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)

Human monocyte-derived macrophages ingest diamide-treated red blood cells (RBC), anti-D immunoglobulin (Ig)G-opsonized RBC, or Plasmodium falciparum ring-stage parasitized RBC (RPRBC), degrade ingested hemoglobin rapidly, and can repeat the phagocytic cycle. Monocytes fed with trophozoite-parasitized RBC (TPRBC), which contain malarial pigment, or fed with isolated pigment are virtually unable to degrade the ingested material and to repeat the phagocytic cycle. Monocytes fed with pigment display a long-lasting oxidative burst that does not occur when they phagocytose diamide-treated RBC or RPRBC. The phorbol myristate acetate-elicited oxidative burst is irreversibly suppressed in monocytes fed with TPRBC or pigment, but not in monocytes fed with diamide-treated or IgG-opsonized RBC. This pattern of inhibition of phagocytosis and oxidative burst suggests that malarial pigment is responsible for the toxic effects. Pigment iron released in the monocyte phagolysosome may be the responsible element. 3% of total pigment iron is labile and easily detached under conditions simulating the internal environment of the phagolysosome, i.e., pH 5.5 and 10 microM H2O2. Iron liberated from pigment could account for the lipid peroxidation and increased production of malondialdehyde observed in monocytes fed with pigment or in RBC ghosts and liposomes incubated at pH 6.5 in presence of pigment and low amounts of H2O2. Removal of the labile iron fraction from pigment by repeated treatments with 0.1 mM H2O2 at pH 5.5 reduces pigment toxicity. It is suggested that iron released from ingested pigment is responsible for the intoxication of monocytes. In acute and chronic falciparum infections, circulating and tissue-resident phagocytes are seen filled with TPRBC and pigment particles over long periods of time. Moreover, human monocytes previously fed with TPRBC are unable to neutralize pathogenic bacteria, fungi, and tumor cells, and macrophage responses decline during the course of human and animal malaria. The present results may offer a mechanistic explanation for depression of cellular immunity in malaria.
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PMID:Impairment of macrophage functions after ingestion of Plasmodium falciparum-infected erythrocytes or isolated malarial pigment. 140 49

1. Head and neck tumors occur predominantly in men between 50 and 70 years of age who typically abuse tobacco or alcohol. These individuals often have poor oral hygiene and dentition as well as nutritional deficits, and achlorhydria, anemia, and iron and riboflavin deficits are common. 2. The tumor and treatment of head and neck cancer may cause many devastating effects, such as facial disfigurement, dysphagia, alterations in airway and communication, partial or total loss of taste and smell, xerostomia, pain, or fatigue. Treatment and rehabilitation may take months. 3. Although advances in technology and reconstructive surgery have not improved the overall survival rate, they preserve appearance, function, and, ultimately, the patient's quality of life.
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PMID:Head and neck cancer resection and reconstruction: from past to present. 141 30

Localized plasma cell type Castleman's disease (CD) is an unusual pathologic entity. It is frequently associated with clinical and laboratory characteristics and rarely occurs in children. Total surgical excision results in cure in all aspects. To make early diagnosis of mesenteric CD is not easy, especially for children. An 11-year-old Taiwanese boy was recently evaluated for anemia and delayed growth. His clinical findings included a syndrome of severe hypochromic microcytic anemia, neutropenia, thrombocytosis, hypoferremia, hypergammaglobulinemia, and growth failure. Radiological examinations (abdominal ultrasound, small intestinal series, and computerized tomography) identified hepatosplenomegaly, nephromegaly, and huge masses in the middle abdomen with precaval, celiac, and paraaortic lymph nodal enlargement. However, detailed physical examination failed to detect a mass. At laparotomy a double-fist-sized confluent mass was found arising from the mesenteric root. Most masses were discrete and were excised individually. The pathologic diagnosis was plasma-cell type angiofollicular lymph node hyperplasia (Castleman's disease). Seven weeks after surgery, he had an episode of acute hepatitis B. Postoperatively, he exhibited a dramatic growth spurt; the hemoglobin, red blood cell indices, serum iron, and immunoglobulins returned to normal in 2 months. Neutropenia, which has not been previously related to mesenteric CD, was an unexpected finding in our case; however, it resolved spontaneously 3 months after the surgery, suggesting its causal relationship with the tumor.
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PMID:New observations in a child with angiofollicular lymph node hyperplasia (Castleman's disease) originated from the mesenteric root. 151 Jan 96

Nickel is a toxic, mutagenic, and carcinogenic metal of significant occupational and environmental concern. Although several cellular targets of nickel have been identified, considerable evidence suggests that it can act indirectly upon DNA by inducing the formation of oxidized purines or pyrimidines that constitute promutagenic lesions. In this study, we examined nickel subsulfide (Ni3S2)- or Ni3S2/iron-induced renal sarcomas in F344 rats for the presence of transforming mutations in the K-ras oncogene. Selective oligonucleotide hybridization analysis of K-ras gene sequences amplified by polymerase chain reaction revealed that 1 of 12 primary tumors induced with Ni3S2 and 7 of 9 primary tumors induced with Ni3S2/iron contained exclusively GGT to GTT activating mutations in codon 12. These mutations are consistent with the known ability of nickel, in the presence of an oxidizing agent, to catalyze formation of 8-hydroxydeoxyguanosine, which in turn promotes misincorporation of dATP opposite the oxidized guanine residue. The presence of GGT to GTT transversions was confirmed by direct sequencing of the polymerase chain reaction products. Sequencing also revealed that there were no transforming mutations in codons 13 or 59-61. Additionally, a direct correlation between shortened tumor latency and the presence of activating ras mutations was noted. These results show that, in rat kidney, Ni3S2 can induce transforming mutations that are consistent with the ability of nickel to produce oxidative lesions and that iron, which exacerbates the extent of cellular oxidative damage, can enhance the frequency of these transforming mutations.
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PMID:GGT to GTT transversions in codon 12 of the K-ras oncogene in rat renal sarcomas induced with nickel subsulfide or nickel subsulfide/iron are consistent with oxidative damage to DNA. 151 40

Iron-enriched diets caused an increase of tumor rate in two models of dimethylhydrazine(DMH)-induced colon tumorigenesis in mice. The effect was independent of the time the iron-diet was fed, i.e. during DMH-treatment or following the DMH-treatment period. The increase of tumor rate depended on the iron concentration in the diet (0.5-3.5%). The concentration-dependent iron accumulation in the colonic mucosa of mice was paralleled by increments of malonaldehyde contents indicating lipid peroxidation, another factor known to be involved in tumor development. It is suggested that iron exerts cocarcinogenic activity in the DMH-model by stimulating cell proliferation and inducing oxidative stress in the colonic mucosa. This effect of iron is independent of the time of tumor-initiation by DMH, as it is also observed in the period of tumor-promotion/progression after DMH-treatment.
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PMID:Influence of dietary iron overload on cell proliferation and intestinal tumorigenesis in mice. 151 40

Using [59Fe] ferric lactate, a direct relationship between iron concentration and [59Fe] uptake by Ehrlich ascites tumor cells was found. Deferoxamine and albumin inhibited this uptake. Electrophoresis showed that both molecules complexed iron from ferric lactate. [45Ca] uptake in the presence of ferric lactate showed the same inhibition, and an iron mass-dependence, these findings suggest an iron--cell membrane interaction as the cause of this phenomenon. The implication of iron--tumor cell membrane interaction in tumor growth regulation is discussed.
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PMID:Iron-tumor cell interaction and regulation of Ca2+ homeostasis: their implication in tumor growth. 152 20

Nutrition is a critical determinant of immunocompetence and risk of illness and death largely due to infectious disease. It is now established that undernourished individuals have impaired immune responses. The most consistent abnormalities are seen in cell-mediated immunity, complement system, phagocytes, mucosal secretory antibody response and antibody affinity. These changes, together with other handicapping factors observed in underprivileged societies, lead to more infections. It is now recognized that deficiencies of single nutrients also impair immune responses. The best studied are zinc, iron, vitamin B-6, vitamin A, copper and selenium. If malnutrition occurs during fetal life, as epitomized by small-for-gestational age infants, the effects on cell-mediated immunity are very significant and long lasting. There is much recent evidence to suggest that at the other end of the age spectrum, namely old age, nutrition plays an important role in maintenance of optimum immunity. Based on these data, several studies have documented the critical importance of nutrition in resistance to a variety of infectious challenges, including Salmonella, Listeria and coxsackie B. Similarly, in vitro and in vivo responses to tumor cells are modulated by nutrition. These interactions of nutrition and immunity have several practical applications, including resistance to infections and tumors and the development of designer formulas that might help reduce the occurrence of opportunistic infections in immunocompromised hosts.
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PMID:Nutrition and immunoregulation. Significance for host resistance to tumors and infectious diseases in humans and rodents. 154 43

One approach to creating a state of iron deprivation in tumors is to expose them to monoclonal antibodies against the transferrin receptor (ATRAs). This paper reviews the recent history of studies with ATRAs. Both multivalent (IgM or IgA) and bivalent (IgG) ATRAs exhibit anti-tumor activity in vitro and in vivo, but IgG ATRAs appear to be most effective when used with an iron chelator such as deferoxamine or when used in pairs. Much more information is needed in order to understand: (1) how ATRAs work by themselves and in conjunction with chelators; (2) why ATRAs differ from one another in terms of their inhibitory potency; (3) whether ATRAs can be used successfully in conjunction with other anti-tumor agents, and (4) why tumors exhibit marked differences in their sensitivity to the effects of ATRAs. The toxicity of iron deprivation arising from ATRA treatment alone seems modest, but only further experimental work in vivo and in phase-1 clinical trials can determine whether the most recent observations can be converted into truly useful therapeutic tools.
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PMID:Effects of anti-transferrin receptor antibodies on the growth of neoplastic cells. 154 48

Spin echo MR imaging has not permitted reliable differentiation between intraluminal blood clot and tumor thrombus. This study assessed the role of ECG referenced repetitive gradient refocused echo (cine GRE) imaging for the differentiation of intravascular tumor from blood clot. Cine GRE images were reviewed in 23 patients, 11 of whom had intravascular tumor and 12 of whom had intravascular blood clots. Percentage contrast between the lesion and skeletal muscle as the reference tissue was determined from a subjective review of the images and objective signal intensity measurements. Intravascular clots were found to be lower in signal intensity than muscle (mean -55 +/- 29%). Intravascular tumors showed higher signal intensity relative to muscle (mean +17 +/- 9%) with the exception of myxomas (n = 2), which had signal intensity values relative to muscle as low as clots (mean -41 +/- 17%). Three masses in the inferior vena cava were composed of central tumor and peripheral clot; the two components could be differentiated with cine GRE imaging. Cine GRE imaging provides adequate signal intensity differences to visualize intravascular masses and helps to differentiate intravascular clot from tumor thrombus. However, if the tumor contains substantial amounts of iron, then the signal is also low and consequently clot and thrombus may not be distinguishable. This can occur in some atrial myxomas.
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PMID:Cine gradient refocused echo (GRE) imaging of intravascular masses: differentiation between tumor and nontumor thrombus. 154 12

Cytotoxicity of peritoneal macrophages (pMs) and peritoneal natural killer (pNK) cells toward xenogenic tumor cells was studied in anemic, suckling rats. Dams were fed 6, 12, or 250 mg Fe/kg diet ad libitum throughout gestation and lactation. Pups were injected intraperitoneally with 10(5) plaque-forming units of virus. Four days later cytotoxicity of pMs and pNK cells against YAC-1 mouse lymphoma cells was measured. Body weight, hemoglobin, hematocrit, and viable cell yield of pups were significantly decreased with decreasing dietary iron. pM cytotoxicity was significantly impaired in anemic pups at pM-target-cell ratios of 10:1 and 30:1 at 4 and 16 h (P less than or equal to 0.03). pNK-cell cytotoxicity was significantly impaired in anemic pups at pNK-target-cell ratios of 10:1 and 50:1 at 16 h. Iron-deficient diet consumed by dams throughout gestation and lactation resulted in anemic offspring whose immunologic defense by pMs and pNK cells against xenogenic tumor cells was significantly reduced.
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PMID:Maternal-iron-deficiency effects on peritoneal macrophage and peritoneal natural-killer-cell cytotoxicity in rat pups. 155 51


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