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)

The cytostatic agent 5'-deoxy-5-fluorouridine (5'-dFUrd) improves cachexia and prolongs survival, suppressing tumor growth in mice bearing large burdens of colon 26 adenocarcinoma. To investigate the mode of this anticachectic action, we isolated colon 26 variants that were resistant to the anticachectic activity in vivo in tumor-bearing mice that initially responded to 5'-dFUrd in terms of tumor growth and cachexia but again became cachectic and refractory to the drug after prolonged treatment. The original line and variants were equally susceptible to the antiproliferative action of 5'-dFUrd, and their growth was stopped. However, 5'-dFUrd given to cachectic mice exhibiting large burdens of these variants could not reverse wasting and only slightly prolonged the survival period. These results indicate that the anticachectic activity of 5'-dFUrd is independent of its antiproliferative action and that the survival of colon 26-bearing mice is shorter when the size of the tumors is not reduced to levels below those that cause cachexia.
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PMID:5'-Deoxy-5-fluorouridine improves cachexia by a mechanism independent of its antiproliferative action in colon 26 adenocarcinoma-bearing mice. 183 6

A 28 year old man suffering from calcifying carcinoma of the stomach underwent a gastrectomy which was histologically classified as being a noncurative resection. As postoperative adjuvant chemotherapy, he received 116 mg of Mitomycin C and 454.8 g of Tegafur as well as 5690 g of ascorbic acid. He showed carcinoma cells histologically at both oral and anal edges of the resected specimen, and peritoneal metastases of tumor cells were also observed, but he nevertheless kept a performance status of 1 until 5 years after surgery. The patient finally died of cachexia 5 years and 6 months after his operation. Among 42 patients with calcifying carcinoma of the stomach reported in the foreign literature and 19 patients reported in Japanese, those patients for whom the postoperative survival time was clearly indicated did not necessarily survive longer than those patients without calcification.
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PMID:A case of calcifying carcinoma of the stomach with long-term postoperative survival. 185 37

Growth hormone (hGH) has been reported to improve nitrogen balances and accrue lean mass tissue in stable subjects. However, the ability of hGH to positively influence host preservation in stressed catabolic states such as cancer-induced cachexia remains unproven. Thirty-seven sham or tumor implanted Fischer 344 rats were randomized to receive either 0.5 mg/kg/day hGH or saline (SAL) subcutaneously from Days 14 to 23 postimplantation. Plasma levels of hGh and somatomedin C/insulin-like growth factor I (IGF I) as well as IGF I bioactivity were determined at sacrifice. Gastrocnemius muscle protein content was used as a index of host lean tissue mass and the tumor response was evaluated via flow cytometry for analysis of cell-cycle distribution. Host cachexia was not attenuated by hGH as muscle protein content was similar in hGH and saline-treated groups. Despite elevated hGH levels (range, 77-222 ng/ml (GH) vs less than 2 ng/ml (SAL], IGF I levels and bioactivity were not elevated in GH-treated groups. In contrast, cancer-induced anorexia markedly decreased IGF I levels (4 U/ml vs 9 U/ml, NTB; P less than 0.01) and this response remained refractory to hGH administration. While final tumor weights were similar between GH- and SAL-treated groups, hGH treatment caused a twofold increase in the proportion of aneuploid cells (P less than 0.05). In conclusion, hGH failed to attenuate lean mass dissolution in the tumor bearing host and this response may be related to the failure of IGF I induction. Conversely, the altered proportion of tumor aneuploid cells suggests a direct influence on tumor cell-cycling populations.
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PMID:Impact of exogenous growth hormone on host preservation and tumor cell-cycle distribution in a rat sarcoma model. 186 78

The relationship between the dynamics of tumor growth and the development of cachexia in C57b1/6j mice bearing the syngeneic transplantable adenocarcinoma EO 771 has been studied. The tumors grow independently of the inoculum size according to the Gompertzian mode of growth, with a maximum growth rate at a tumor size of about 3 g. As a dynamic measure of the degree of cachexia, the cachexia index "K", i.e. the quotient of the alteration of the carcass weight of the animal divided by the alteration of the tumor weight during the same time interval, is introduced. K is superior to a simple estimation of the alteration of the carcass animal weight because it also considers local weight-reducing effects of the infiltrating tumor growth. With respect to cachexia, three phases of tumor growth can be distinguished; cachexia develops mainly during the 2nd phase, i.e. for tumor sizes between 1.0 to 3.5 g which strongly correlates with the maximum growth rate of the tumor.
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PMID:Relationship between tumor growth and cachexia during progressive malignant disease: a new measure of the extent of cachexia, the cachexia index. 188 55

Two problems associated with supplemental nutrition of tumor-bearing organisms are control of tumor growth and reduction of cachexia. To investigate these problems, rats bearing methylcholanthrene-induced sarcomas were maintained on total parenteral nutrition (TPN) for 10 to 12 days beginning 23 days after tumor inoculation. Combined treatment of one group of these rats with the glutamine antimetabolite, acivicin, and the beta 2-adrenergic agonist, clenbuterol, arrested tumor growth, increased skeletal muscle mass and protein content, increased gut mass, and decreased total plasma lipid levels. Resting energy expenditure and cardiac mass were increased by TPN and were increased further by acivicin plus clenbuterol. These results demonstrate that tumor growth and muscle wasting can be controlled during TPN of tumor-bearing organisms. Therefore, cachectic depletion of lean body tissue may not be obligatory in neoplastic disease.
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PMID:Clenbuterol plus acivicin decrease tumor growth and increase muscle mass in rats maintained on total parenteral nutrition. 189 11

Administration of repetitive sublethal doses of either recombinant human tumor necrosis factor (TNF) or recombinant murine gamma-interferon (IFN) to non-tumor-bearing (NTB) rats caused a significant decline in food intake and body weight. After 3 days rats became resistant to the anorectic and weight loss effects of TNF but maintained persistent diminished food intake and diminished body weight gain while receiving recombinant murine IFN. Passive immunization against recombinant rat gamma-interferon allowed cachectic tumor-bearing (TB) rats to eat more food, have a lesser decline in body weight, live longer, and tolerate larger tumors than similar TB rats given nonspecific control antibody. TB rats treated with an antisera to recombinant murine TNF, which was 100% protective when given to NTB rats 6 h before a lethal endotoxin challenge, did not differ significantly from TB rats treated with control antibody with respect to food intake, body weight, survival, or tumor size. Serum levels of TNF or IFN were not detectable in cachectic tumor-bearing rats. The data indicate that the administration of exogenous IFN can simulate cachexia in NTB rats and that passive immunization against it can partially reverse the cachectic changes associated with cancer and prolong survival. These findings suggest that gamma-interferon may be an important mediator of cachexia in this rat tumor model.
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PMID:The roles of gamma-interferon and tumor necrosis factor alpha in an experimental rat model of cancer cachexia. 190 58

Malnutrition is extremely common in patients with malignant disease. Whereas the causes are multifactorial, the predominant factor is the imbalance between nutrient intake and host nutrient requirements. Furthermore, the evidence suggests that cachexia is related to abnormal changes in host intermediary metabolism induced by host-tumor interactions, and endogenous peptides such as TNF may be important mediators. The role of nutritional therapy in cancer patients remains to be defined. Clearly, patients with severe malnutrition benefit from nutritional intervention. However, the benefit of nutritional therapy in less severe cases of malnutrition as an adjuvant to oncologic therapy has yet to be established.
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PMID:Nutritional support of patients with cancer of the gastrointestinal tract. 190 41

Nude mice were inoculated with CHO/IFN-gamma cells, a line of Chinese hamster ovary tumor cells, that had been genetically engineered to produce murine IFN-gamma. Severe cachexia, as evident from body weight loss and reduced food intake, occurred in these mice, but not in those injected with CHO/control cells, i.e. the original, non-IFN-gamma-producing line. The essential role of IFN-gamma in the pathogenesis of cachexia was confirmed by the demonstration that monoclonal antibodies (MAbs) against IFN-gamma, given prior to injection of the tumor cells, prevented cachexia. In addition to IFN-gamma, the presence of the tumor cells was also required for cachexia to develop. As evident from pair-feeding experiments, reduced food intake could only partially account for the rapid and extensive body-weight loss. Cachexia was characterized by a marked reduction in the amount of interscapular fat tissue. Injected tumor cells exclusively invaded intraperitoneal adipose tissue and elicited an inflammatory cell infiltrate, indicating that interscapular fat loss was due to humoral factors. Our data suggest that, among the humoral factors responsible for cancer-associated cachexia, IFN-gamma plays a prominent role.
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PMID:Severe cachexia in mice inoculated with interferon-gamma-producing tumor cells. 190 42

The haemolytic activity of the total Complement (CH50) and the fractions C3 and C4 were assayed in rats transplanted with Yoshida's tumor and then treated with hCG, LH-FSH and PGE2. A relevant increase, only concerning the values of the CH50 and C3 fraction, was observed in all animals in the early days after the transplantation, probably due to a sort of stress "by transplantation". Afterwards, hCG and PGE2 induced an increase in CH50 and C3 values, but not in the C4 fraction. Treatment with LH and FSH led to a very slight increase in the CH50 and C3. In the following days, as a consequence of the cachexia, a progressive reduction of the values of the Complement was observed in all animals. Those treated with hCG also showed a little increase of survival. The authors suggest that the increase in CH50 and C3 fraction induced by the treatment with hCG and PGE2 could be an expression of increase of the aspecific humoral immunity, as a compensatory mechanism of the cell-mediated immunological depression which occurs during neoplasias.
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PMID:[Complement behavior in rats bearing Yoshida tumors subjected to treatment with gonadotropin and PGE2]. 193 Sep 5

A 63-year-old Japanese man complained of hematuria and pollakisuria for several months. Computed tomography and cystography disclosed an infiltrative tumor mass in the irregularly thickened apical and posterior walls of the urinary bladder. Narrowing of the vesical lumen and posterior extension of the tumor into the pelvic cavity were also noted. After palliative ureterocutaneostomy, 60 Gy irradiation was given locally. The patient died of cachexia seven months later. Autopsy revealed neuroendocrine carcinoma of the urinary bladder with extensive invasions and metastases to the pelvic and peritoneal cavities, liver, lungs, vertebrae, left kidney and retroperitoneal lymph nodes. Histologically, atypical tumor cells with eosinophilic cytoplasm formed solid nests and anastomosing cords with pseudoglandular structures. No other histologic tumor components were included. An intact urachal remnant was found at the vesical apex while features of metaplastic cystitis were absent. In addition to positive carcinoembryonic antigen and cytokeratin, the argyrophilic cancer cells were immunoreactive for neuron-specific enolase, chromogranin A, serotonin, neuropeptide Y, glicentin, somatostatin, neurotensin and calcitonin. Ultrastructurally, neurosecretory-type granules, with a mean diameter of 166 nm, were identified in the cytoplasm of the tumor cells. To discuss the histogenesis of the tumor, 44 previously reported cases of neuroendocrine carcinoma of the urinary bladder were reviewed.
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PMID:Neuroendocrine carcinoma of the urinary bladder: case report and review of the literature. 194 51


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