[Tumoral processes and characteristics of their pathogenesis].
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Humans↗
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Neoplastic transformation and cytogenetic aberrations of rat tracheal epithelial cells induced by alpha-particle irradiation.
Primary rat tracheal epithelium (RTE) cells can be transformed in vitro by alpha-particles irradiation. One out of 3 isolated morphologically transformed colonies gave rise to an immortal cell line and ultimately became neoplastic by successive passaging. Cytogenetic analysis was performed on the cell line in order to understand how the specific chromosome alterations participate in the process of neoplastic transformation of RTE cells. The 5th, 18th, 39th passage cells and the colony cells isolated from soft agar (SA) culturing of the 40th passage cells were analyzed. The results showed that the 20th passage cells were nontumorigenic, but the 40th passage cells were tumorigenic. The increase of the length of the long arm of chromosome 15 (15q+) was frequent at the 5th passage (67.8%), especially in SA cells in which it occurred in a clonal fashion (100%). Therefore, 15q+ might be the critical gene lesion after alpha-particles irradiation. Monosomy of chromosome 8 that occurred frequently at passage 5 (54%) and 40 (53%) might be correlated with earlier transformation of RTE cells. In addition, three marker chromosomes (M1, M2 and M3) showed a passage-dependent increase. In particular M1 and M2 that were highly frequent at passage 39 (90%) suggested that they might play an important role in the process of cell transformation.
Alpha Particles↗
Platelet-derived growth factor as a mediator of normal and neoplastic cell proliferation.
Human platelet-derived growth factor is the major mitogen in serum for connective-tissue-derived cells in culture. The factor is 30,000 mol. wt protein composed of two disulphide-linked polypeptide chains, named A and B. The B-chain is virtually identical to part of the transforming protein of simian sarcoma virus (SSV), implying that SSV-transformation is mediated by a PDGF-like growth factor. This notion is supported by the finding that specific as well as nonspecific inhibitors of PDGF-action (PDGF antibodies and suramin, respectively) are efficient inhibitors of SSV-transformation and revert the transformed phenotype of SSV-transformed cells. Expression of the genes encoding the PDGF subunits and production of PDGF-like growth factors is a common feature of human sarcoma cell lines, suggesting a role of PDGF in the pathogenesis of sarcomas, although direct support in favor of this notion is lacking. An involvement of PDGF in autocrine and paracrine stimulation of normal cell growth is suggested by the finding that responsive (arterial smooth muscle cells and placental cytotrophoblasts) as well as nonresponsive (endothelial cells and macrophages) cells produce PDGF-like growth factors. In conclusion, PDGF-like growth factors may be widely implicated in normal as well as neoplastic growth processes.
Amino Acid Sequence↗
[Intestinal hemorrhages in tumor processes of the digestive tract].
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Digestive System Neoplasms↗
Protective role of potentially lethal damage repair in the neoplastic transformation of Balb/c 3T3 cells treated with N-methyl-N'-nitro-N-nitrosoguanidine.
To determine the role of repair of potentially lethal damage (PLD) in the initiation process of neoplastic transformation, Balb/c 3T3 cells treated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were temporarily exposed to conditioned medium obtained from density-inhibited Chinese hamster cell cultures, as a post-treatment for the induction of PLD repair. With or without this exposure, cell survival and transformation frequencies were simultaneously determined by colony-formation and focus-formation assays, respectively. Temporary exposure to conditioned medium resulted in a 20-30% increase in cell survival compared with no exposure. Post-treatment with conditioned medium resulted in a 60-65% reduction in transformation frequencies. At the molecular level, the repair of MNNG-induced single-strand breaks of DNA occurred much more rapidly in conditioned medium. These data suggest that PLD repair reduces the in vitro neoplastic transformation through excision repair operative during the cessation of DNA replication. Thus, PLD repair appears to be preventive against neoplastic fixation in initiation of neoplastic development.
Animals↗
Effect of magnesium on nickel-induced genotoxicity and cell transformation.
Raising the extracellular level of magnesium ions inhibited nickel-induced DNA strand breaks, DNA-protein crosslinks, sister chromatid exchanges, chromosomal aberrations and cell transformation. Carcinogenic nickel ions preferentially damaged centromeres and other heterochromatic regions of Chinese hamster ovary cell chromosomes. Elevation of extracellular magnesium levels prevented the effects of nickel on heterochromatin and inhibited cell transformation, but did not substantially reduce the DNA damage induced by nickel in euchromatic regions. This study suggests that heterochromatic DNA damage may be important to the nickel-induced neoplastic transformation process.
Animals↗
Neoplastic transformation of human epidermal keratinocytes by AD12-SV40 and Kirsten sarcoma viruses.
Recent investigations have begun to dissect the number and nature of genetic alterations associated with cancer cells. In the present study, primary human epidermal keratinocytes acquired indefinite life-span in culture but did not undergo malignant conversion in response to infection with a hybrid of adenovirus 12 and simian virus 40. Addition of Kirsten murine sarcoma virus, which contains a K-ras oncogene, to these cells induced morphological alterations associated with the acquisition of neoplastic properties. These findings demonstrate the malignant transformation of human primary epithelial cells in culture and support a multiple-step process for neoplastic conversion.
Adenoviruses, Human↗
Complex expression of the genes coding for plasminogen activators and their inhibitors in HeLa-smooth muscle cell hybrids.
As cells progress through the multistep process of neoplastic transformation, they eventually acquire the property of invasive behavior. Although both plasminogen activators (PA) and their inhibitors (PAI) contribute to this process, their regulation in normal and transformed cells remains poorly defined. Because somatic cell hybrids provide useful tools for examining the transformation pathway, tumorigenic and invasive HeLa cells were fused with human normal vascular smooth muscle cells and tested for invasion-related parameters, including the expression of PA and PAI genes, and matrix degradation. Both parental cell lines produced large amounts of PAI activities with no detectable PA in either cellular or secreted form. Opposite findings were obtained with the hybrid cell lines, which demonstrated the presence of receptor-bound and secreted PA but absence of enzymatically measurable PAI activities. Both urokinase-type and tissue-type PA were found in cell-associated and secreted form in the hybrid cells. In addition, expression of the urokinase-type PA receptor gene was found in the three hybrid cells and the vascular smooth muscle cells but not in the HeLa cells. Expression of active, receptor-bound and secreted PA provided the nontumorigenic hybrid cells with the enzymatic tools to degrade extracellular proteins in a plasminogen-dependent manner. Thus, the hybrid cells lost tumorigenicity while retaining the tissue-degrading capability of HeLa cells. These hybrid cell lines should prove to be important reagents for investigating the complex regulatory control of PA and PAI gene expression.
Extracellular Matrix↗
[Simple roentgen findings in expansive tumor processes in the area of the optic nerve, chiasm and optic tracts].
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Brain Neoplasms↗
Contrasting responses of normal and transformed rat tracheal epithelial cells to the tumor promoter 12-O-tetradecanoylphorbol-13-acetate.
The data presented here are part of an ongoing effort to examine the response of rat tracheal epithelium to tumor promoting agents and to elucidate the mechanisms of tumor promotion in that epithelial tissue (see Steele, this volume). Previous studies indicated that airway epithelium is responsive to the tumor promoter TPA and that TPA can promote the tumor response in rat tracheal epithelium But what are the mechanisms involved? We have divided this question into two main elements: 1) Which stages of neoplastic development are affected by TPA, i.e., which preneoplastic cell populations are targets for TPA action resulting in the acceleration and enhancement of the process of neoplastic development? 2) What effects does TPA have on various preneoplastic cell populations and how do such effects result in promotion? The experiments discussed here relate to the second part of the question. They suggested that TPA elicits a marked cytotoxic response in stably transformed RTE cell variants (see Fig. 1). These preneoplastic cell variants are clearly different from untransformed RTE cells which are triggered into cell cycle as indicated by an increase in CFE. This difference between normal and transformed cells is of considerable interest in itself since it points to a fundamental, biochemical alteration in the transformed cells. Evidence exists that transformed RTE cell lines have TPA receptors and that at least some of the responses elicited by TPA exposure, such as the induction of ornithine decarboxylase activity, are receptor-mediated. Whether the cytotoxic response elicited by TPA is receptor-mediated is presently not known.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Neoplastic progression evidenced in the L929 cell system. II. In vitro growth properties and biochemical characteristics of cell variants with different malignant behavior.
Using a culture cell system, derived from a low-tumorigenic strain of L929 mouse fibroblasts, including cell variants with different malignant behavior in vivo, we have tried to dissociate a group of biological and biochemical transformation-associated properties with respect to the process of neoplastic progression. It is shown that morphologic changes, nonalignment in vitro, and growth in soft-agar are not sufficient alterations for in vivo malignant behavior and, also, not useful indicators for further neoplastic progression. The rate of hexose uptake should also be considered as unrelated to this process. The increase in tumorigenicity, but without the concomitant development of metastasis ability of the cells, was associated with the decrease of a 160k cell surface protein and the diminution of the tumor dose 50%. Finally, further alteration in morphology and the appearance of a 177k cell surface protein were associated with the development of metastasis ability, in an early stage; loss of fibronectin and the ability to grow as macrocolonies in increasing concentrations of deoxyglucose appeared as associated to more advanced stages of neoplastic progression. On the whole, the approach of taking the in vivo behavior, and not the in vitro properties, as end-point for the study of transformation is recommended on the basis of this and a previous paper.
Animals↗
Induced type-B reticulum cell neoplasia of CBA mice. II. Functional similarities between tumorigenic reticulum cells and normal accessory cells.
In a previous report, it was proposed on the basis of phenotypic evidence that the population of transplantable cells which constituted the major component of experimentally induced type-B reticulum cell neoplasms of CBA strain mice could be a neoplastic counterpart of lymphoid dendritic or veiled accessory cells. This has been further tested by an in vitro examination of their accessory function. Both similarities and differences in behaviour between the neoplastic cells and accessory cells prepared from spleens of normal mice were found. The possible significance of these properties is discussed in relation to the process of neoplastic change.
Animals↗
Roles of reactive oxygen species and selected antioxidants in regulation of cellular metabolism.
Reactive oxygen species (ROS) are essential for life of aerobic organisms. They are produced in normal cells and formed as a result of exposure to numerous factors, both chemical and physical. In normal cells, oxygen derivatives are neutralized or eliminated owing to the presence of a natural defense mechanism that involves enzymatic antioxidants (glutathione peroxidase, superoxide dismutase, catalase) and water or fat-soluble non-enzymatic antioxidants (vitamins C and E, glutathione, selenium). Under certain conditions, however, ROS production during cellular metabolism also stimulated by external agents may exceed the natural ability of cells to eliminate them from the organism. The disturbed balance leads to the state known as oxidative stress inducing damage of DNA, proteins, and lipids. An inefficient repair mechanism may finally trigger the process of neoplastic transformation or cell death. Reactive oxygen species are also an integral part of signal transduction essential for intercellular communication. The balance between pro- and antioxidative processes determines normal cellular metabolism manifested by genes activation and/or proteins expression in response to exo- and endogenous stimuli.
Antioxidants↗
[PSEUDO-TUMORAL EXPANSIVE PROCESS OF THE BASE OF THE SKULL AND SYPHILITIC MENINGOENCEPHALITIS].
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Brain Neoplasms↗
Cervical wart virus infection, intraepithelial neoplasia and carcinoma; an immunohistological study using a panel of monoclonal antibodies.
The pattern of epithelial antigen expression has been examined in normal and disordered cervical squamous epithelium using immunohistological methods and a range of monoclonal antibodies. It was demonstrated that wart virus infection (WVI) is associated with disordered staining for a keratin-associated component and for HLA-DR antigen. Furthermore, wart-infected epithelium shows strong labelling for carcinoembryonic antigen (CEA) and for human milk fat globule antigens 1 and 2 (HMFG1 and 2). In addition these antigens (CEA, HMFG1 and 2) are also expressed in mixed WVI and cervical intraepithelial neoplasia (CIN), CIN III and in carcinoma. While these findings do not allow immunohistological discrimination between non-neoplastic and neoplastic cervical epithelia, they do provide support for the view that cellular proliferation of the type induced by papilloma virus may represent an initiator stage in the process of neoplastic transformation.
Adenocarcinoma↗
Dissimilar modes of expression of beta- and gamma-actin in normal and leukemic human T lymphocytes.
Actin polypeptides are the most abundant protein components of replicating normal human T lymphocytes, comprising 16% of the total cellular protein. Unlike other replicating cell types which synthesize equal proportions of beta- and gamma-actin polypeptides, T cells synthesize beta-actin as the predominant species. By contrast, leukemic T cells (the Molt-4 cell line) synthesize nearly equal proportions of beta- and gamma-actin. In addition, novel forms of beta-actin in normal T cells and of beta- and gamma-actin in Molt-4 cells appear to be present, perhaps resulting from a post-translational modification process. Otherwise, both divergent T cell types express a relatively common spectrum of polypeptide species, thereby suggesting that regulation of actin biosynthesis may be involved in the neoplastic transformation process.
Actins↗
[The fine structure of cell processes in astrocytoma (author's transl)].
Astrocytes, in normal tissue, may be characterized by their extensive processes which may be cylindrical in part but are sheet-like at their periphery where they serve to cover other structures. It becomes of interest ot determine the morphology of astrocytic processes after neoplastic transformation. We, therefore, examined the fine structure of 14 cases of astrocytomas. In general the fine structure of the cell bodies and the interior of the processes are fundamentally similar to those of normal or developing astrocytes. Differences are apparent at the cell periphery. These include less well developed cell junctions and usually only poorly formed peripheral expansions of the processes. Most sections through the processes appear round or oval rather than laminar in normal astrocytes. They often consist of small microvilli or pseudopodia-like protrusions. Whether these changes are due to the immaturity of the cell or to the lack of appropriate nearby target cells is not known.
Astrocytes↗
Differential expression of mucins 1-6 in papillary thyroid carcinoma: evidence for transformation-dependent post-translational modifications of MUC1 in situ.
Mucins are primary glycoproteins of epithelia that are known to undergo major changes in their post-translational processing during neoplastic transformation. This study has examined the expression pattern of seven primary mucins, ie mucin (MUC) 1, 2, 3, 4, 5AC, 5B and 6, in normal, hyperplastic, benign neoplastic, and papillary-type carcinoma (PTC) tissues of the thyroid. MUC1 and MUC5B were the only mucins to be widely transcribed in both benign and malignant tissues. In contrast, MUC4 transcripts were undetectable in normal thyroids, and were present in only 40% of the hyperplastic and malignant thyroid tissues. In PTC, MUC1 was identified as a single mRNA transcript, rejecting the idea that this mucin may undergo transformation-dependent alternative splicing in thyroid tumours. The tissue distribution of MUC1 and MUC4 proteins was highly heterogeneous: this largely paralleled their mRNA expression profiles and supported the conclusion that whereas MUC1 was ubiquitously expressed in PTC, MUC4 was detectable in less than 20% of the cases analysed. In order to determine whether post-translational modifications of MUC1, putatively associated with malignancy, also occurred in the mucin produced by PTC, immunohistochemistry was performed with a panel of well-characterized anti-MUC1 antibodies in conjunction with digestion of the tissue sections with deglycosylating enzymes. These experiments, which were supported by immunochemical analyses of the MUC1 and MUC4 glycoforms extracted from tissues, collectively demonstrated markedly divergent MUC1 glycosylation profiles in normal and benign thyroid tissues when compared with PTC. Characteristically, these latter neoplastic cells produced mucin molecules carrying complex poly-N-lactosamine-type glycans capped with fucose and neuraminic acid residues. The present study also found evidence in PTC for the potential presence of proteolytically processed MUC1 isoforms which differ in their post-translational traits depending on whether they are retained on the cell surface or secreted into the extracellular space. It is proposed that the observed differences in the glycosylation properties of normal and neoplastic MUC1 may be exploitable as an ancillary tool in the diagnosis of PTC.
Antibodies, Neoplasm↗
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