 liters ascitic fluid and the substitution of part of it by physiological fluid, perioperative prophylactic antibiotics and heparinisation, flow-rate control in the postoperative period by changing patients position, respiratory exercises, daily flushing, all those measures limit the risk of fibrinolysis (DIC), shunt occlusion, fluid overload and infection. The fear of metastasis by shunt is unfounded, since the survival of the primary tumor is mostly too short (41). The postoperative follow up in an intensive care unit is necessary during 24-72 hours.
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PMID:[The Denver shunt in malignant ascites]. 258 Apr 8

CGP 6809 is a water-soluble nitrosourea derivative with quite distinct chemical and biological properties as compared with the well-known representatives of this class of compounds. It is related to the antibiotic streptozotocin, from which it is distinguished in the structure of the sugar moiety and the position of the methylnitrosourea residue. CGP 6809 possesses practically the same alkylating potential as streptozotocin; however, its carbamoylating activity is comparable with that of CCNU. In contrast to other nitrosourea derivatives, CGP 6809 showed relatively little activity in murine leukemias but was markedly active in solid transplantable melanomas (Harding-Passay, B16), in the 11095 prostate carcinoma, and in a substrain of Yoshida hepatoma (AH 7974) resistant to BCNU and CCNU. In the Ehrlich and Yoshida ascitic tumors complete responses were seen with no toxic death. Dose-dependent activity was found in the human lung carcinoma MBA 9812 and almost complete growth inhibition was achieved in the human melanoma WM 47 by both the oral and parenteral routes of administration. However, mammary tumor lines (Ca 755, 2661/61, R-3230AC), the Guerin-T8 uterus epithelioma, and the Rous sarcoma/S-R proved to be relatively refractory to this drug. This was also the case for the Lewis lung carcinoma implanted i.m. or s.c. However, development of lung metastases was markedly inhibited. Combination therapy using CGP 6809 with cyclophosphamide, 5-fluorouracil, or chlorambucil in the same model led to partial responses of the primary tumor as well as almost total eradication of lung metastases.
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PMID:CGP 6809, a sugar-containing nitrosourea derivative: pharmacological and physicochemical properties. 271 56

We have shown earlier that a decline in splenic natural killer (NK) activity during the development of transplanted or spontaneous tumors in mice results from an inactivation of NK lineage cells, mediated by prostaglandins (primarily PGE2) secreted by NK suppressor cells of the monocyte-macrophage lineage. In the present study we have used a C3H mouse mammary carcinoma model to examine whether this mechanism of NK suppression is conducive to tumor metastasis in vivo and whether a reversal of this suppression by a chronic indomethacin therapy can prevent metastatic spread from the primary tumor site. Three mammary tumor lines, all derived in our laboratory from a spontaneous C3H mammary tumor were employed: T-58 (uncloned parental line, having weak lung metastasizing ability from the subcutaneous site), C3 (a clone of T-58, showing high metastatic ability), and C10 (a nonmetastatic clone of T-58). Although the degree of NK susceptibility of these lines varied inversely with their metastatic potential, none was NK resistant. A chronic administration of indomethacin in the drinking water (14 micrograms/ml) to mice beginning on Day 4 after subcutaneous transplantation of 10(6) tumor cells resulted in a significant reduction in the growth rate of primary tumors in all hosts and led to a complete or nearly complete abrogation of lung metastasis in T-58- or C3-transplanted hosts examined at 1 month after tumor transplantation; C10-transplanted mice showed no metastasis in the control or the treated group. Concomitantly, there was a substantial restoration of splenic NK activity in all indomethacin-treated hosts. Plastic-adherent cells (greater than 95% macrophages) isolated from tumors growing in control mice, when coincubated for 20 hr with normal splenic effector cells caused a suppression of NK activity, reversible in the presence of indomethacin (10(-5) M) in vitro. Similar cells recovered from the residual primary tumors in indomethacin-treated mice had no suppressor ability. Chemically pure PGE2 (at concentrations of 0.5 to 1 X 10(-6) M, but not 0.25 X 10(-6) to 10(-8) M) also caused a suppression of NK activity of normal splenic effector cells, when added during the 4-hr 51Cr-release assay or allowed to interact with effector cells alone for a 20-hr incubation period; a removal of the cell-free PGE2 in the latter case prior to the NK assay did not relieve the suppression.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Indomethacin therapy abrogates the prostaglandin-mediated suppression of natural killer activity in tumor-bearing mice and prevents tumor metastasis. 294 21

Increased sialylation and branching of asparagine-linked oligosaccharides have recently been associated with both neoplastic transformation and the metastatic phenotype. Swainsonine, an inhibitor of Golgi alpha-mannosidase II blocks the synthesis of sialylated tri- and tetraantennary asparagine-linked oligosaccharides and results in the expression of hybrid-type oligosaccharides at the cell surface. Both the lymphoid tumor line MDAY-D2 and B16F10 melanoma cells were less metastatic when grown in swainsonine (0.3 micrograms/ml) for 48 h prior to injection of the cells into the lateral tail veins of mice. The addition of swainsonine (2.5 micrograms/ml) to the drinking water of the mice further reduced the incidence of lung colonization by B16F10 melanoma cells. MDAY-D2 tumors removed from mice on swainsonine-supplemented drinking water showed a loss of leukoagglutinin-binding complex-type oligosaccharides similar to that of tumor cells cultured in medium containing swainsonine. The growth rate of s.c. MDAY-D2 tumors was not reduced by the addition of swainsonine to the drinking water of the host; however, when mice were given two i.p. injections of the interferon-inducing agent polyinosinic:polycytidylic acid in addition to swainsonine, the primary tumor grew at a reduced rate compared to either treatment alone. Swainsonine alone did not inhibit tumor cell growth in vitro; however, the drug enhanced the antiproliferative effect of interferon. The survival time of mice bearing established MDAY-D2 metastases was extended by treating the animals with swainsonine and polyinosinic:polycytidylic acid; however, the number of long-term survival was unchanged. Swainsonine-treated tumor cells appeared to be compromised in two ways: reduced organ colonization potential; and drug-treated MDAY-D2 cells were more sensitive to the antiproliferative effects of interferon in vitro and in vivo.
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PMID:Effects of swainsonine and polyinosinic:polycytidylic acid on murine tumor cell growth and metastasis. 309 60

At the Finsen Institute, Copenhagen, from 1971 to 1981, 134 patients were treated for lymph node metastases from primary cutaneous malignant melanoma of axial localization (e.g., in the head and neck and trunk), where metastases to regional lymph node groups were the first sign of dissemination. Due to the lack of sufficient clinical data, 27 patients were excluded from the study. Median time from excision of primary tumor to diagnosis of node metastases was 11 months. In 42 of 85 (49%) patients with truncal melanoma, the primary tumor was placed in the lymphatic water-shed areas. Two patients among this group showed bilateral simultaneous metastases to two different node groups. In the remaining 43 patients with truncal tumors located outside water-shed areas, node metastases developed in unexpected groups in seven (16%) patients. Of 22 patients with head and neck tumors, two (9%) patients demonstrated metastases to distant lymph node groups without metastases to the regional node basins.
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PMID:Patterns of the first lymph node metastases in patients with cutaneous malignant melanoma of axial localization. 316 20

Previous studies have indicated the efficacy of adoptive immunotherapy utilizing recombinant interleukin-2 (rIL-2) and lymphokine-activated killer (LAK) cells in the treatment of advanced neoplastic disease. However, this therapeutic approach is associated with considerable toxicity, primarily due to the systemic administration of rIL-2. The present study was undertaken to determine the efficacy of a newly developed water-soluble glucan, when administered in combination with LAK cells, in the therapy of experimental hepatic metastases. Mice were challenged subcutaneously (1 X 10(4) cells) with reticulum cell sarcoma M5076 on day 0. Therapy was initiated on day 15, when a palpable primary tumor mass and hepatic micrometastases were evident, and continued at 3-day intervals up to day 54. Sarcoma-bearing mice received glucan (250 mg/kg) intravenously, either alone or in combination with LAK cells (1 X 10(7)/mouse). Control mice received 5% (wt/vol) dextrose in water. Glucan-LAK cell therapy significantly suppressed primary tumor growth, inhibited the progression of hepatic metastases and prolonged survival in sarcoma-bearing mice. Splenocytes, incubated with rIL-2 for 72 h, exhibited significant natural killer (NK) cell activity and were cytotoxic to sarcoma cells in vitro. Glucan-LAK cell administration resulted in significant increases in splenic NK cell activity and Kupffer cell-mediated tumoricidal activity. In addition, bone marrow proliferation was enhanced following the co-administration of glucan and LAK cells. Due to its nontoxic nature and immunostimulating properties, soluble glucan may prove to be an attractive biological response modifying agent for utilization in adoptive immunotherapy of advanced neoplastic disease.
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PMID:Soluble glucan and lymphokine-activated killer (LAK) cells in the therapy of experimental hepatic metastases. 328 99

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