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

Under observation were 140 children with retroperitoneal neurogenic tumors. In 69 of 125 patients with malignant neoplasms metastases were detected. Hemographic and myelographic findings were analysed depending on the degree of malignancy and tumor spread. Anemia usually moderate and normochromatic was observed only in neuroblastomas. This group of patients is also characterized by frequent shifts to the left leucograms and high sedimentation test, contrary to benigh tumors. The investigation of bone marrow allows one to reveal the suppression, and more rarely irritation of various blood stems.
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PMID:[Hematopoiesis in children with retroperitoneal neurogenic tumors]. 17 13

Sixty-seven specific-pathogen-free cats of various ages (newborn, 2 wk, 1 mo, 2 mo, 4 mo, and 1 yr) were inoculated ip with either the Rickard (R) or the Kawakami-Theilen (KT) strain of feline leukemia virus (FeLV). Susceptibility to FeLV was judged by induction of a) FeLV group-specific antigens (gsa) in leukocytes, b) FeLV-related disease, c) antibody to feline oncornavirus-associated cell membrane antigen (FOCMA), and d) virus-neutralizing (VN) antibody. Susceptibility to FeLV-decreased with age. Persistent viremia and FeLV-related disease developed in 100% of cats inoculated as newborns, in 85% of cats inoculated at 2 weeks to 2 months of age, and in 15% of cats inoculated at 4 months or 1 year of age. Cats susceptible to FeLV leukemogenesis became persistently FeLV gsa-positive (viremic) at 4 weeks post inoculation and thereafter and produced little or no FOCMA or VN antibody. Cats that resisted leukemogenesis by FeLV all developed persistent FOCMA and VN titers and never became FeLV gsa-positive. The disease in inoculated cats was influenced by virus strain; FeLV-R induced predominantly thymic lymphosarcoma, whereas FeLV-KT caused fatal nonregenerative anemia without concurrent neoplasia.
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PMID:Feline leukemia virus infection: age-related variation in response of cats to experimental infection. 18 71

Described here is a patient who had an islet cell carcinoma containing both glucagon (glucagonoma) and insulin (insulinoma). Complete removal of the tumor was possible. Immunoreactive glucagon (IRG) could be extracted from all parts of the tumor (approximately 50 mug./gm.) and was shown to be fully bioactive. Immunoreactive insulin (IRI) could be extracted only from one section of the tumor (approximately 30 mug./gm.). The clinical and biochemical manifestations of the disease were dermatitis, diabetes, weight loss, anemia, hypoaminoacidemia, and hyperketonemia. The diabetes was characterized by low or normal fasting blood glucose concentrations and by impaired glucose tolerance (Kg = 0.4). After complete removal of the tumor, the dermatitis cleared, the catabolic state changed into an anabolic state, blood amino acid concentrations increased, and blood ketone-body concentrations decreased. Fasting blood glucose concentrations, however, rose above 200 mg./dl., and glucose tolerance declined further (Kg = 0.15). Hourly blood sampling for 24 hours, intravenous and oral glucose tolerance tests, intravenous arginine and tolbutamide tolerance tests with serial determinations of IRG, IRI, and blood glucose were performed preoperatively and again two weeks and two months postoperatively. The results of these studies demonstrated marked abnormalities in the stimulation and suppression of glucagon and insulin release. In addition, they failed to demonstrate a glycemic effect on the chronically elevated glucagon concentrations in this patient, while identifying insulin as the dominant factor determining blood glucose homeostasis.
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PMID:An islet cell carcinoma containing glucagon and insulin. Chronic glucagon excess and glucose homeostasis. 19 71

The glucagonoma syndrome is characterized by dermatitis, stomatitis, elevated serum glucagon levels, abnormal glucose tolerance, weight loss, and anemia--all in association with a glucagon-secreting alpha-cell tumor of the pancreas. A review of 21 cases showed strikingly similar features. A generalized, symmetrical dermatitis initially appeared to be asteatotic or eczematous over the perineum, buttocks, and lower extremities. Gradually, a more characteristic migratory necrolytic erythema with transient bulla formation and erosions developed in intertriginous and dependent areas. Histologically, the most specific features included necrolysis of the upper epidermis, with liquefaction necrosis of the granular cell layer and subcorneal clefting or blister formation. The dermatologist is often first to examine such patients; early recognition of this syndrome with prompt surgical removal of the primary pancreatic lesion may afford cure of the neoplasm.
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PMID:Glucagonoma syndrome. Report of two cases and literature review. 19 36

Glucagon-secreting tumors of the pancreatic islets (glucagonomas) produce a distinctive syndrome in which weight loss, diabetes mellitus, anemia,and prominent mucocutaneous findings occur. The cutaneous component-necrolytic migratory erythema--may be polymorphous, but most commonly manifests as erosions and crusts of the groin, perineum, buttocks, distal part of the extremities, and central area of the face. Alternatively, scaly papules and plaques may predominate in these areas. The eruption may resemble such dermatoses as pemphigus foliaceus, acrodermatitis enteropathica, chronic mucocutaneous candidiasis, psoriasis, and severe seborrheic dermatitis. Two patients with chronic, previously undiagnosed dermatoses had necrolytic migratory erythemia, which led to the discovery of glucagonomas present in each. In one patient surgical resection of the tumor resulted in total clearing of the rash within 48 hours. Awareness of this distinctive entity may lead to early diagnosis and, possibly, cure.
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PMID:Necrolytic migratory erythema. Distinctive dermatosis of the glucagonoma syndrome. 19 37

Three of nine children of possibly consanguineous American Indian parents developed typical osteosarcoma in a 2-year period. Etiologic investigations detected limb anomalies and elevated mean corpuscular volumes (98--109 micrometer3) in the surviving tumor patient, several of her sibs, and her father. Limb anomalies included simple clinodactyly with brachymesophalangy, absence of one digital ray of the foot, and bilateral radioulnar synostosis. The red cell macrocytosis was not accompanied by anemia or explained by the usual causes. No unusual environmental exposures were found and screening for possible oncogenic viruses by culture, electron microscopy, and serology was negative. All family members had elevated antibody titers to Epstein-Barr viral antigens. The proband and her father had excessive chromosomal breaks in the bone marrow. This unusual familial pattern of osseous malignancy and malformation and defective erythropoiesis, tentatively called OSLAM syndrome, may represent impaired regulation of bone development.
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PMID:Multiple childhood osteosarcomas in an American Indian family with erythroid macrocytosis and skeletal anomalies. 20 63

The glucagonoma syndrome occurs in some but not all patients with a benign or malignant islet cell tumor and hyperglucagonemia. Manifestations may include anemia, diabetes mellitus, pruritic skin rash, glossitis, stomatitis, weight loss, diarrhea, flexible fingernails, venous thromboses, low plasma amino acid levels, and coarse folds of the jejunum and ileum. Most patients are postmenopausal women, but men and women ages 40 to 65 have been affected. The course is variable depending upon the nature of the underlying tumor. Twenty-two cases of probable glucagonoma syndrome have been reported; twelve documented with glucagon levels. The hyperglucagonemia results from elevation of the proglucagon and true glucagon immunoreactive fractions of pancreatic glucagon. Management of the rash can be accomplished rarely with topical or systemic antibiotics or corticosteroids. If the tumor is resectable, surgery reverses the syndrome. Patients with metastatic disease have responded to streptozotocin and DTIC.
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PMID:The glucagonoma syndrome and its management. 20 9

The glucagonoma syndrome is a rare clinical condition characterized by a distinctive cutaneous eruption associated with a glucagon-secreting islet cell neoplasm of the pancreas. A 19-year-old woman manifested typical features of this condition: a polymorphous skin eruption with characteristic distribution of lesions in perioral and paragenital regions; lesions in sites of cutaneous trauma; a skin biopsy that showed epidermal cleavage; glossitis; weight loss; mild anemia; abnormal glucose tolerance test results. Plasma glucagon levels, determined by radioimmunoassay, were approximately five times normal. Angiography indicated a pancreatic tumor with liver metastases. Islet cell origin was confirmed histologically. It is hoped that wider recognition of the distinctive clinical features of this syndrome will result in earlier detection and possible surgical cure of the underlying malignancy.
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PMID:The glucagonoma syndrome. A distinctive cutaneous marker of systemic disease. 20 56

The glucagonoma syndrome is characterized by necrolytic migratory erythema, glossitis, ungual dystrophy, diabetes mellitus, anemia, weight loss, elevated plasma glucagon levels and an alpha-cell glucagon-secreting neoplasm of the pancreas. We are reporting a case of this syndrome in a middle-aged woman, in whom the first complaints and signs were cutaneous. The recognition of the distinctive skin manifestations of the syndrome led to early diagnosis and treatment of the underlying malignant pancreatic tumor.
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PMID:The glucagonoma syndrome. 20 68

The concentration of iron (III)-transferrin (IT) in whole blood and serum, along with another high-spin (five unpaired electrons) iron complex (probably IT) accumulated by tumor tissue, was investigated by electron paramagnetic resonance (EPR) spectroscopy during the development of Murphy-Sturm rat lymphosarcoma. The observed changes in concentration (microgram/ml) of IT in sera/blood were generally complementary to those from tissue and the character of the modifications suggested the existence of three distinct phases of systemic response to the implantation: (1) an initial response, evidenced by a sharp reduction in serum IT and somewhat high tissue-IT concentration (microgram/g); (2) a period in which the tumor is (2) a period in which the tumor is becoming established, indicated by relatively constant tissue IT levels and near normal serum IT; and (3) the onset of rapid cell multiplication, characterized by increased total tissue-IT accumulation that rises to above 200% of normal available serum iron, increasing tissue-IT concentration, and rapidly declining serum-IT concentration. The results suggest that, in the face of an implanted tumor there are two detectable abnormal serum-IT responses: (1) an initial change, probably due to systemic blockage of iron reutilization; and (2) extraction of IT from serum by multiplying tumor cells, which is probably a major contributor to reduced serum-IT levels and ultimately anemia.
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PMID:Electron paramagnetic resonance investigation of high-spin iron (III) in cancer. 21 Mar 66


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