Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of a 78-year old woman, complaining of epigastralgia, is reported. A series of gastrointestinal examinations revealed a small, elevated lesion with a central depression in the antrum. Since a fiberoptic biopsy had shown a Group V classification, a partial gastrectomy was performed. Tumor nodules, judged to be metastatic, were noticed in the liver and regional lymph nodes. Histologic scrutiny disclosed a keratinizing tumor that measured 1.0 X 0.9 cm in diameter and was largely a squamous cell carcinoma with a small focus indicating an adenocarcinoma. This tumor was confined to the muco-submucosal layers with prominent vascular permeation. No adenocarcinomatous components were found in the metastatic foci. The patient died eight months after operation. In light of our experience, together with what has been found in a review of the literature, we feel that a squamous carcinoma and an adenosquamous carcinoma of the stomach to be more aggressive than an ordinary adenocarcinoma and keeping this point in mind, they should be considered differentiated from an adenoacanthoma.
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PMID:[A case of small squamous cell carcinoma with a grading of IIa + IIc, an early gastric cancer type]. 340 55

PSK (Krestin) is a protein-bound polysaccharide isolated from cultured mycelia of Coriolus versicolor in basidiomycetes. PSK is a biological response modifier which possesses unique characteristics. We investigated the effects of PSK on the immune response of aged C57BL/6 mice bearing a syngeneic transplantable tumor adenocarcinoma 755. (a) In C57BL/6 mice, the delayed foot pad reaction against sheep erythrocytes and resistance to syngeneic tumor challenge reached a peak when the mice were at 30 weeks of age, and decreased at 50-60 weeks of age. The serum of normal mice exerts a modifying effect on blastogenesis of lymphocytes to phytohemagglutinin. The positive effect reached a peak at 30 weeks of age, and thereafter declined with age. (b) When adenocarcinoma 755 was inoculated to C57BL/6 mice at 10-, 30- and 60-weeks of age, immune responses were depressed in 10-week-old and 60-week-old mice. PSK prevented such depression. However, in 30-week-old mice, tumor-induced suppression was slight, and administration of PSK to them increased proportion of mice which did not develop a tumor. (c) In 60-week-old tumor-bearing mice, the antitumor effects was increased with a combination of PSK and adoptive transfer of spleen cells from 10-week-old normal mice. The immune responses of mice, which change with the progress of age, are depressed by tumor burden. The administration of PSK to aged mice is effective to restore immune responses from tumor-induced suppression.
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PMID:Restoration of immune responsiveness by a biological response modifier, PSK, in aged mice bearing syngeneic transplantable tumor. 343 May 62

This experimental study in rats examines tumour take and growth after RES modulation in an organ rich in macrophages--the liver--vs. an organ poor in macrophages--the kidney. A control group of 16 rats had 1.0 X 10(6) transplantable adenocarcinoma cells inoculated in the liver and the same number in the left kidney. They were compared with a RE-stimulated group of 16 rats treated i.v. with Zymosan (3 mg/100 g for 3 days) and a RE-depressed group of 16 rats treated with i.v. methylpalmitate (100 mg/100 g for 3 days) before tumour inoculation. Tumour size was measured on days 7 and 14. The animals were killed on day 14. Mortality was significantly higher in methylpalmitate-treated rats than in control groups. Tumour take in the kidney was not affected by RES stimulation or depression. In the liver, RES stimulation caused significantly less tumour take. Depression of RES with methylpalmitate did not increase tumour take or tumour growth in the liver, which was very high in the control group.
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PMID:RES function and tumour take and tumour growth in the liver and in the kidney--an experimental study in rats. 343 52

Using a tracer technique, loss of cells from perivascular and average tumor cells of the syngeneic mammary adenocarcinoma EO 771 in male C57Bl/6J mice may be measured in the living animal, by the use of 125-labelled 5-iodo-2'-deoxyuridine (125I-UdR). It was the purpose of this paper to compare measurements in vivo with those made in vitro following local 60Co-gamma irradiation in the absorbed dose range from 10 to 27.5 Gy, incorporation of radioactivity into DNA of tumor cells and activity loss from labelled tumor cells were measured externally by a special scintillation counter device. In addition, by injecting the vital dye "light green" into the mice the I-125-activity of the stained viable and unstained necrotic regions were separately measured for loss of activity following gamma irradiation. A comparison was made between radiation induced growth delay and the depression of 125I-UdR incorporation into DNA of the proliferating tumor cells. After local tumor irradiation with a dose of 27.5 Gy 60Co gamma rays an enhancement of the activity loss by 0.5% per hour was externally observed for the perivascular tumor cell population. A lower enhancement of 0.4% per hour was externally registered in the average tumor cell population. Both values were evaluated relative to sham-irradiated control tumors. The measurements on isolated tumors were in comparatively good agreement with the external values. The activity loss rate from the viable, euoxic tissue increased by 0.4% per hour after 27.5 Gy 60Co gamma rays and by 0.3% per hour in the average cell population, the latter representing a mixture of euoxic and hypoxic cells. The results demonstrate, that the external measurements are a good indicator for radiation effects under in vivo-conditions.
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PMID:Cell loss from viable and necrotic tumor regions after local gamma irradiation measured by 125I-UdR. 356 71

A 58-year-old male visited the Kochi Municipal Central Hospital on May 17, 1984. A barium meal study and endoscopy revealed a huge crater surrounded by a thick embankment on the posterior wall of the stomach body. Biopsy specimens taken from the lesion revealed tubular adenocarcinoma, UFT (600 mg/day) and anti-tuberculous drugs were administered due to the complication of pulmonary tuberculosis. Endoscopic examination on August 6, 1984, revealed a remarkable improvement, showing a shallow irregular depression with converging folds. The patient underwent surgery on August 7, 1984, because from the endoscopic appearance, residual cancer was highly suspect, and also tuberculosis had improved. The histology of the surgically resected specimen showed a chronic peptic ulcer, the base of which was covered with regenerating mucosa. No cancer nests were demonstrated even by serial tissue sections.
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PMID:[A case of gastric carcinoma disappearing after short-term preoperative chemotherapy]. 361 65

We studied the effect of treatment with Thymosin Fraction 5 (Fr-5) on the restoration of T-cell functions and the induction of antitumor immunity in spontaneously hypertensive rats (SHR) with congenital T-cell depression. SHR showed a reduced number of rosette-forming thymocytes early in their lives, and in vitro incubation of SHR thymocytes with Fr-5 restored the numbers of rosette-forming T-cells to the normal level for Wistar/HMK rats, the original strain of SHR. In vivo treatment of SHR with various doses of Fr-5 (0.5, 1.0, or 2.0 mg/kg, 6 times every other day) also increased significantly the blastogenic responses of their spleen cells to phytohemagglutinin but failed to promote plaque-forming cell responses to sheep red blood cells. These immunological restorative effects by Fr-5 were dose dependent. In contrast, treatment with lower doses of Fr-5 (0.25 or 0.50 mg/kg) showed greater curative effects on a high antigenic fibrosarcoma (SMT-6) than did treatment with higher doses of Fr-5 (1.0 or 2.0 mg/kg). This was confirmed by the fact that treatment with a 0.5-mg/kg dose of Fr-5 caused a significant suppressive effect on the growth of a weakly antigenic and highly metastatic adenocarcinoma (SST-2) in SHR with a consequent prolongation of survival days, whereas treatment with a 1.0- or 2.0-mg/kg dose of Fr-5 was without any effect. In order to clarify this mechanism, we studied the effect of pretreatment with cyclophosphamide (CY) on the development of antitumor delayed-type hypersensitivity (DTH) reaction in the SMT-6-bearing SHR treated with Fr-5 (0.5 or 2.0 mg/kg). Treatment with 0.5 mg of Fr-5 per kg significantly increased the DTH reaction to SMT-6 cells in both CY-pretreated and untreated SHR. In contrast, treatment with 2.0 mg of Fr-5 per kg produced a significant antitumor DTH reaction in SHR pretreated with CY but failed to induce the DTH reaction in SHR untreated with CY. These results suggest that higher doses of Fr-5 may induce preferentially suppressor T-cells rather than killer T-cells in tumor-bearing SHR with congenital T-cell depression.
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PMID:Restoration of T-cell function and induction of antitumor immune response in T-cell-depressed spontaneously hypertensive rats by treatment with thymosin fraction 5. 387 52

We report here our study of the role of natural host defense mechanisms mediated by macrophages and natural killer (NK) cells in an experimental model of spontaneous pulmonary metastases of a mammary adenocarcinoma SST-2 in spontaneously hypertensive rats (SHR) with congenital T-cell depression. To activate macrophages and NK cells, Listeria monocytogenes (LM) was injected IV into SHR which had received a transplantation of SST-2. To assess the antimetastatic responses induced by LM, the number of lung nodules and the lung weight in SHR were evaluated 30 days after tumor inoculation. The growth of lung metastases, though not of primary tumors, was significantly reduced if 10(7) LM were injected IV into SHR 2, 10 and 20 days after the SC transplantation of 5 X 10(4) or 5 X 10(5) SST-2. An inhibitory effect of LM on pulmonary metastases was also observed in tumor-excised rats, in which the number of lung metastases and the lung weight were enhanced as compared with those in tumor-bearing rats which had not undergone surgery. Peritoneal resident cells which were harvested from rats injected with LM showed a significant augmentation of tumoricidal activity against SST-2 cells as measured by in vitro cytotoxicity. Similarly, the NK activity of spleen cells of SHR injected with LM increased significantly when compared with untreated SHR. These data suggest that the inhibition of metastatic growth, though not of primary tumor growth, was accomplished by the, possibly T-cell independent, activation of macrophages and NK cells.
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PMID:Activation of natural resistance against lung metastasis of an adenocarcinoma in T-cell depressed spontaneously hypertensive rats by infection with Listeria monocytogenes. 387 51

Aroclor 1254 was fed to groups of 24 male and 24 female F344 rats, from 7 weeks of age, at dietary concentrations of 25, 50 and 100 ppm for up to 105 weeks. There was a dose- related depression of body weight gain for both sexes and decrease in survival for male rats. Histologically, an increased incidence of gastric intestinal metaplasia and adenocarcinoma was found in both sexes. Hepatocellular adenomas, carcinomas, and eosinophilic and vacuolated hepatocellular foci were usually found in dosed rats only. The number of these foci per unit area of liver was significantly increased in dosed rats, although eosinophilic foci were only found in rats exposed to Aroclor 1254. Basophilic hepatocellular foci were found in similar numbers per square centimeter of liver in controls and treated rats. This finding suggested that eosinophilic hepatocellular foci and tumors arose de novo rather than from the naturally occurring basophilic foci. The appearance of unique, potentially preneoplastic lesions and tumors in the liver and stomach in dosed rats which do not usually occur spontaneously in control rats would support the hypothesis that Aroclor 1254 induced or initiated these unique lesions de novo rather than promoted the growth of any naturally occurring lesions. Nonneoplastic hepatic lesions included degenerative hepatocellular changes and aggregates of macrophages with crystalline cytoplasmic structures and pigment granules.
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PMID:Proliferative lesions of the glandular stomach and liver in F344 rats fed diets containing Aroclor 1254. 392 67

Development of 1,2-dimethylhydrazine (DMH) induced colonic neoplasia were studied using male Wistar rats given 120 mg DMH per kg s.c. weekly for 5 weeks. During the course of colon carcinogenesis, changes in cellular proteins of colonic mucosa were analysed by two-dimensional gel electrophoresis. Rats were sacrificed just before and at 10, 15 and 20 weeks after the initial DMH treatment together with controls. Incidence and number of colorectal tumors gradually increased. At the 20th week, colon carcinoma was found in every rat. Most tumors (92%) were found in the major flexure and the distal colon and rectum, while only 1% and 7% were found in the cecum and proximal colon, respectively. Histologically, most (92%) were classified as well differentiated or moderately differentiated adenocarcinoma. Eighty-five percent of the tumors were semipedunculated or sessile without depression, and the remainder were sessile with depression. All of the latter were carcinomas with invasion to the submucosa or further. Two-dimensional gel electrophoresis revealed 180 spots in cellular proteins before and after the initial treatment. Three new spots appeared and four spots greatly increased during the course of carcinogenesis, while one spot disappeared. The above results suggest that the appearing and increasing spots may be associated with cancer and that the disappearing spot may be associated with the normal colon.
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PMID:[Development of 1,2-dimethylhydrazine-induced colonic neoplasia in rats and changes in cellular proteins of colonic mucosa]. 408 89

80 patients with inoperable non-small cell bronchial carcinoma were treated, at an interval of 4 weeks between them, with ifosfamide (2 g/m2 on days 1-5) and cisplatin (75 mg/m2, day 1). All diagnoses had been confirmed histologically. The course of 72 patients (36 with squamous carcinoma, 25 with adenocarcinoma, two with alveolar-cell carcinoma and nine with large-cell carcinoma) could be evaluated. There were four complete and 21 partial remissions (response rate 35%). In a further 14 patients temporary arrest of tumor growth was registered. Median survival time of all patients was 8.3 months, for those with complete and partial remission 11.5 months. Patients in whom the tumor progressed lived on average 3.9 months. Age and general state of the patients, as well as histological tumor type, had no influence on the results of treatment. Patients in stage IV lived, at seven months, significantly less long than those with only loco-regional spread (11 months). Main side-effects were vomiting, bone-marrow depression and neuropathy. Urotoxicity was not significant, as a result of treatment with mesna. Remission rate and survival time of these patients corresponded with the results obtained with other cisplatin combinations.
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PMID:[Chemotherapy of the non-small cell carcinoma of the lung with ifosfamide and cisplatin]. 608 64


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