Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1326912 (tumorigenesis)
 57,481 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Blood group ABH determinants in human erythrocytes are carried by four kinds of glycolipid carbohydrate chains, differing in their structural complexity. They are Aa, Ab, Ac, and Ad for A variants, and H1, H2, H3, and H4 for H variants (Table I and Fig 1). Based on the surface labeling of A variants and on the reactivity of erythrocytes to antibodies directed against H3 and against its degradation products, it is concluded that complex variants of A or H determinants (Ac and Ad/or H3 and H4) are absent or significantly low in fetal erythrocytes (80-150 days after gestation) and in new born erythrocytes, whereas these complex structures are fully developed in adult erythrocytes. In contrast, A determinants linked to simpler carbohydrate chains (Aa, Ab variants) are fully developed before birth and do not show significant change after birth. The precursor of blood group carbohydrate chains seems to be abundant in fetal or newborn erythrocytes. This assumption is based on the higher reactivity of fetal or newborn erythrocytes to an antibody, which is directed against the precursor N-acetylglucosaminly beta1 leads to 3 galactosyl beta1 leads to 4 glucosylceramide than in adult erythorocytes. Reactions of glycolipids of gastrointestinal mucosa, with antibodies directed against H3 glycolipid and its degradation products, were compared to that of gastrointestinal tumors. The reaction to bela Glc NAc1 leads to 3 beta Gall leads to 4 Glc leads to ceramide (structure 4), which is the precursor of all blood group glycolipids, was consistently high in many cases of tumor glycolipid than that of normal glycolipid. This as well as other evidence supports a general concept that the process of ontogenesis of a blood group carbohydrate chain occurs as step-by-step elongation and arborization, and that blocking of such a development of a carbohydrate chain occurs in the process of oncogenesis.
J Exp Med 1976 Sep 01
PMID:Status of blood group carbohydrate chains in ontogenesis and in oncogenesis. 6 Apr 62

"Fingerprints" of 0.9% NaCl solution extracts obtained from fetal guts and individual adenocarcinoma of the colon show a randomized pattern of expression of carcinoembryonic antigen (CEA) determinants by CEA radioimmunoassay and isoelectric focusing. All CEA-containing antigens found in a pool of 20 primary adenomas were found at some stage in fetal development. No single CEA-reacting peak was typical of any one period of fetal development. When fetal gut profiles were grouped according to trimester in utero, however, an expanded gene pool was found in the second trimester which correlates well with maximum gastrointestinal growth and differentiation. Isoelectric focusing-CEA radioimmunoassay profiles of individual primary adenomas were similar to but never identical with individual fetal gut profiles. "Fingerprints" of metastatic adenomas of entodermal origin showed quantitative and qualitative increases in molecules with CEA determinants unlike these latter categories. Such data suggest that both integrator and controller gene activities may be lost in metastatic disease. Rather than "phase-specific gene sets" on different chromosomes being activated by various oncogenic modalities, it is more probable that individual chromosomes are involved in oncogenesis. While more data are needed to confirm this idea, it is safe to say that the expression of molecules with CEA determinants need not be caused by either derepressive or reexpressive gene activation. These data point to the individuality of gene expression of molecules with CEA determinants both in fetal development and in early neoplasia. Since CEA-reacting molecules were not found in tumors of ectodermal or mesodermal origin by these methods, such products should be termed carcino-developmental antigens of entodermal or colonic origin.
Cancer Res 1976 Sep
PMID:Gene activation of molecules with carcinoembryonic antigen determinants in fetal development and in adenocarcinoma of the colon. 6 12

Preneoplastic mammary nodule outgrowth lines were examined for their ability to grow and produce tumors in ovariectomized BALB/c mice. In addition, these nodule outgrowth lines and tumors derived from them were investigated for cytoplasmic estrogen receptor proteins by qualitative and quantitative techniques. Early ovariectomy, performed within 4 weeks after transplantation, slightly delayed but did not permanently block the ability of three different nodule lines to completely fill the fat pad with nodule tissue. Ovariectomy performed later than 4 weeks after transplantation or adrenalectomy performed early or late had no effect on nodule growth. Neither early nor late ovariectomy or adrenalectomy had an effect on the maintenance of the nodule alveolar phenotype. Ovariectomy performed 3 weeks after transplantation had little effect on the tumor potential of the low oncogenic line D1 or the high oncogenic line D2. Samples of nodule outgrowths transplanted from ovariectomized mice responded to a chemical carcinogen in a similar manner, as did nodule outgrowths transplanted from control experiments. Thus, the altered hormonal environmenment in ovariectomized mice apparently did not select for subpopulations of nodule cells with altered tumorigenic potentials. The ovarian independence of the nodule lines and tumors derived from them was correlated with a very low level of cytoplasmic estrogen receptor. These results, along with other data, illustrate the nature of the independence on ovarian hormonal control for tumorigenesis in these mammary tumor virus-free nodule lines.
Cancer Res 1975 Sep
PMID:Hormone dependence and estradiol receptors in the D series of mammary nodule outgrowth lines and tumors. 16 55

Large subcutaneous doses (2 mg/21 days) of estradiol valerate (EV) given over several months will induce a prolactin and growth hormone-secreting pituitary tumor in female rats. The medial basal hypothalami (MBHs) of such EV-treated animals were examined at different time intervals with light and electron microscopes to determine whether EV affects the MBH and to relate any observed effects to the process of tumorigenesis. The MBHs of extensively treated rats exhibited profound glial and neuronal changes. The filament content of astrocytes was greatly increased and large dense pleomorphic inclusions filled both astrocytic perikarya and processes. Degenerating neuronal elements have been observed in the neuropil of extensively treated animals. Dark cells identified as M cells were seen to engage in phagocytosis and were loaded with dense inclusions. Some neurons in MBH contained large quantities of lipofuscin that was different in appearance from that of normal females of the same age. The glial reaction developed gradually. At earlier stages of EV treatment there were fewer reactive glia and these contained fewer inclusions. Myelin figures often occurred in these early inclusions. Reactive glia in EV-treated rats did not appear in the preoptic area, dorsomedial nucleus or lateral hypothalamus but were found in ventromedial nucleus. Retired breeders and starvation-stressed rats resembled normal controls. These pathological changes in MBH may result from a direct effect of EV on the hypothalamus. It is possible that, in addition to its effects on the hypophysis, EV suppresses or injures hypophysiotropic cells in MBH, thus releasing pituitary chromophobes from inhibitory hypothalamic influences. This could result in hypersecretion and neoplasia.
Am J Anat 1975 Sep
PMID:Cytopathological effects of estradiol on the arcuate nucleus of the female rat. A possible mechanism for pituitary tumorigenesis. 17 Aug 18

The ecologic aspects of the distribution of adeno-associated satellite virus (ASV) in the human population are of great interest because of its unconditional defectiveness and dependence on adenovirus for full and herpesvirus for partial complementation. Adenoviruses and herpesviruses are extremely common and persistent infections in man. We have developed immunofluorescent procedures for detecting the presence of satellite virus antibodies in human sera. The percentage of sera with antibodies to the ASV 2-3 complex was significantly higher in the normal group than in the cancer patients whereas there were no significant differences in herpes antibodies between the groups. The low incidence of satellite antibodies was particularly striking in patients with genital malignancies. The role of ASV's in human disease is not known. Their role in possible abrogation of oncogenesis mediated through adenoviruses or herpesviruses is worthy of further investigation.
Am J Obstet Gynecol 1976 Sep 01
PMID:Antibodies to adeno-associated satellite virus and herpes simplex in sera from cancer patients and normal adults. 18 3

Case reports of neuroblastoma revealed that some individuals are genetically predisposed and that this genetic predisposition may have other consequences. According to a mutation model, two classes of individuals could acquire neuroblastoma. One (prezygotic) was a rare class that carried a dominant gene imparting high risk of the tumor. The other (postzygotic) comprised all other individuals, each at low risk. The model related tumor incidence to germinal and somatic mutation rates and thereby carried implications for environmental modification of tumorigenesis and demographic variation in incidence. Case reports also revealed associations of neuroblastoma with congenital defects and a susceptibility to second tumors. Analogy with retinoblastoma and Wilms' tumor of the kidney suggested that these associations could result from action of a neuroblastoma gene or from chromosomal aberration. One known dominantly inherited condition, von Recklinghausen's disease, could dispose to neuroblastoma and create some associations. According to the two-mutation model, neuroblastoma may have been a single recessive gene disorder at the level of the cell. The phenomena of aganglionosis, neuroblastoma in situ, maturation of neuroblastoma to ganglioneuroma, and spontaneous regression suggested that such a neuroblastoma gene interfered with normal developmental processes. The specificities of this gene and of those for von Recklinghausen's disease and pheochromocytoma suggested that the functiof a membrane macromolecule.
J Natl Cancer Inst 1976 Sep
PMID:Developmental genetics of neuroblastoma. 18 2

We have studied the sequential morphological events of glial tumorigenesis in neonatal dogs, using high titer subgroup C Bratislava-77 Avian Sarcoma Virus, given as 0.01 ml by intraventricular inoculation. The cells of the subependymal plate are those which seem to form the gliomas; cytoplasmic alterations are evident within 24 h after inoculation and microfoci of gliomas, contiguous with the subependymal plate of the lateral ventricles, are visible within 7 days. Independent tumors are present by the 10th post-inoculation day. These studies support the hypothesis of Globus and Kuhlenbeck, which implicates the cells of the subependymal palte in glial tumorigenesis.
Acta Neuropathol 1977 Sep 26
PMID:The role of the subependymal plate in glial tumorigenesis. 19 34

Female and male CBA/H mice were infected with lactate dehydrogenase virus (LDV). Two weeks later, these mice and noninfected controls received double sc implants of unplasticized vinyl chloride-vinyl acetate copolymer films (0.2 X 15 X 22 mm). Foreign-body (FB) tumorigenesis was delayed in LDV-infected females and males by 2 months. This result could not be explained by an effect of LDV on cellular immunity, inasmuch as cellular immunity does not influence the course of FB tumorigenesis.
J Natl Cancer Inst 1977 Sep
PMID:Delayed foreign-body tumorigenesis in mice infected with lactate dehydrogenase-elevating virus: Brief communication. 33 Aug 68

A study begun by a drug company and taken over by the FDA (Food and Drug Administration) in 1970 attempted to assess the role of oral contraceptives in tumorigenesis and clotting abnormalities in animals. The study used ethynerone (MK 665) + mestranol; chloroethynyl norgestrel (Wy-4355) + mestranol; anagestone acetate + mestranol; ethynerone, and; mestranol administered at levels up to 25 times the human use level to female beagle dogs and 50 times the human use level to female rhesus monkeys. No behavioral changes related to compound or dose were observed in either species. Both species exhibited pharmacologic effects of hormone administration. Inhibition of the estrous cycle and vulvar enlargement were seen in all dosed dogs. Both species exhibited a dose-dependent, nonprogressive decrease in hemoglobin and hematocrits, with the anagestone acetate-mestranol combination showing the greatest effect. More nodules developed in the mammary glands of dogs who received the progestogen-mestranol combinations and who received ethynerone alone than control dogs. The 3 progestogen-mestranol combination showed the greatest tumorigenic effect as expressed by the number of dogs affected and by numbers of mammary nodules. This effect was dose-dependent for the ethynerone-mestranol and chloroethynyl norgestrel-mestranol combinations, but for the anagestone acetate-mestranol combination was maximal at the lower dose. A small number of dogs that received each progestogen-mestranol combination developed clinically malignant tumors; control dogs or dogs that received only mestranol or ethynerone were unaffected. In contrast, none of the drugs was associated with an increased incidence of mammary nodules in the monkeys. Some monkeys that received each drug showed ductal epithelial hyperplasia in mammary gland biopsies. Diabetes mellitus occurred in 10 dogs from the chloroethynyl norgestrel-mestranol and anagestone acetate-mestranol groups and in 3 monkeys from the ethynerone-mestranol high dose and anagestone acetate-mestranol high dose groups. Generalized cystic hyperplasia of the gallbladder mucosa was seen in a small number of dogs from the anagestone acetate-mestranol group. The suitability of the dog as test species for the tumorigenic and carcinogenic study of oral contraceptives is indicated.
J Toxicol Environ Health 1977 Sep
PMID:FDA studies of estrogen, progestogens, and estrogen/progestogen combinations in the dog and monkey. 41 41

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), an extraordinarily potent toxin, has recently been found to be a potent carcinogen producing mucosal, lung, and liver tumors in female rats. In light of this carcinogenicity, we reexamined the in vivo covalent binding of [3H]TCDD to rat liver macromolecules. Immature Sprague-Dawley rats, receiving [3H]TCDD (0.87 mCi/kg; specific activity, 39 Ci/mmol) concentrated 18 to 64% of the total administered dose in their livers, but virtually all of this radioactivity (greater than 99.9%) was extractable. The maximum unextractable radioactivity was: protein, 60 pmol TCDD per mol of amino acid residue; rRNA, 12 pmol TCDD per mol of nucleotide residue; and DNA, 6 pmol TCDD per mol of nucleotide residue. If one assumes that this small residual amount of radioactivity represents covalent binding, this binding is 4 to 6 orders of magnitude lower than that of most chemical carcinogens, and the binding to DNA is equivalent to one molecule of TCDD per DNA, equivalent to 35 cells. The results suggest it is unlikely that TCDD-induced oncogenesis is through a mechanism of covalent binding to DNA and somatic mutation.
Cancer Res 1979 Sep
PMID:An estimate of the maximum in vivo covalent binding of 2,3,7,8-tetrachlorodibenzo-p-dioxin to rat liver protein, ribosomal RNA, and DNA. 47 64


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