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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Resting energy expenditure is abnormal in most patients with cancer and may contribute to cancer cachexia. These metabolic abnormalities may be a direct measure of tumor metabolism, or represent alterations in the size or activity of the body cell mass, or both. To unravel this pathogenesis, we prospectively studied 68 preoperative patients with cancer about to undergo curative resection by measuring resting energy expenditure before and after tumor resection. The preoperative measured resting energy expenditure was compared with expected resting energy expenditure based on Harris-Benedict resting energy expenditure predictions: 10 patients were hypometabolic (less than 90% Harris-Benedict); 35 were normometabolic (90% to 110% Harris-Benedict); and 23 were hypermetabolic (greater than 110% Harris-Benedict). Using each patient as his or her own control, resting energy expenditure normalized or remained normal following curative resection. In contrast, after palliative resection, resting energy expenditure remained hypermetabolic or significantly increased toward hypermetabolism. Tumor induces an abnormal metabolic rate, since tumor removal results in prompt normalization of resting energy expenditure. The abnormal energy expenditure of patients with cancer cannot be solely attributed to abnormal host body composition.
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PMID:Ablation of abnormal energy expenditure by curative tumor resection. 168 65

Deterioration in nutritional status occurs late in the progress of cancers at certain sites, but at all stages in patients with gastrointestinal cancer. Weight loss with decrease in body fat and muscle wastage, occurs to a varying degree. Superficially, the clinical condition resembles simple food deprivation. However, the derangements in metabolism are often and some patients show an elevated resting energy expenditure, disturbances of carbohydrate, fat and protein metabolism and generally, a failure to adapt to reduced food intake, which is characteristic of cachexia. Cancer cachexia then becomes characterized by signs of marked negative energy and protein balance, including hypoalbuminemia, weight loss, and anemia. On the other hand, toxohormone extracted from tumor tissues was considered as the main cause to produce cancer cachexia. However, it has become clearer that cytokines, e.g. cachectin/TNF, IL-1, LT and IFN gamma play an important role to produce cachexia. Patients who are malnourished have an incidence of postoperative complications double that seen in adequately nourished patients. The effectiveness of cancer-chemotherapy is also different in nutritional status of patients. Although in patients requiring hyperalimentation, enteral nutritional support may feasible and enteral feeding has a distinct metabolic advantage compared with parenteral feeding, there is a definite role for total parenteral nutrition in patients who have severe chronic radiation enteritis, side effect of chemotherapy, weight loss and malabsorption. Tentative weight gain and correction of hypoalbuminemia without improving patient survival may be expected by this intravenous hyperalimentation.
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PMID:[Palliative therapy in cancer 2. Nutrition control]. 169 91

Murine colon 26 adenocarcinoma causes a progressive weight loss and physiological changes associated with cachexia when it grows to a certain size. By the use of this tumor model several types of cytostatics were examined for their ability to alleviate cachexia. Among them, 5'-deoxy-5-fluorouridine could reverse a progressive weight loss and improve hypoglycemia, hyperglucocorticism, and hepatic malfunctions, as well as inhibiting the tumor growth. Cyclophosphamide, nimustine, and 2'-deoxy-5-fluorouridine were only slightly effective in reversing the wasting, while 5-fluorouracil, tegafur, mitomycin C, cis-platinum, and doxorubicin were not active. Within 3 days after 5'-deoxy-5-fluorouridine was administered to cachectic mice with large tumor burdens, the wasting was immediately reversed even at doses in which there was increase or no significant reduction in tumor growth. These results indicate that the anticachectic activity of 5'-deoxy-5-fluorouridine is independent of its antiproliferative activity.
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PMID:Anticachectic activity of 5'-deoxy-5-fluorouridine in a murine tumor cachexia model, colon 26 adenocarcinoma. 169 21

The aim of this study was to evaluate to what extent tumor necrosis factor alpha (TNF-alpha) and interleukin 1 may explain the development of experimental cancer cachexia. For this purpose, C57BL/6J mice bearing a transplantable low differentiated rapidly growing tumor were passively immunized every other day with rabbit or rat neutralizing immunoglobulins against either TNF-alpha (anti-TNF) or against an interleukin 1 receptor (anti-IL-1r). Anti-IL-1r in itself had no agonistic effect to the type I, T-cell/fibroblast IL-receptor. Tumor-bearing mice receiving either preimmune antiserum or nonimmune rat hybridoma IgG served as controls. Anti-TNF and anti-IL-1r inhibited tumor growth significantly, as measured by a lower wet and dry tumor weight at the end of 11 days of antiserum treatment (P less than 0.05). The acute phase response in tumor-bearing animals, measured as an increase in liver weight, hepatic RNA content, and increases in plasma concentrations of circulating IL-6, serum amyloid P, transferrin, complement (C3), and a decrease in plasma albumin, were unaffected by the specific antiserum treatments. Food intake, which declined significantly in pre/nonimmune injected tumor-bearing controls, was significantly improved in tumor-bearing animals immunized against TNF-alpha or the IL-1r. Whole body lipid content showed a trend to improvement in specifically immunized animals (P less than 0.07). The effects on whole body fat-free dry weight were insignificant, although numerically higher in specifically immunized tumor-bearing animals. The combination of anti-TNF and anti-IL-1r antiserum had no additive effects compared to single antiserum treatment suggesting that the two antibody treatments acted through a common mechanism. Cultured tumor cells, established from growing tumors, were sensitive to anti-TNF and anti-IL-1r, which both reduced tumor growth in vitro. This inhibitory effect by the antiserum could in part be reversed by the addition of recombinant IL-1 alpha and TNF alpha. We conclude that both TNF and IL-1 are involved in tumor growth and thus the progression of cancer cachexia. It seems as if the role of TNF and IL-1 was to promote tumor growth rather than restrict tumor growth in the present model. In this sense both TNF and IL-1 may act as tumor growth factors.
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PMID:Role of endogenous tumor necrosis factor alpha and interleukin 1 for experimental tumor growth and the development of cancer cachexia. 170 40

The aim of this study was to evaluate whether spontaneous physical exercise can modify cancer anorexia and cachexia in tumour-bearing rats. Two transplantable experimental tumours were evaluated. Tumour-bearing Wistar Furth rats fed ad libitum and with free access to a running wheel had a delayed onset of anorexia compared with their non-exercised tumour-bearing controls, retained normal behaviour and were able to run the same daily distance as non-tumour controls until the onset of cachexia. Exercise resulted in a decreased carcass wet weight and lipid stores but in an increased carcass dry weight in the tumour-bearing animals. Despite increased food intake, physical exercise resulted in a reduced final tumour weight without any change in water content. Skeletal and cardiac muscle tissue did not show any difference in water content but there was an increased RNA/protein quotient in the exercising tumour-bearing animals. Thus the deleterious alterations induced by the malignancy on tumour host metabolism are not inevitable but can be modified by spontaneous physical exercise.
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PMID:Effects of spontaneous physical exercise on experimental cancer anorexia and cachexia. 170 20

Pentoxifylline (Trental), used routinely for the treatment of intermittent claudication, has been shown previously to decrease the levels of tumor necrosis factors-alpha (TNF-alpha) RNA in cancer patients and to lead to a general improvement of well being. Increased TNF-alpha levels have been observed not only in cancer patients but also in cachectic patients with the acquired immunodeficiency syndrome (AIDS), and TNF-alpha is known to increase the expression of the human immunodeficiency virus type 1 (HIV-1) via activating its long terminal repeat (LTR). Moreover, TNF-alpha decreases the therapeutic efficacy of zidovudine (AZT). Here we show a significant decrease in HIV-1 replication by pentoxifylline in infected human peripheral blood mononuclear cells. The reduction was proportional to the downregulation of expression of a reporter gene, the bacterial gene for chloramphenicol acetyl transferase, linked to the HIV-1 LTR in human monocytoid cells. We conclude that patients with AIDS may benefit from pentoxifylline treatment because of its blockage of TNF-alpha-mediated HIV-1 upregulation, from increased efficacy of AZT, and also from improvement in TNF-alpha-induced cachexia.
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PMID:Pentoxifylline (Trental) decreases the replication of the human immunodeficiency virus type 1 in human peripheral blood mononuclear cells and in cultured T cells. 130 72

Our previous studies have demonstrated the production and release of a tumor-derived factor that promoted lipolysis in normal adipocytes. We further demonstrated that this in vitro lipolysis was correlated with the in vivo loss of total carcass lipids induced by the presence of the same tumor. This study identified and isolated this "lipolysis-promoting" factor (LPF), released into the extracellular environment (conditioned media) by the human A375 melanoma cell line, which appears to be responsible for the previously demonstrated induction of in vitro and in vivo lipolytic activity. Unlike previously described non-tumor-derived molecules, such as tumor necrosis factor-alpha/cachectin, which have been implicated in cancer cachexia, the LPF induces alterations in lipid metabolism similar to those observed in cancer patients. The biochemical nature of human tumor-derived LPF appears to be a heat-stable molecule with an apparent molecular weight of approximately 6000. The lipolysis-promoting activity was trichloroacetic acid precipitable, but not precipitable with protamine sulfate or extractable with chloroform:methanol. Its activity appears to be resistant to enzymatic treatments with protease K, trypsin, Pronase, RNase, and DNase, as well as to periodate oxidation. Immunochemically, LPF appears to be distinct from tumor necrosis factor-alpha/cachectin. Furthermore, in contrast to the mechanism of action of tumor necrosis factor-alpha/cachectin, the mechanism of "lipolysis promotion" by LPF appears to be by the induction of cellular lipase activity.
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PMID:Identification of a human tumor-derived lipolysis-promoting factor. 173 44

Melanoma-derived lipoprotein lipase inhibitor (MLPLI) is a factor purified from the conditioned medium of a human melanoma cell line, SEKI, which induced severe cachexia in tumor-bearing nude mice. Amino acid sequencing revealed that the amino-terminal portion was identical to that of leukemia-inhibitory factor (LIF). To determine whether MLPLI is actually LIF, the expression of LIF mRNA was examined in the SEKI melanoma cell line. Northern blot analyses revealed that the cell line displayed an intense hybridizable band with a molecular size of 3.8 kilobases, suggesting that MLPLI is identical to LIF. The relationship between the development of the cancer cachexia syndrome and the expression of LIF mRNA was examined in four melanoma xenografts, SEKI, G361, A375 and MEWO, in nude mice. SEKI- and G361-bearing nude mice developed cancer cachexia syndrome, and their body weights decreased by the 25th day after the transplantation to 73.6% and 73.8% of the control, respectively. A375- and MEWO-bearing nude mice, however, did not develop the syndrome. Northern blot analyses revealed that G361 as well as SEKI expressed a large amount of LIF mRNA, but A375 and MEWO did not, suggesting a close relationship between the expression of LIF mRNA and the development of the syndrome. These data support the concept that MLPLI, or LIF, plays an important role in the development of the cancer cachexia syndrome observed in melanoma-bearing nude mice.
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PMID:Cancer cachexia syndrome developed in nude mice bearing melanoma cells producing leukemia-inhibitory factor. 174 40

Angiosarcoma of the face and scalp developed in 12 patients. The patients were five women and seven men with an average age of 71 years. Initial features were solitary or multiple violaceous vascular nodules or plaques. The clinical course was complicated by ulceration, secondary infection, bleeding, anemia, infiltration into the underlying bones, tumor cachexia, and death. Metastases were not observed. Histologically, seemingly benign hemangiomatous capillary-like structures were found in some areas of the tumors, with richly cellular, solid sarcomatous proliferations in other areas. Early and extensive surgical excision is the therapy of choice, but generally it does not alter the relentless course of the disease. Neither palliative radiation therapy nor polychemotherapy is capable of interfering with tumor progression.
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PMID:Angiosarcoma of the face and scalp. 181 27

C57BL/6N mice bearing Lewis lung tumours were treated with anti-gamma-interferon (IFN-gamma) monoclonal antibodies. Early, but not late, treatment inhibited tumour growth, suggesting that endogenous IFN-gamma promotes initial tumour cell proliferation. Tumour development was associated with failure to gain weight or with progressive weight loss. Anti-IFN-gamma given early or late counteracted this wasting syndrome, which indicates that IFN-gamma production subsists during tumour growth and is directly or indirectly responsible for tumour-associated cachexia. Studies of body composition in cachectic mice revealed fat tissue to be particularly affected. Fat loss was enhanced by IFN-gamma and antagonised by anti-IFN-gamma. Tumour-bearing mice were also hypersensitive to the lethal effect of endotoxin; anti-IFN-gamma was unable to mitigate this sensitisation, suggesting that IFN-gamma does not exert its cachexia-inducing effect through augmentation of the host response to an endogenous endotoxin source.
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PMID:Anti-interferon-gamma antibody treatment, growth of Lewis lung tumours in mice and tumour-associated cachexia. 182 86


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