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Query: UMLS:C0235394 (wasting)
 8,040 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The importance of maintaining the cancer patient's nutritional status is now recognized as a major part of the medical care. It is necessary for the oncology team to be aware of the psychological and physiological factors that interfere with food acceptance so that the correct food can be offered at the right time in the most palatable form. The oral route is the preferred method of feeding, and nutritional supplements, chosen according to the individual patient's needs, are of great value in assuring an adequate oral intake. Diagnostic tests and therapy are frequent causes of disruption of the meal schedule and the dietary service must be flexible in providing the patient an opportunity to make up for missed meals. Taste disturbance, nausea, vomiting and mucositis caused by therapy may necessitate periods of intravenous hyperalimentation. Food aversions due to therapy can frequently be prevented by avoiding new or unusual foods in the hours before chemotherapy or irradiation. Regular nutrition counseling during clinic visits and/or hospitalization permits diet modification for specific therapeutic needs. The ultimate goal is the prevention of wasting and debilitation due to malnutrition in the cancer patient.
Cancer 1979 May
PMID:Oral feedings in the cancer patient. 10 86

The effects of neonatal and perinatal thymectomy on mammary tumorigenesis in (C57BL X I)F1fC3H hybrid female mice were determined. When hybrid females were neonatally thymectomized by controlled suction, a procedure that removes thymic lobes completely, a large proportion of animals developed stigmas of a fulminant wasting disease and died before tumors developed. However, when hybrid females were subjected to neonatal thymectomy by continuous suction, a procedure that resulted in retention of thymic remnants, they survived and manifested a significant prolongation of latent period before tumorigenesis. When complete removal of the thymus was carried out in the perinatal period, the effect on mammary tumorigenesis was critically dependent on the age at surgery. The procedure was without effect when performed at 1, 3, and 8 weeks of age. However, when it was performed at 9-12 days of age, there was a delay or a decrease in the appearance of mammary tumors. The extent of T-cell depletion and/or its timing in relationship to the introduction of murine mammary tumor virus appeared to play a critical role in determining the effect on eventual tumor development.
J Natl Cancer Inst 1977 Mar
PMID:Inhibition of mammary tumors by incomplete T-cell depletion. 19 Apr 16

Specimens from the deltoid muscle of 210 randomly selected autopsy cases without previous clinical evidence of primary neuromuscular impairment were examined with regard to the influence of extramuscular diseases on voluntary muscle. Differences between malignant tumours and other disorders were of special interest with respect to the question of the possible existence of a remote effect of cancer on skeletal muscle. The number of central nuclei within muscle fibre cross sections was considered as the most simple parameter for myopathic reaction. Atrophic fibre changes were examined quantitatively by measurement of the orthogonal fibre diameters and calculating the variation of fibre size. In addition, a semi-quantitative histological evaluation of the muscles was performed. While tumor cases did not show a significant difference from the remainder with respect to myopathic changes, they did display a significant difference with regard to scattered and small-group fibre atrophy. The reasons for the muscular changes are discussed. From the present investigation the changes seem to be due chiefly to metabolic impairment and wasting. No signs for a specific carcinotoxic effect on skeletal muscles could be demonstrated.
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PMID:Quantitative analysis of voluntary muscles from routine autopsy material with special reference to the problem of remote carcinomatous changes ("neuromyopathy"). 67 79

Malignant melanoma has been induced in the Weiser-Maple guinea pig by prolonged application of 7,12-dimethylbenz(a)anthracene. The tumor shows a biphasic growth pattern analogous to the radial and vertical growth phase of human cutaneous malignant melanoma. It evolves through a predictable series of cellular events classified as intraepidermal melanocytic hyperplasia, dermal melanocytosis, dermal melanocytoma, malignant melanoma without intralesional transformation, and, finally, malignant melanoma with intralesional transformation, which is characterized by the appearance of "new kinds of cells" and is associated with widespread metastases and massive lymph node involvement. Clinically, the lesions evolve from diffuse hyper-pigmentation to brown-black macules, to nodules of increasing size, to overt malignant melanoma associated with metastases, wasting, and death. Examples of intralesional transformation analogous to that in guinea pigs are found not only in human malignant melanomas, but in other human neoplastic systems, and such analogous cellular events are discussed in this paper.
Cancer Res 1976 Nov
PMID:The developmental biology of induced malignant melanoma in guinea pigs and a comparison with other neoplastic systems. 82 48

Seventeen patients with malignant disease developed a complex metabolic syndrome of 2-8 weeks' duration characterized by hypocalcemia, hypomagnesemia and hypokalemia following administration of the aminoglycoside group of antibiotics. Gentamicin, Tobramycin, Amikacin, and Sisomicin were all involved. Other features noted were hypoalbuminemia, hypophosphatemia, and hypouricemia. Low immunoreactive parathyroid hormone (i-PTH) levels in the presence of hypocalcemia and absence of hyperplastic changes in the parathyroid gland examined at postmortem confirmed a diagnosis of hypoparathyroidism. Immunoreactive calcitonin levels (i-CT) were not elevated. Renal tubular wasting of potassium and magnesium was documented in six patients and excessive urinary loss of sodium, phosphate, and uric acid was noticed. Twelve patients died before recovering from the metabolic stress and five patients developed progressive renal impairment. A possible potentiating action of chemotherapeutic agents, especially Adriamycin, is suggested.
Cancer 1977 Apr
PMID:Hypocalcemia with hypoparathyroidism and renal tubular dysfunction associated with aminoglycoside therapy. 85 39

Cell suspension of a human breast cancer cell line (Hattori line) was injected intraperitoneally into an athymic nude mouse to produce ascites form breast cancer (peritoneal carcinomatosis). Subsequent serail transfers of cancer cells in ascites were also successful in mice. All male and female nude mice injected 1 X 10(7) tumor cells died of accumulation of ascites after a latency period averaging 4 weeks, with one exception which died of a wasting disease. Multiple lung metastases were observed in some mice. The tumor cells retained cytological characteristics of the original cell line, and histology of the infiltrating tumor in the peritoneum and omentum was that of poorly differentiated adenocarcinoma. Differentiation not only toward acinar or duct lining cells but also toward myoepithelial cells was observed by histochemistry, immunohistochemistry, and electron microscopy.
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PMID:Human breast cancer serially transplantable in nude mice in ascites form. 100 68

The theory has been advanced that the anorexia of cancer is the result of anorexigenic peptides and of other intermediary metabolites produced by the cancer and the tumor-bearing host. These metabolites are the signals to peripheral receptors and to the brain centers and are responsible for the state of satiety and aversion to food. Although the only effective way to stimulate the appetite of the cancer patient is to control the cancer, efforts should be made to increase the calorie intake even in the presence of anorexia and to maintain a calorie equilibrium. However, controlled studies have not shown that forced feeding can reverse for long periods the progressive tissue wasting process or prolong the cancer patient's survival.
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PMID:Why cancer patients have anorexia. 106 80

Bilateral and midline symmetry of the normal pelvic anatomy is an aid to the interpretation of computed tomographic (CT) examinations. Following hindquarter amputation (HQA) or partial hemipelvectomy (PHP) the normal anatomical relationships are disturbed. The CT examinations of 15 patients who had undergone either an HQA or a PHP for an advanced musculoskeletal malignancy are reviewed. The new "normal" anatomy revealed displacement of the bladder and small bowel to the side of surgery in one third of patients, more commonly in the PHP cases. There were varying degrees of wasting of the ipsilateral musculature, gluteus maximus muscle flap, erector spinae and psoas muscles, etc., because of partial denervation and disruption of their origin or insertion. Recurrent tumour was identified in eight of 10 cases in which it was clinically suspected prior to the CT examination. Invariably the recurrence arose within the muscle flap at the resection margin. Bone involvement by direct tumour spread was present in three cases. Pitfalls in differentiating recurrent tumour from scar tissue are discussed.
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PMID:Computed tomographic appearances of the pelvis following hindquarter amputation. 128 16

There is, at present, considerable interest in the possible role for the proinflammatory cytokines, tumor necrosis factor-alpha, interleukin-1, interleukin-6, and interferon-gamma in the pathogenesis of cancer cachexia. Indirect evidence for such a role is based on the observation that chronic administration of many of these cytokines, either alone or in combination, can reproduce the myriad of host responses seen in experimental and human cancer cachexia. Elevated plasma levels of tumor necrosis factor-alpha, interleukin-2, and interferon-gamma have rarely been detected in patients or experimental animals with cancer, although interleukin-6 levels appear to correlate with tumor progression in animal models. The strongest evidence for a causal role for cytokines has come from rodent studies in which tumor-bearing animals have been passively immunized with antibodies directed against individual cytokines. Several groups have shown modest but significant improvements in food intake and lean tissue retention with antibodies directed against tumor necrosis factor-alpha, interleukin-1, interleukin-6, and interferon-gamma. However, there has been no consistent finding that one cytokine is universally involved in cancer cachexia in histologically distinct tumor models. One ominous finding in several tumor models has been that the endogenous production of cytokines appears to support tumor growth. Such findings raise the intriguing possibility that these cytokines, although contributors to tissue wasting and anorexia, may also serve the tumor as either direct or indirect cell growth factors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of cytokines in cancer cachexia. 128 23

Cancer cachexia describes a syndrome that consists of weight loss, and abnormalities in carbohydrate, protein, and lipid metabolism, which result in a state of persistent net negative energy balance. Patients suffering from cancer cachexia have a significantly shortened survival after cancer treatment. Recent experimental studies have focused on the belief that the mechanisms of cancer cachexia involve the host's production of inflammatory cytokines, which through broad physiologic actions ultimately lead to a chronic state of wasting, malnourishment, and death. Cytokines that have been thought to play a role in the pathophysiology of cachexia include tumor necrosis factor, interleukin-1, interleukin-6, interferon-gamma and differentiation factor. It has become clear that these cytokines have overlapping physiologic activities, which makes it likely that no single substance is the sole cause of cachexia in most cancer patients. Only further investigation may make it possible to more clearly define the role of cytokines in the pathophysiology of cancer cachexia. Specific strategies to reverse the cachectic effects of these substances may then be developed to ultimately improve cancer treatment.
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PMID:Cytokines and their role in the pathophysiology of cancer cachexia. 128 24


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