Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cancer often causes malnutrition and specific vitamin and protein deficiencies. Chemotherapy also causes deficiencies by promoting anorexia, stomatitis, and alimentary tract disturbances. Antimetabolite drugs in particular inhibit synthesis of essential vitamins, purines, and pyrimidines. Because vitamin levels in the blood are often nondiagnostic, nutritional deficiency is identified almost exclusively on the basis of clinical signs and symptoms and the patient's response to therapy. Signs and symptoms of cachexia and hypoalbuminemia are common in patients with advanced cancer. Deficiencies of vitamins B1, B2, and K and of niacin, folic acid, and thymine also may result from chemotherapy. Nutritional deficiencies are chemically correctable; however, the tumor must be eradicated to relieve cachexia.
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PMID:Nutritional deficiencies in patients receiving cancer chemotherapy. 229 64

The present study investigates a tumor model for cachectic mice. Among various murine transplantable tumors, used for assessing cytostatics, we identified colon 26 adenocarcinoma (colon 26) as capable of causing cachexia. Fifteen days after inoculation, the tumor grew to about 6% of the body weight causing substantial carcass weight loss of 3.4 g (14.5% of the carcass weight). When the tumor size was 2.7 g at 3 weeks after the inoculation, the carcass weight was 12 g less than the age-matched control. The tumor continued to grow while the mice maintained this weight, surviving for an average of 45 days. This extensive weight loss was essentially the wasting of adipose and muscle tissues. Hypoglycemia and hypercorticism occurred during the time of the weight loss. In addition, the colon 26 caused disorders of hepatic functions: the concentration of acute phase proteins in serum increased; the number of hepatic glucocorticoid-cytosol receptors decreased; and activities of hepatic catalase and drug-metabolizing enzymes decreased. On the other hand, noncachectic mice with Meth A fibrosarcoma gained weight, which was somewhat less than the control, and had neither hypoglycemia nor hypercorticism, although some mild disorders of hepatic functions were found. Mice bearing colon 26 is an appropriate model for elucidating the mechanism that causes cachexia.
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PMID:Experimental cancer cachexia induced by transplantable colon 26 adenocarcinoma in mice. 231 17

Tumor necrosis factor may be a mediator of the syndrome of cancer cachexia. Tachyphylaxis or tolerance to the cachectic effects of recombinant tumor necrosis factor (rTNF) has been previously described. In this study, we investigate whether repetitive exposure to rTNF can induce similar tolerance in tumor-bearing (TB) rats and ameliorate cachexia induced by the tumor. In experiment 1, non-tumor-bearing (NTB) and TB rats were randomized to either escalating low doses of rTNF or saline i.p. twice daily for 9 consecutive days. NTB rats treated with rTNF demonstrated a significant decline in food intake and weight change (P less than 0.00001) but soon developed tolerance to the cachectic effects of rTNF; they consumed significantly more food than on the first day of treatment and had weight change similar to NTB rats treated with saline. TB rats treated with rTNF showed a similar significant decline in food intake and weight change (P less than 0.0001) and also demonstrated similar tolerance to the cachectic effects of rTNF with continued treatment. Following treatment, TB rats that had been treated with rTNF ate significantly more and lost less weight than TB rats that had been treated with saline (P less than 0.00001). rTNF treatment of TB rats also demonstrated antineoplastic activity, as estimated tumor weight of tumors from rats treated with rTNF were significantly less than controls (P = 0.003). The anticachexia and antineoplastic effects of rTNF resulted in prolonged survival of TB rats treated with rTNF compared to control TB rats (P = 0.015). Experiment 2 utilized two different rTNF treatment regimens in TB rats: one group received 12 days of escalating doses of rTNF, and another group received 15 days of rTNF treatment. TB rats treated with rTNF again had a significantly greater food intake (P less than 0.00001) and delayed weight loss (P = 0.0001) posttreatment that was further augmented by additional doses of rTNF. Antineoplastic activity of rTNF was less clear, and overall tumor growth curves were not affected by rTNF treatment. Survival of TB rats treated with rTNF was again significantly increased in a dose-dependent manner (P = 0.006). Repeated administration of low doses of rTNF to TB rats induces mild reduction in tumor growth, tolerance to the cachectic effects of rTNF that results in tolerance to the cachectic effects of tumor, and prolongation of survival.
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PMID:Prolonged survival of tumor-bearing rats with repetitive low-dose recombinant tumor necrosis factor. 235 41

Single snapshot measurements of resting energy expenditure (REE) suggest that hypermetabolism contributes to cancer cachexia, but tumor impact on total 24-hr energy expenditure (TEE) is unknown. Automated multicage indirect calorimetry was employed to measure daily energy expenditure in adult Buffalo rats (n = 16) randomized to tumor inoculation or controls. Measurements included baseline REE, activity EE (AEE), thermic response to food (TEF), and TEE. Rats (n = 16) were randomized. Metabolic measurements, tumor size, and body weight were recorded weekly. Animals were sacrificed at Week 5 for analysis of host and tumor composition. Significant depletion of total lean body mass occurred in TB rats (greater than 15% wt loss, ANOVA P less than 0.001) which inversely correlated with tumor growth (r = -0.81, P less than 0.001). REE, TEF, AEE, and TEE did not change in controls (ANOVA P = n.s.). In TB rats, a 19.5% increase in REE occurred (119.4 +/- 3.3 to 138.7 +/- 1.8 kcal/kg LBM/day, P less than 0.01). TEE remained unchanged (157.3 +/- 5.6 vs 152.9 +/- 3.6 kcal/kg LBM/day, P = n.s.) due to a 66% decrease in AEE (32.9 +/- 3.1 to 10.5 +/- 1.7 kcal/kg LBM/day, P = 0.01). TEF did not change (4.7 +/- 0.8 vs 5.0 +/- 0.3 kcal/kg LBM/day, P = n.s.). Both TB and controls demonstrated a decreased REE in response to a 24-hr fast (7.9% vs 4.8%, P = n.s.). Respiratory quotient decreased in both groups when comparing fed to fasted values: TB (0.86 to 0.76) and controls (0.86 to 0.71), but the decline was greater in controls (P = 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Components of energy expenditure in tumor-bearing animals. 236 17

Twenty bladder biopsies from patients with primary transitional cell carcinoma were inoculated into nude mice. To date, eleven of these have grown as primary implants and three serially transplantable xenograft lines (UCRU-BL-12, UCRU-BL-13, UCRU-BL-14) have been established. The histological and ultrastructural features of human transitional cell carcinoma have been maintained in each line. Despite a relatively uniform histological appearance, several indices of occult tumor heterogeneity have been revealed. Immunocytochemical staining was negative for beta-subunit human chorionic gonadotrophin but positive for carcinoembryonic antigen only in areas of squamous differentiation. All three tumors bound peanut lectin. Flow cytometric DNA analysis of UCRU-BL-13 showed multiple aneuploid peaks, separate populations being demonstrated in different xenografts of the same generation. However, the morphologies of these tumors remained identical. On initial implantation UCRU-BL-12 and UCRU-BL-14 were near diploid but aneuploid populations became apparent with increasing passage number. Each xenograft line caused cachexia in the host mice. Treatment with the cisplatin analogue, isopropyl platinum, ameliorated the cachexia displayed by mice carrying UCRU-BL-14 but did not cause tumor regression. UCRU-BL-12, when tested with cisplatin, isopropyl platinum, and carboplatin, showed equivalent growth retardation with each drug. These xenografted human bladder cancers may be useful models for the study of heterogeneity of the tumor populations in bladder cancer and for the evaluation of new approaches to treatment.
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PMID:Bladder cancer xenografts: a model of tumor cell heterogeneity. 241 59

Surgical palliation of advanced gastrointestinal malignancy is often accompanied by high morbidity and limited success. To evaluate the role of ablative laser therapy in palliation, we reviewed our experience with 30 consecutive patients who presented with symptoms of obstruction, bleeding, or pain from unresectable tumors of the esophagus (20), Stomach (4), or rectum (6). Overall, 97 laser treatments were administered endoscopically with a Neodymium Yttrium Aluminum Garnet (Nd:YAG) laser using average energy per treatment of 4525 joules. Forty per cent of the patients received their therapy as outpatients and all were given only light intravenous sedation. The symptomatic response was good to excellent in 70 per cent of patients but five (16.7%) subsequently developed recurrences requiring further laser ablation. Performance status was improved in 19 of 20 patients with esophageal cancer. Few of the gastric or colorectal cancer patients noted changes in performance status since concomitant medical illnesses often limited their overall function. There was one mortality within 30 days from esophageal tumor cachexia and two patients experienced moderately severe visceral pain. No perforation or fistulizations occurred. This experience confirms that a Nd:YAG laser photo-ablation is safe and effective when palliation is indicated for advanced cancers of the gastrointestinal tract.
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PMID:Laser palliation for gastrointestinal malignancy. 244 6

Endoscopic laser therapy (ELT) for palliation of cancer of the esophagus and the gastroesophageal junction was evaluated in 31 patients with far advanced disease. Initial technical success (94%) and initial improvement of symptoms (81%) were comparable to data reported previously. Complications were bleeding (6%), sepsis (6%), and tracheoesophageal fistula (6%). This analysis, however, addressed the impact of ELT on the remaining life of the patients. In 9 patients (29%) ELT was the only palliative alternative, and in 7 of these patients a fair functional success was achieved. In 13/21 (63%) of the patients with good initial functional result palliation could be preserved by repeated ELT until death from cachexia. Eight patients, however, were intubated in the follow-up period because of failure to keep the esophagus open. The dysphagia-free interval was only 4 weeks, and repeated ELT became progressively more difficult because of increased tumor load and increasing debility of the patient. 32% of the patients experienced ELT as more difficult than repeated dilations. Our data also suggest that duration of palliation after ELT alone lasts longer than palliation after dilation followed by ELT. Results of ELT were best in patients with recurrent cancer at the esophagogastric or esophagojejunal anastomosis.
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PMID:Palliative Nd:YAG laser therapy for cancer of the esophagus and gastroesophageal junction: impact on the quality of remaining life. 245 64

Endoscopic neodymium yttrium aluminium garnet (Nd YAG) laser therapy, is a new and simple method for the palliative treatment of inoperable colorectal cancer. To date the authors have treated 70 patients and the value of this method was assessed prospectively in 14 patients. Quality of life was measured before, during, and after treatment. The quality of life (QL) index, a physician's assessment and a linear analogue self-assessment (LASA) were used. A close correlation was found between the two assessment methods (r = 0.79). Overall there was a significant improvement from the mean pretreatment score and the best score achieved posttreatment (QL: P = 0.002; LASA: P = 0.002). Patients with diarrhea, rectal bleeding, mucus discharge, or pain secondary to tumor bulk, will benefit most from this treatment. Malignant cachexia, pain secondary to sacral plexus involvement, tumor encroachment on the anal canal and/or sphincter dysfunction resulting from tumor invasion should be viewed as relative contraindications to laser therapy. The authors conclude that in selected patients endoscopic laser therapy can provide effective palliation in patients with malignant tumors of the rectum and descending colon.
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PMID:Palliative laser therapy for inoperable rectal cancer--does it work? A prospective study of quality of life. 246 30

We have established four lines of transplantable gastric carcinoma in WF Osaka rats. They were derived from adenocarcinomas of the glandular stomach, which were developed along with the lesser curvature, measuring less than 1.0 square centimeter. Morphology of these four lines of the transplantable tumor showed essentially an identical figure in their respective generations. Histology in the early generation of transplanted tumors showed well differentiated tubular adenocarcinoma similar to the primary lesion of the stomach. Later the histological appearance of these four lines of the transplanted tumor altered from glandular structure to keratinizing squamous cell metaplasia of cancer cells. The lines of S4 and S5 transplantable tumor were recently established, but the lines of S1 and S3 transplantable tumor have been transplanted as far as more than the 60th generation, and changed their histological appearance to scirrhous carcinoma in the line of S1 and medullary carcinoma in the line of S3. The growth speed of S1 line became slow in the later generations compared to the former ones, and that of S3 line became extremely rapid and recipient rats died with cachexia within two weeks. Effectual activities of tumor enhancement for the gastric and the colon cancer, previously reported elsewhere, recently decreased, and gastric carcinoma was rarely induced by these two lines. Lately established S4 and S5 transplantable tumor lines showed vigorous flourish of inducing gastric and colon cancers.
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PMID:Morphology on the transplantable gastric carcinoma in WF Osaka rat strain. 248 93

Tumour necrosis factor (TNF) is a polypeptide hormone produced in vivo by activated macrophages and lymphocytes. TNF has diverse effects in vivo and has a physiological role as an immune modulator, as a mediator of the immune response, both through activation of neutrophils and eosinophils, and also affects the vascular endothelium. TNF also has antiviral activity and causes alterations in lipid metabolism. In disease states excessive production of TNF may have adverse affects. TNF has been implicated as a mediator of endotoxic shock, inflammatory joint disease, immune deficiency states, allograft rejection, and in the cachexia associated with malignant disease and some parasitic infections. When used in pharmacological doses, TNF is cytotoxic to many malignant cells in vitro and in vivo. The mechanisms underlying cytotoxicity are not fully elucidated but involve both a direct toxic effect to the cell and an indirect effect on tumour vasculature. Cytotoxicity is not universal and TNF may act as a differentiating agent or growth factor for some haematological cell types. So far the clinical application of TNF has been as a treatment for cancer in Phase I and II trials in patients with advanced disease and its efficacy here is still unproven. TNF may have potential for clinical application in combination therapy for cancer. There is experimental evidence for its interaction with other biological agents and cytotoxic drugs. The use of specific antibodies to inhibit production of TNF, or other agents to antagonise the toxic effects of TNF may have clinical relevance in counteracting septic shock and the clinical manifestations of TNF in inflammatory and neoplastic disease.
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PMID:Clinical applications of tumour necrosis factor. 249 Dec 55


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