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)

Phenothiazine-induced bone marrow depression (BMD) was evaluated in three separate but complementary data bases: (1) Among 1,048 patients admitted to psychiatric hospitals, there was no evidence of subclinical depression of the white blood cell (WBC) count attributable to phenothiazines used before admission. (2) Among 18,587 medical inpatients, there were 34 patients admitted for BMD in the absence of neoplasia or prior cytotoxic drug therapy; one of the latter reported using chlorpromazine hydrochloride, but it is doubtful whether this drug was the cause of the BMD. (3) Among 24,795 medical, surgical, and gynecological patients surveyed over a ten-month period in 1972, there were four who were admitted for BMD; one of the latter had a reversible leukopenia attributed to trifluoperazine hydrochloride.
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PMID:Outpatient phenothiazine use and bone marrow depression. A report from the drug epidemiology unit and the Boston collaborative drug surveillance program. 0 Sep 78

Three human lung tumor-associated antigens (TAA's) have been identified in soluble and membrane-solubilized extracts of human squamous cell lung carcinoma with the use of antisera raised in rabbits. The antigens were identified and partially characterized by means of an agarose adsorption technique. These antigens, termed lung TAA's 1,2, and 3, are all soluble in 50% ammonium sulfate, are antigenically distinct, and do not cross-react with carcinoembryonic antigen or alpha-fetoprotein. Lung TAA's 1 and 2 are oncofetal antigens demonstrable in soluble extracts from 24-week-old but not from 26-week-old fetal lungs. Rabbit antibodies to these lung TAA's were not adsorbed by types A, B, and O human red blood cells, serum proteins as well as soluble or insoluble lung preparations. Of several commercial antisera to human proteins, none cross-reacted with lung TTA 1, but anti-human liver ferritin cross-reacted with lung TAA 2, and anti-human lactoferrin cross-reacted with lung TAA 3. Lung TAA 1 was partially adsorbed and cross-reacted with certain normal serum or plasma preparations used and appears to be a normal serum protein in Cohn Fraction IV-4. Lung TAA 2 and 3 appear only in lung tumor-soluble extracts, whereas the lung TAA 1 was demonstrable in soluble extracts of breast, colon, cervical and head and neck carcinoma. All may be tumor markers of value in immunodiagnosis.
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PMID:Isolation and identification of human lung tumor-associated antigens. 6 79

Membrane glycoproteins have been studied in the normal lactating mammary gland and R3230 AC mammary tumor of the rat. Plasma membrane-enriched fractions were obtained from these tissues by discontinuous sucrose gradient centrifugation of a microsomal preparation from the tissue homogenates. The lightest membrane fractions (F-1 and F-2) have the greatest enrichment of plasma membrane markers, with a 14- to 20-fold purification of 5'-nucleotidase and Na+-K+ -adenosine triphosphatase over the homogenate values in both tumor and normal tissues for F-1. Electron microscopy shows smooth membrane vesicles for these fractions. Polypeptide analysis by acrylamide gel electrophoresis shows essentially the same patterns for F-1 and F-2 and only relatively minor differences between membrane components of tumor and normal tissues. Glycoprotein analysis of the polyacrylamide gels by periodate-Schiff staining indicates more dramatic differences. Membrane Fraction F-1 from normal tissue contains two major glycoproteins, GP-II and GP-III, while Fractions F-2 and F-3 contain an additional glycoprotein, GP-I, with a higher apparent molecular weight. In the tumor, the component corresponding to GP-III is decreased or absent and a new component GP-IV is seen at a lower apparent molecular weight.
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PMID:Membrane glycoprotein differences between normal lactating mammary tissue and the R3230 AC mammary tumor. 12 79

We have solubilized by limited papain digestion and partially purified the tumor rejection antigen, tumor-specific transplantation antigens (TSTA), from membranes of a simian virus 40-induced sarcoma. Uniform-sized materials with a molecular weight range of 50,000 have retained their tumor rejection activities through the purification procedures. The simian virus 40 TSTA have been separated from H-2 activity by affinity chromatography on concanavalin A columns and no evidence was found for H-2 antigens in the unbound fraction (I) of concanavalin A containing TSTA activity. A reduced yield from the crude soluble fraction was observed with Fraction I of concanavalin A material and this may indeed represent fragmentation of antigen during papain digestion. These results stand in contrast to purification of histocompatibility antigens (H-2alpha) using the same methods and techniques. Low concentrations of simian virus 40 TSTA crude soluble materials were nervertheless biologically active. A concentration as low as 4 mug protein provided 50% tumor rejection and 0.1 mug protein provided lymphocyte stimulation. Both assays reflected specificity of response.
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PMID:Biological and biochemical properties of soluble tumor-specific transplantation antigen of a simian virus 40-induced neoplasm. 18 51

RNA fractions were prepared by sucrose density gradient centrifugation from hot-cold phenol, RNA-rich extracts of lymphoid tissues from strain 2 guinea pigs hyperimmunized to line 1 or line 10 tumors. Each RNA fraction was assessed for its ability to convert nonsensitized strain 2 peritoneal exudate cells to a state of specific sensitivity for line 1- or line 10-solubilized tumor antigens. An RNA fraction residing between the 4 S and 18 S peaks, designated as Fraction "B", transferred line 10 or line 1 sensitivity in 12 experiments. Twelve additional RNA extracts containing 2 subfractions prepared from RNA fraction B, designated as B1 and B2, also transferred line 1 or line 10 sensitivity in 14 experiments. Except for 3 experiments where the 4 S or 18 S material transferred tumor-specific sensitivity, RNA fractions corresponding to approximately 4 S, 18 S, 22 S, and 28 S were unable to transfer tumor-specific sensitivity to nonsensitized peritoneal exudate cells. Treatment of fraction B with RNase results in complete loss of ability to transfer immunobiological activity.
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PMID:Isolation and localization of RNA fractions able to transfer tumor-specific delayed hypersensitivity in vitro. 18 27

One must know tumor cell kinetics in order to devise a rational drug regimen for gliomas. With tritiated thymidine, the Labelling Index of astrocytomas is less than 1 per 100; of glioblastomas from 5-10 per 100. The duration of S phase is fairly constant, ranging from 7 to 10 hours. Double radioautography reveals a cell cycle time of 2 to 3 days and a Growth Fraction of 10 to 30 per 100 in glioblastomas. Calculations based on volume of tumor at recurrence after a gross total resection, analysis of primer dependent D.N.A. polymerase (P.D.P.), and analysis of cells by Flow Microfluorometer, all confirm these approximate figures. Thus most of the cells of a glioma are not sensitive to a cell-cycle phase specific drug. Such an agent, if given, should be administered over a 2 to 3 day period, in order to affect as many cells as possible. The most important part of a drug regimen should be an agent which attacks non-proliferating as well as proliferating cells, such as an alkylating agent. The effects of various drugs and schedules can be examined by animal models with the technqiue of colony forming efficiency.
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PMID:Current status of population kinetics in gliomas. 19 96

Rheumatoid factors (RF) were associated with alterations of antibody reactions to melanoma cells in vitro by two serologic assays. Removal of RF from melanoma patients' sera by absorption with Cohn's Fraction II coated latex particles enhanced seroreactivity in the Immune Adherence (IA) assay and diminished IgM detection by the Indirect Membrane Immunofluorescence (IMI) assay. The addition of serum with high titers of RF to these assay systems led to diminution of IA reactivity and enhancement of IgM detection by IMI. Since these factors are found in cancer patients' sera and can alter humoral immune reactions directed against antigens on the membranes of tumor cells, their presence should be recognized when performing assays with tumor target cells. RF may be of significance in the host-tumor relationship in vivo.
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PMID:Rheumatoid factor in melanoma patients: alterations of humoral tumor immunity in vitro. 37 97

Erythroid burst forming units (BFU-E) are proliferative cells present in peripheral blood and bone marrow which may be precursors of the erythroid colony forming cell found in the bone marrow. To examine the possible role of monocyte-macrophages in the modulation of erythropoiesis, the effect of monocytes on peripheral blood BFU-E proliferation in response to erythropoietin was investigated in the plasma clot culture system. Peripheral blood mononuclear cells from normal human donors were separated into four fractions. Fraction-I cells were obtained from the interface of Ficoll-Hypaque gradients (20-30% monocytes; 60-80% lymphocytes); fraction-II cells were fraction-I cells that were nonadherent to plastic (2-10% monocytes; 90-98% lymphocytes); fraction-III cells were obtained by incubation of fraction-II cells with carbonyl iron followed by Ficoll-Hypaque centrifugation (>99% lymphocytes); and fraction-IV cells represented the adherent population of fraction-II cells released from the plastic by lidocaine (>95% monocytes). When cells from these fractions were cultured in the presence of erythropoietin, the number of BFU-E-derived colonies was inversely proportional to the number of monocytes present (r = -0.96, P < 0.001). The suppressive effect of monocytes on BFU-E proliferation was confirmed by admixing autologous purified monocytes (fraction-IV cells) with fraction-III cells. Monocyte concentrations of >/=20% completely suppressed BFU-E activity. Reduction in the number of plated BFU-E by monocyte dilution could not account for these findings: a 15% reduction in the number of fraction-III cells plated resulted in only a 15% reduction in colony formation. These results indicate that monocyte-macrophages may play a significant role in the regulation of erythropoiesis and be involved in the pathogenesis of the hypoproliferative anemias associated with infection and certain neoplasia in which increased monocyte activity and monopoiesis also occur.
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PMID:Cell-cell interaction in erythropoiesis. Role of human monocytes. 71 62

Tumors from 40 patients and 7 established human xenograft tumor lines were grown in three-dimensional histoculture. A Viable-Cell-Index (VCI) based on fluorescent dyes and Growth Fraction Index (GFI) based on [3H]thymidine incorporation were measured by confocal microscopy and histological autoradiography, respectively, after treatment with cytotoxic agents. Chemosensitivity in vitro with the two methods was correlated with chemosensitivity of the same set of human xenografted tumor lines grown in nude mice. The percent accuracy of in vitro to in vivo correlation with VCI (73%) was higher than GFI (63%). The number of false positives with VCI was 12.1% (4/33), and with GFI was 31.3% (10/32). The results thus indicated that in vitro histoculture with fluorescent vital-dye end-points to measure cell viability is of potential use to determine tumor chemosensitivity.
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PMID:In vitro histoculture of human tumors with fluorescent dye end-points measured by confocal microscopy: high correlation of in vitro and in vivo chemosensitivity. 132 46

Our previous studies have indicated that the protein-bound polysaccharide Kreha (PSK) enhances the cytotoxic activity of peripheral blood lymphocytes (PBL) against the T24 human urinary bladder tumor cell line in patients with bladder tumor. Since PSK consists of a mixture of various kinds of protein-bound polysaccharides, the present study was designed to examine which subfractions of PSK mediated the enhancement of cytotoxicity. When PSK was separated according to size, treatment of PBL with the 50 kilodalton (kd) or less fraction killed T24 cells more efficiently than unfractionated PSK-treated PBL. The higher molecular weight fractions did not enhance killing above the control level. PSK was fractionated on a diethylaminoethyl (DEAE)-cellulose column to obtain a protein rich fraction that absorbed onto the column and a polysaccharide rich fraction that did not. PBL treated with the polysaccharide rich fraction were able to kill T24 cells more effectively than unfractionated PSK-treated PBL. The protein rich fraction had no effect on the killing. Further fractionation of the polysaccharide rich fraction was performed by differential precipitation with ammonium sulfate. PBL treated with the precipitated fraction at 70-80% saturation (PSK Fraction D) enhanced cytotoxicity equal to that of the polysaccharide rich fraction. Treatment of PBL with the other fractions did not augment the cytotoxicity. These enhancement by PSK fractions were observed in healthy donors and also in patients with bladder tumor. An increase of the proliferative response of PBL to PSK Fraction D as well as unfractionated PSK was observed. Treatment of PBL with PSK Fraction D had no effect on the proportion of PBL binding to T24 cells, thus suggesting a post-binding effect. The structure of PSK Fraction D as inferred from the results of methylation analysis was mainly an alpha-glucan. These results demonstrate that PSK mediated enhancement of cytotoxicity and proliferation of PBL may be largely due to an alpha-glucan of less than 50 kd.
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PMID:Effect of PSK and its subfractions on peripheral blood lymphocytes mediated cytotoxicity against urinary bladder tumor cells. 143 70


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