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

The levels of glucosamine-6-phosphate synthetase in various rat tissues including those undergoing differentiation or regeneration revealed that the enzyme is related to tissue proliferation and differentiation. In the liver upon neoplastic transformation, the level of glucosamine 6-phosphate synthetase rises and the liver form of the enzyme having a pI at 5.0 is replaced by a form with a pI of 4.1. Since the latter form has also been found present in whole embryos (12- and 14-day) and brain, the molecular alterations of glucosamine-6-phosphate synthetase in liver neoplasia can be considered to be carcinofetal.
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PMID:Carcinofetal alterations in glucosamine-6-phosphate synthetase. 0 Sep 47

Experimental data supporting a Unifying Concept of the molecular mechanisms of cellular aging and cellular neoplastic transformation of dividing cells in mass culture and clonal culture systems will be described. The Unifying Concept combines the hitherto antithetically presented Differentiation Theory, the Mutation Theory, the Error Catastrophy Theory and the Degradation Deficiency Theory with a newly worked out Virus Theory of the cellular aging and the cellular neoplastic transformation. Quantitative in vitro studies of embryonic fibroblast cell systems of two closely related inbred rat strains L.BN and Lewis were undertaken. The data obtained from the experimental analysis of the molecular mechanisms of the cellular aging and the cellular neoplastic transformation demonstrate, that the cellular aging of dividing cells is a Three-Stage-Differentiation Sequence under the control of three different genetic programs. The genetic constitution of the senescent cell regulates the expression of virogenes and oncogenes of the endogenous RNA tumor viruses of the C-type, resulting either in the cellular degeneration of the senescent cell under the control of the virogenes or in the cellular neoplastic transformation regulated by the oncogenes.
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PMID:Experimental evidence for a unifying concept of the molecular mechanisms of the cellular aging and the cellular neoplastic transformation. 2 5

Nuclear fluorescence metachromasia of heated fixed cells subsequently stained with acridine orange was compared in smears and isolated nuclei of various types of primary tumors and normal cells from the tissues that gave rise to the tumors. The ratios of fluorescence emission at 590 and 530 nm reflect the thermal stability of chromatin in situ. The results show that the mean thermal stability of the chromatin in neoplastic cells was lower than the stability of their normal counterparts in all cases. This was found in both spontaneous and chemically induced tumors as divergent in type as a dog vaginal tumor and murine lymphocytic leukemia. These data, together with our previous observations in other neoplastic systems, indicate that reduced chromatin thermal stability may be a general characteristic of cells that have undergone neoplastic transformation and is not confined to rapidly growing tumors. The present investigation identifies the sources of variability encountered in measuring fluorescence metachromasia in slide preparations, and methods of minimizing this variability for potential cytodiagnostic application are discussed.
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PMID:Microfluorometric comparisons of heat-induced nuclear acridine orange metachromasia between normal cells and neoplastic cells from primary tumors of diverse origin. 4 93

The "virogene-oncogene" hypothesis of Huebner and Todaro and the "provirus" hypothesis of Temin implicate RNA tumor viruses in the neoplastic transformation of mammalian cells. These hypotheses have been substantiated in several animal systems including primates and, presumably, in man. Because the detection in a tissue of one or two activities allegedly related to RNA tumor virus may not be conclusive evidence for viral presence, we have developed a scheme of coordinated morphologic, biologic, and biochemical investigations of human prostatic tissues. We report here the more recent progress we have made in one of the segments of our scheme of investigations. Two, possibly three, DNA polymerase activities from human prostatic tissue have been isolated and partially purified by DEAE-cellulose and phosphocellulose chromatography. These activities have been partially characterized. Based on template preferences and non-inhibition by selective inhibitors of reverse transcriptase, neither of the major polymerase activities appears to be the reverse transcriptase-type activity.
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PMID:The search for "virogene" in human prostatic tissues: prostatic DNA polymerases. 4 15

The close relationship at the molecular level between cellular differentiation and neoplasia has been evidenced by the discovery in adult individuals of fetospecific antigens and fetal type isozymes associated with many spontaneous and experimentally induced malignant tumors. One question in relation with this finding is whether cancerous tumors develop from the differentiation of a tissue reserve of stem cells or by a process of retrodifferentiation, i.e., the nucleocytoplasmic stepwise reversion of cells toward stationary states with simplified structure and less information content. The question is not merely academic; elucidation of the nature of the target cells from which neoplastic growth emerges has obviously physiopathological and therapeutic implications. This contribution is an analysis of the nature and the mechanism of cellular retrodifferentiation and a discussion of its possible role in regeneration and metaplasia, as well as in neoplastic development. Throughout living systems, retrodifferentiation appears as a common adaptive process for the maintenance of cell integrity against deleterious agents of varied etiology (physical, chemical,and viral). While preserving the entire information encoded on its genome, cells undergoing retrodifferentiation lose morphological and functional complexity by virtue of a process of self-deletion of cytoplasmic structures and the transition to a more juvenile pattern of gene expression. This results in a progressive uniformization of originally distinct cell phenotypes and to a decrease of responsiveness to regulatory signals operational in adult cells. Retrodifferentiation is normally counterbalanced by a process of reontogeny that tends to restore the terminal phenotypes from where the reversion started. This explains why retrodifferentiation remains invariably associated to cell regeneration and tissue repair. There is an ever growing evidence that neoplastic transformation in vivo and in vitro is frequently preceded and/or accompanied by biochemical, morphological, and behavioral transitions characteristic of a cell undergoing retrodifferentiation. Contrary to what occurs in regenerating tissues, the "unbalanced" character of tumor-associated retrodifferentiation seems to be a property linked to cancer. The question arises why a unique mechanism of cell rejuvenation is in physiological conditions (regeneration), followed by a process of reontogeny, while in neoplasia the process remains incomplete or does not occur and leads to the emergence of a population of persistently dividing cells. It is to be hoped that a careful study of retrodifferentiation in physiological and tumoral models will help to distinguish that which in neoplastic development can be relevant to an adaptive cell behavior from that which might eventually be the result of specific or constitutive alterations.
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PMID:Cancer, retrodifferentiation, and the myth of Faust. 6 5

The present work consists in a quantitative cytospectrophotometric investigation of the cytoplasmic hyperbasophilia that characterizes the foci of neoplastic transformation and the tumor cells in rats fed hepatocarcinogens. It reveals that the increase in the dye-binding capacity shown by the cytoplasmic RNA of these cell populations results primarily form a qualitative alteration which raises the affinity for basic dyes by a factor of nearly 2, and also to a change in concentration due to volumetric changes which may again double the staining intensity of these hepatocytes. This phenomenon of hyperbasophilia differs radically from the weak variations in basophilia observed in normal regenerating liver and in hyperplastic liver parenchyma of rats fed the carcinogenic diet in which cases the changes appear to be related mainly to de nova RNA synthesis. Biochemical assays on cellular fractions indicate that the ribosomes are the organelles responsible for the hyperbasophilic properties that hepatocytes acquire in areas of neoplastic transformation.
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PMID:[Cytospectrophotometry of hepatocyte RNA in regenerating and neoplastic liver]. 8 63

The ability to induce formation of new vessels was tested in fragments of rat mammary tissue transplanted onto the rabbit iris and observed through the transparent cornea. Virgin, pregnant, and lactating glands showed an angiogenic capacity in about 5% of implants. In contrast mammary carcinomas induced angiogenesis in 75 to 100% of implants. Fragments of mammary gland previously treated with 7,12-dimethylbenz[alpha]anthracene of N-nitrosomethylurea but without histological evidence of neoplastic transformation showed an angiogenic response in about 5% of implants. The same low angiogenic response was detected in primary hyperplastic alveolar nodules. However, angiogenesis was observed 2 to 3 times more frequently in implants from hyperplastic outgrowths that acquired of continuous transplantability and showed a high degree of neoplastic transformation. These data on the rat mammary gland confirm previous findings on mouse mammary gland, indicating that: (a) neoplastic epithelium has a higher angiogenic capacity than does normal epithelium; and (b) hyperplastic epithelium at high risk of undergoing neoplastic transformation induces angiogenesis more frequently than does hyperplastic epithelium with low tumor potential.
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PMID:Acquisition of angiogenic capacity and neoplastic transformation in the rat mammary gland. 10 22

Biological characteristics of nodule-like alveolar lesions (NLAL) induced by 7,12-dimethylbenz[a]anthracene (DMBA) in organ culture of whole mammary gland (BALB/c female mice) were assessed after transplantation into gland-free mammary fat pads of syngeneic virgin mice. (i) Tissue-fragment explants from NLAL areas of the gland produced abnormal lobuloalveolar (LA) outgrowths in 3 of 10 fat pads. (ii) Transplantation of dissociated cells of NLAL-derived LA outgrowths into 36 fat pads showed 100% LA outgrowths and 3 (8%) of these 36 outgrowths produced mammary carcinomas. (iii) The explants of dissociated cells from whole mammary glands treated with DMBA in culture produced full or partial LA structures in 2 of 56 outgrowths. (iv) The explants of dissociated cells prepared from outgrowths derived from outgrowths derived from explants as in iii produced 9 LA outgrowths in 16 instances; mammary tumor incidence in these outgrowths was 3 of 16 (18%). (v) The explants of tissue fragments from LA outgrowths as in iv produced LA outgrowths in 20 of 20 fat pads; mammary carcinomas appeared in 16 of 20 (80%) of these outgrowths. No NLAL was detectable in control glands treated with dimethyl sulfoxide (solvent for DMBA); explants of the control glands consistently produced ductal outgrowths and no tumor. This accomplishment of chemical carcinogen-induced neoplastic transformation of epithelial cells in vitro provides a model for studying carcinogenesis in an entire isolated organ.
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PMID:Neoplastic transformation of epithelial cells in whole mammary gland in vitro. 11 56

A lifetime study in Swiss mice showed that a single 300microgram application of 7, 12-dimethylbenzanthracene (DMBA) once, or 300 or 30microgram DMBA once followed by 3.2 microgram phorbolester for 15 weeks induced a high number of skin tumors many of which regressed spontaneously. The regression occurred mostly early in the experiment, the number of appearing and regressing tumors following a cynical pattern. The incidence of regressions was only to a limited extent associated with tumor size, tumor duration and total number of tumors. Repeated DMBA treatment, 5 microgram twice a week induced the same types of tumors in larger numbers: with a smaller incidence of regressions and only if they were transient in nature, i.e., lasting less than 3 weeks. These occurred in animals which showed a large number of persisting tumors simultaneously, but which rarely displayed multiple regressions. The results indicate the occurrence of multiple steps of neoplastic transformation from hyperplastic lesions, benign regressing tumors, presistent tumors and frankly malignant ones, the incidence as well as biological behavior depending upon inducing treatment.
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PMID:Tumor persistence and regression in skin carcinogenesis. An experimental study. 15 92

Certain continuous lymphoid and myeloid tumor cell lines of rodent origin are unable to grow in tissue culture in the absence of pre-formed L-cystine (CYS). In contrast, three NZB murine lymphoid cell lines obtained from NZB mice free of hematopoietic neoplasm can grow as well in cystine-deficient media containing L-cystathionine (CSN), the immediate precursor of CYS in the biosynthetic pathway, as in cystine sufficient medium. The former class of cells is, therefore, CYS auxotrophs (CYS-) and the latter CYS prototrophs (CYS+). Compared to CYS+ cells, the CYS- lines appear to be relatively deficient in the enzyme cystathionase, which catalyzes the cleavage of CSN to CYS and alpha-ketobutyrate. Using protein synthetic capacity as a criterion, normal thymocytes from mixed-bred Swiss mice behave like CYS prototrophs, while those from littermates bearing Moloney type C virus-induced thymic tumors behave like CYS auxotrophs. The former are also characterized by substantially higher levels of cystathionase than the latter. Extracts of thymocytes from tumor-free AKR mouse thymus are also characterized by higher levels of cystathionase activity than extracts of spontaneous AKR thymomas. Exogenous in vitro type C virus infection of a CYS+ cell results in vigorous virus production but no concomitant reduction in cystathionase activity. Thus viral replication alone in any random lymphoid cell is not sufficient to alter the enzyme level. The data therefore suggests that CYS auxotrophy may closely accompany neoplastic transformation of certain hematopoietic cells in vivo, including that induced by certain "thymic" type C viruses.
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PMID:Accumulation of cystine auxotrophic thymocytes accompanying type C viral leukemogenesis in the mouse. 18 Nov 39


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