Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1261473 (sarcoma)
 25,952 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A phase II study of Vindesine (VDS) was carried out in 20 patients with carcinoma of the lung (14 adenocarcinomas, 3 squamous cell carcinomas, 2 large cell carcinomas and 1 small cell carcinoma), and in 18 patients with metastatic pulmonary tumor (primary organ: 4 colons, 2 uteri, 2 lungs, one each tongue, pharynx, maxillary sinus, esophagus, mediastinum, bile duct, pancreas, kidney, rectum and sarcoma). VDS was given weekly by i. v. push at a dose of 3 mg/m2. Patients should be given at least three times of VDS for eligibility. Of 18 evaluable patients with carcinoma of the lung, 3 patients with adenocarcinoma showed a partial response. Response rates were 17% for patients with carcinoma of the lung, and 25% for 12 patients with adenocarcinoma. Two responders (uterine cervical carcinoma and mediastinal embryonal carcinoma) were observed in 14 evaluable patients with metastatic pulmonary tumor. In addition, one patient with metastatic maxillary sinus tumor showed a minor response. Major hematologic toxicities of VDS were leukopenia (less than 4000 cells/mm3--92%, less than 2000 cells/mm3--28%), anemia (less than 10.0 g/dl, 38%) and thrombocytopenia (less than 10 X 10(4) cells/mm3, 11%). Major non-hematologic toxicities were numbness (24%), constipation (11%), anorexia (21%), fever (16%) and liver dysfunction (21%). The dose limiting factor of VDS was leukopenia.
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PMID:[Phase II study of vindesine in patients with carcinoma of the lung and metastatic pulmonary tumor]. 630 76

The interaction of cholecystokinin-induced hypophagia with cancer anorexia was investigated within both acute (Walker 256 carcinosarcoma) and chronic (methylcholanthrene-induced sarcoma) animal models of cancer anorexia. Cholecystokinin octapeptide (CCK8) effectively reduced feeding for at least one hour in both groups of rats. However, this peptide was no more effective in inducing hypophagia in tumor-bearing rats than in nontumor-bearing control rats when tested at a variety of doses (0.5, 5.0 and 50.0 microgram/kg; IP) both prior to and after the development of anorexia. Therefore, these data do not support a role of cholecystokinin in the mediation of experimental cancer anorexia, since no synergism of CCK8-induced hypophagia with the anorexia was observed.
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PMID:Cholecystokinin-induced hypophagia is not potentiated by cancer anorexia. 632 52

Eighty-three patients with advanced soft tissue sarcoma who had received no prior chemotherapy entered a randomised phase II study comparing carminomycin (CMM) 20 mg/m2 with adriamycin (ADM) 75 mg/m2, both administered i.v. bolus every 3 weeks. Six patients were ineligible and response could not be evaluated in 6 additional patients. Thirty-eight evaluable patients received ADM and 33 received CMM. There was one complete response to ADM and 10 partial responses, an overall response rate of 29%. CMM showed significantly (P = 0.01) lower antitumour activity--one partial response (3%). Stabilisation of disease was similar in both arms (47 and 45%), but fewer patients progressed on ADM (24 compared to 52%). Durations of response dating from the start of chemotherapy were 5 months for complete remission on ADM, a median of 7 months (range 4-17) for partial response on ADM and 14 months for the one partial remission on CMM. Although the median time to progression for all patients receiving CMM (2 months) was significantly (P = 0.001) shorter than for those receiving ADM (5 months), patients on ADM had only a marginally significant longer duration of survival (P = 0.06) than the patients receiving CMM. A leucocyte nadir less than 2.0 X 10(9)/l occurred in 38% of patients receiving ADM and 43% receiving CMM. Anaemia and thrombocytopoenia were uncommon. Other toxicities such as nausea, vomiting, anorexia and alopecia were more severe in the ADM group. There was one infective death secondary to leucopoenia in the ADM arm, and one patient who had received 109 mg/m2 CMM + 255 mg/m2 ADM developed progressively fatal cardiomyopathy.
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PMID:Carminomycin vs adriamycin in advanced soft tissue sarcomas: an EORTC randomised phase II study. 635 80

Two hundred forty-six adults with advanced progressive soft tissue sarcoma received combination chemotherapy with cyclophosphamide, vincristine, Adriamycin (doxorubicin), and DTIC. They were randomly allocated to receive the four drugs simultaneously every 4 weeks (S1: CYVADIC), or pairs of drugs (S2: ADIC-CYV) alternating at 4 weekly intervals. One hundred sixty-two patients completed 8 weeks of chemotherapy, and were considered to be evaluable for response. There were 18 complete remissions and 25 partial remissions, an overall response rate of 26%, with a highly significant difference between the two arms in favor of S1 (38% versus 14%, P = 0.001). There were no significant differences between S1 and S2 in terms of median duration of remissions (62 versus 39 weeks), and median survival of responders (85 versus 80 weeks) and of all evaluable patients (43 versus 45 weeks). Karnofsky index (KI) was the single most important prognostic factor. Patients with KI 90-100 showed a remission rate of 41% (56% on the S1 regimen) in contrast with 14% in those with KI 50-80. No patient with a KI of 50 responded to chemotherapy. The main toxicities were nausea, vomiting, anorexia, alopecia and myelosuppression, but did not differ significantly between the two regimens. Our findings suggest that stratification according to KI is essential for studies on chemotherapy for advanced soft tissue sarcomas in order to make a valuable comparison of treatment results.
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PMID:Cyvadic in advanced soft tissue sarcoma: a randomized study comparing two schedules. A study of the EORTC Soft Tissue and Bone Sarcoma Group. 636 47

AT1727 is a derivative of ICRF 154. The purpose of this study was to evaluate its "radiosensitizer" properties. From October 1979 until the end of December 1980, 89 patients with radiation resistant cancers such as soft tissue sarcoma, squamous lung cancer (with large lesion, 6-8 cm diameter) and other cancers had been included in trial. Radiation therapy was carried out using CO60 or 8 Mev Linac. Fifty-five patients had a remarkable objective remission rate of 61.8% (55/89). Eighteen of 30 patients with soft tissue sarcomas obtained obvious remission (60%), and 26 of 38 patients with lung cancer had remission (68.4%). Patients with esophageal cancer (5/6) and nasopharyngeal cancer (5/5) also had good remission rates. The side-effects of this treatment were very mild: anorexia and vomiting were noted in 50% and no significant changes were noted in liver and kidney function tests and blood platelet count. Leucopenia was slight in all but one patient. No difference in the lung fibrosis rate was noted between the two randomized groups. From the results of this study we concluded that AT1727 had some effect as a "radiosensitizer" but much more work is needed to confirm this.
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PMID:Preliminary report on AT1727 as a potential radiosensitizer. 639 23

The independent effects of total parenteral nutrition (TPN) on tumor growth and host carcass are important in designing effective nutritional support. In this study, a TPN regimen was used to keep substrate intake at normal levels during a 10-day period of tumor-induced anorexia and cachexia in rats transplanted with a sarcoma. Tumor mass was increased in TPN-supported animals compared to orally-fed controls. Tumor composition (water, fat, nitrogen) was similar in all tumors. Host carcass mass in tumor-bearing (TB) animals was increased by TPN as compared to orally-fed TB controls, but not to the same extent as in orally-fed or TPN-supported nontumor-bearing controls. Host carcass composition determinations demonstrated significantly increased fat content but no significant change in protein or water content in TB-TPN animals compared to orally-fed TB animals. This study demonstrates increased tumor growth and increased host carcass fat stores secondary to TPN.
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PMID:Tumor and host carcass changes during total parenteral nutrition in an anorectic rat-tumor system. 642 Dec 54

This study was designed to ascertain whether the overall availability of whole-body lipids and nitrogen is a limiting factor for survival in tumor-bearing mice suffering from anorexia and cachexia. Three-month-old nongrowing mice (C57BL/6J) were given s.c. transplants of a methylcholanthrene-induced sarcoma. Freely fed, starved, and pair-fed animals were used. Body and lipid composition, tumor growth, and survival time were measured. Freely fed sarcoma-bearing mice died with profoundly altered body composition. This was not explained by the anorexia assessed in pair-feeding experiments. Starvation had caused a more severe depletion in body composition in both tumor-bearing and nontumor-bearing animals than the tumor alone did in freely fed tumor-bearing mice. Freely fed tumor-bearing animals had normal proportions of whole-body triglycerides, cholesterol, and polar lipids, but they lost palmitic acid quantitatively more than any other fatty acid. It is unlikely that any single fatty acid became limiting during tumor growth. The results show that the overall availability of lipids, nitrogen, and glucose precursors is not a limiting factor for survival in experimental tumor cachexia. Other factors considered to be more likely as determining factors for the death of tumor-bearing animals are discussed.
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PMID:Role of whole-body lipids and nitrogen as limiting factors for survival in tumor-bearing mice with anorexia and cachexia. 657 17

The syndrome of cancer anorexia includes early satiety in man and a reduction in the duration of feeding in experimental animals. These aberrations suggest dysfunction of peripheral and/or central nervous system satiety mechanisms in tumor-bearing individuals. Since the gut peptide, cholecystokinin (CCK), has been implicated as a potent satiety cue in man and animals, plasma and brain concentrations of CCK were measured by radioimmunoassay in anorectic tumor-bearing rats. Plasma concentrations of immunoreactive CCK were not significantly altered in either an acute Walker 256 carcinosarcoma or more chronic methylcholanthrene-induced sarcoma animal model of cancer anorexia. However, levels of immunoreactive CCK were significantly reduced in the hypothalamus and cerebral cortex of animals bearing the methylcholanthrene sarcoma during both mild and severe anorexia. These data demonstrate that elevations in immunoreactive CCK are not a major factor in the etiology of cancer anorexia. If brain CCK is involved in satiety, tumor-bearing rats may be attempting to compensate for their anorexia by down-regulating CCK production.
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PMID:Plasma and brain cholecystokinin levels in cancer anorexia. 658 66

Lonidamine, a substituted indazole carboxylic acid with unique effects on cellular respiration, was studied in 27 patients with advanced malignancies. Of the 18 evaluable patients, 5 had small-cell lung cancer, 3 had non-small-cell lung cancer, 3 sarcoma, 2 breast cancer, and 5 other tumour types. All but 1 had had extensive prior treatment. A partial response was seen in 1 patient with metastatic synovial sarcoma, and tumour growth inhibition was demonstrated in 2 other cases. The major toxicity encountered was myalgia (66.6%) which was incompletely ameliorated by prednisone and required dose reduction in 2 patients and cessation of drug in 3. Other toxicities included auditory changes, anorexia, nausea and vomiting, diarrhoea, skin sensitivity, and conjunctivitis. No added toxicity was seen, when Lonidamine was combined with other chemotherapeutic agents. No correlation between Lonidamine dose and serum lactate levels was seen, although 4 patients showed a progressive increase in lactate levels over time, thought to be related to their increasing tumour burden. 5 patients demonstrated a dramatic fall in serum testosterone levels 4-8 weeks after starting Lonidamine which was accompanied by an increase in luteinizing hormone levels in 3 patients. In summary, modest antitumour activity was demonstrated in 3 patients; moderate toxicity was seen in most patients, but was usually tolerable. Further studies of Lonidamine are warranted in less heavily treated patients, alone or in combination with other chemotherapeutic agents.
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PMID:Phase II evaluation of Lonidamine in patients with advanced malignancy. 671 99

The time course of energy metabolism has been studied in weight-stable and nongrowing mice with a transplantable methylcholanthrene-induced sarcoma. Daily oxygen consumption and carbon dioxide production were measured in relation to the tumor growth from the time of tumor implantation. The time course of energy dynamics was related to the end-state changes in body composition. Freely fed sarcoma-bearing mice decreased their whole-body energy expenditure in proportion to the tumor growth. This was due to the accompanying anorexia. The alteration in oxygen consumption and carbon dioxide production was continuously evident 24 hr/day in sarcoma-bearing mice. The tumor-bearing mice lost body fat and had decreased respiratory quotient, while pair-fed controls maintained their body composition, and their respiratory quotients agreed with the food respiratory quotient. Loss of body lipids in freely fed sarcoma-bearing mice reflected a negative energy balance, accompanied with increased fat oxidation, while maintenance of body composition in pair-fed controls reflected a decreased metabolic rate. Sarcoma-bearing mice showed a significantly higher energy expenditure in relation to their food intake compared to that of pair-fed controls. Estimates of partition of oxygen uptake in sarcoma-bearing mice support that both the host and the tumor account for the elevated energy expenditure. This study has confirmed a small but significantly increased energy expenditure in sarcoma-bearing mice, which was continuously present 24 hr/day in spite of unlimited availability of food. This illustrates the fatal outcome of experimental cancer.
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PMID:Energy metabolism in nongrowing mice with sarcoma. 686 Nov 35


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