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At least 19 recordsLinked to original sources

PubMed1992

An overview of oncogenesis.

The paper reviews the actual knowledge in the field of oncogenesis, according to the oncogene theory of cancer. The main actions of proto-oncogenes during cellular proliferation are outlined and oncogenes are classified to their specific roles. The relationships between proto-, viral-, and cellular oncogenes are analyzed and the several steps of the evolution of a p-onc towards a c-onc are described. Several examples of better known oncogenes are presented to illustrate the interrelations between the families of genes and their interactions during oncogenesis are evoked. As the implication of each c-onc in distinct neoplasia can be suspected according to the most frequent genomic alteration of each type of cancer, information about the chromosomal localization of oncogenes is comprised. The oncogenes' products, their weight and cellular position are also presented. The onco-suppressor genes, oncogenes' counterparts are also described, their localization being deduced from analysis of frequent breakpoints or mutation site/s in cancers. Finally, future perspectives of oncogene research are also outlined.

Genes, Tumor Suppressor↗

PubMed2025

How Have Massively Parallel Sequencing Technologies Furthered Our Understanding of Oncogenesis and Cancer Progression?

Massively parallel sequencing technologies have been a boon to many fields of biological science, including oncology. Cancer is an umbrella term for many diseases featuring abnormal cellular growth due to genetic and epigenetic aberrations. Advances in sequencing technology allow for interrogation of the DNA and RNA of cancer cells and other cells in the tumor microenvironment down to a single-base resolution. However, these strides come after a rich history of ground-breaking biological assays, like the discovery of the Philadelphia chromosome in the context of leukemia. Many specific genetic and epigenetic modifications have been implicated in oncogenesis, cancer progression, and response to treatment. Sequencing technologies have also helped to associate populations of bacteria in the microbiome to cancer development and prognosis. However, all this new information, especially when procured via high-throughput methods, comes at the cost of being more computationally and staff-resource intensive. There is also more risk to the privacy of the individuals with sequenced genomes. Notwithstanding, the overall benefit of sequencing technologies can greatly outweigh the risks with careful advancements and continued focus on the goal: helping those affected by cancer via precision medicine. Cancer biology has been and will continue to be elucidated by sequencing innovations in ways unimaginable without it.

Humans↗

PubMed1979

Enhancement by asbestos of oncogenesis by Moloney murine sarcoma virus in CBA mice.

Five micrograms of finely ground crocidolite asbestos (UICC standard sample) were injected intraperitoneally into 3-week-old CBA mice, together with 10(5) FFU of Moloney murine sarcoma virus. Altogether 44 out of 61 mice (72.1%) so treated developed palpable intraperitoneal tumours, and half of these died of such tumours within 100 days. The same amount of quartz and carbon similarly administered gave lower tumour incidences, namely, 19.4% (3.2% fatal) and 11.9% (1.5% fatal) respectively. Only 1 out of 59 mice inoculated with the virus alone developed a palpable intraperitoneal tumour, and this regressed spontaneously within 10 days of its first appearance. No tumours were encountered in mice treated with either asbestos, quartz or carbon alone. All the neoplasms had the appearance, under the light microscope, of anaplastic sarcomas. Most of them were confined to the serosal surface of the abdominal cavity, although invasion of underlying tissues was observed in some of the animals that died. Electron microscopical examination of tumours revealed the presence of C-type particles budding off from cellular surface. Some neoplastic cells showed characteristic features of mesothelial lining cells. The role of milky spots (taches laiteuses) in oncogenesis by asbestos and virus, especially in the induction of mesothelioma, is discussed.

Animals↗

PubMed1976

Oncogenesis in human acute leukemia.

By selecting, for discussion, some aspects of oncogenesis in human acute leukemia, we hope to focus attention on areas of current interest which promise to provide important advances in our knowledge and understanding of human neoplasia, and, in time, may lead us nearer to the goal of disease control and eventual eradication.

Acute Disease↗

PubMed1978

Glial-mesenchymal tropism of in vivo avian sarcoma virus neuro-oncogenesis in rats.

Intracerebral inoculation of avian sarcoma virus (ASV) in postnatal animals induces gliomas and sarcomas but no neuronal tumors. High titer Bratislava-77 strain ASV was inoculated intracerebrally in fetal F-344 rats between 17 and 20 days of gestation: a time of active neuronal proliferation. Following birth inoculated rats developed gliomas and sarcomas but no neuronal tumors. The results are evidence that the glial-mesenchymal tropism of in vivo ASV neuro-oncogenesis is independent of stage of neurocytodifferentiation at inoculation.

Animals↗

PubMed1992

Genetic alterations by human papillomaviruses in oncogenesis.

The integration sites in the cellular genome of human papillomavirus are located in chromosomal regions always associated with oncogenes or other known tumor phenotypes. Two regions, 8q24 and 12q13, are common to several cases of cervical carcinoma and can have integrated more than one type of papillomavirus DNA. These two chromosomal regions contain several genes implicated in oncogenesis. These observations strongly imply that viral integration sites of DNA tumor viruses can be used as the access point to chromosomal regions where genes implicated in the tumor phenotype are located, a situation similar to that of non-transforming retroviruses.

Chromosomes, Human, Pair 12↗

PubMed1979

Cellular regulation of mammalian sarcoma virus expression: a gene regulation model for oncogenesis.

Investigations aimed at defining cellular functions required for expression of transformation by mammalian sarcoma viruses have led to the isolation of a class of revertants that contain biologically active feline sarcoma virus, yet possess in vitro and in vivo properties of normal cells. The block to expression of the transformed state in these cellular revertants was spontaneously reversible at low frequency. Moreover, infection with certain helper viruses reversed the block at very high efficiency. Helper virus complementation was shown not to be a direct effect of helper virus functions expressed in the initially infected revertant cell. Rather, the helper virus acted indirectly by rescuing sarcoma virus and allowing it to infect and transform another cell within the revertant population. Using biochemical and immunologic techniques, it was possible to demonstrate a specific and very marked reduction in transcriptional and translational products of the sarcoma viral genome in the revertant cells. Findings that the reversal of this block was associated with reacquisition of the transformed phenotype, together with other evidence, suggest that reversion results from cellular transcriptional regulation of the integrated sarcoma virus genome. Reversion in this virus transformation system provides a model for oncogenesis resulting from derepression of cellular genes that possess malignant potential.

Animals↗

PubMed1992

Chromosome abnormalities and oncogenesis in cat leukemias.

Chromosome abnormalities are found in feline leukemia virus (FeLV)-infected tumor cells as well as in tumor cells free of the virus. Three cell lines derived from tumors in the domestic cat (Felis catus), two of thymic origin and one of multicentric lymphoma origin, were analyzed cytogenetically to determine whether the FeLV virus was associated with chromosomal abnormalities in these tumor cell lines. One thymic tumor and the multicentric lymphoma were FeLV infected. The other thymic tumor cell line was FeLV-free. The normal diploid number in the domestic cat is 38. All three cell lines had numerical chromosome abnormalities with modal numbers of 37, 38 (pseudodiploid), and 39, respectively and had consistent structural chromosome abnormalities. Three markers in the virus-free cell line (S markers) were shared with one or the other of the virus-positive cell lines. The two FeLV-positive cell lines did not have S markers in common. The finding of chromosome abnormalities in both the virus-infected and the virus-free cell lines suggests that these abnormalities may be important in oncogenesis. The FeLV virus could not be considered the only causative agent of the abnormalities observed.

Animals↗

PubMed1976

Status of blood group carbohydrate chains in ontogenesis and in oncogenesis.

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.

ABO Blood-Group System↗

PubMed1975

Oncogenesis by Marek's disease herpesvirus in chickens lacking expression of endogenous (gs, chick helper factor, Rous-associated virus-O) and exogenous avian RNA tumor viruses.

Chickens free of exogenous avian leukosis virus (ALV) infection, replicating endogenous ALV (Rous-associated virus-O), gs antigen, and chick helper factor were fully susceptible to induction of Marek's disease (MD) by ALV-free MD viruses. Dual infection with Rous-associated virus-2 and MD virus did not significantly alter the character of the MD lesions. Thus exogenous ALV infection was not requisite for MD virus-induced oncogenesis. Although participation of endogenous RNA tumor virus genes in MD lesion induction could not be excluded, expression of such genes in MD tumors as gs antigen was not established.

Animals↗

PubMed1977

Short and long term effects of methyl- and ethylnitrosourea (MNU & ENU) on the developing nervous system of the rat. II. Short term effects: concluding remarks on chemical neuro-oncogenesis.

The cytotoxic action of various single doses of MNU and ENU on developing neural and extraneural tissues was studied at different stages of development. Examination revealed lethal damage. (L.I.) and mitotic inhibition (M.I.), confined to proliferating cells only, and caused by the number of alkyl groups administered. In studying the duration of M.I. a difference was found in duration of the cell cycle arrest after MNU or ENU. The arrest lasted longer for MNU than for ENU, and the neural tissues turned out to be more sensitive than the extraneural ones. Moreover, among the reappearing mitotic figures abnormal ones were noticed frequently. After pulse-labeling with thymidine this arrest could be traced to take place in or before entering the S-phase. During the period of this arrest a low, but specific, activity was found that might point to the existence of repair-processes in vivo. Finally, we directly demonstrated alkylations in tissue-sections by the use of (14C-methyl)-MNU. High radioactivity was found with a random distribution over the various tissues, cell types and even cellular compartments. Therefore--in contrast with the cytotoxic effects--alkylation seems to occur in all cell types. In conclusion, it seems justified to consider the matrices of proliferating cells in the central nervous system as the target tissue-areas for the carcinogenic action of both MNU and ENU. Re-entrance of these damaged cells into their cycle prior to the elimination of altered bases from DNA might be of great importance for the problem of oncogenesis.

Age Factors↗

PubMed1992

'Hit and run' oncogenesis by human papillomavirus type 18 DNA.

Transfection of an immortalized cell line (AE), derived from Syrian hamster embryo cells, with human papillomavirus type 18 (HPV 18) DNA induced morphological transformation and these transformed cells were tumorigenic in nude mice. Southern blot analysis revealed that the transfected viral DNA was retained in all the cell lines tested, however, all these transformed cells contained only less than one copy per cell of viral genome. Eleven cloned cell lines were established from a tumor cell line obtained after explantation of a tumor into a nude mouse. Two lines revealed no viral sequences by both Southern blot hybridization and polymerase chain reaction, whereas the nine others contained the remaining viral sequences. These results are highly suggestive of a 'hit and run' oncogenesis by this virus.

Animals↗

PubMed1975

[Participation of Mycoplasmas in oncogenesis (author's transl)].

The conclusions drawn from the presented data are in agreement with previously issued opinions of the author. Mycoplasmas are, synergistically with other factors, esseential and obligatory for oncogenesis. Distince biotypes of Mycoplasmas from different types of tumors could not be isolated. Mycoplasmas possess the ability to induce various tumors, without regard to their origin, either from tumors and fetuses. It is concludet that Mycoplasmas are infectious agents specific for tumor induction in general, but not for a distinct type. The conviction, presented already in 1948, tthat no malignant tumor occurs without the presence of Mycoplasmas, but in contrast, that numerous infections by Mycoplasmas do not provoke the manifestation of malignent tumors, is maintained.

Animals↗

PubMed1976

The effect of modifiers of microsomal enzymes on chemical oncogenesis in cultures of C3H mouse cell lines.

Two cell lines, both derived from the C3H mouse and each having different responses (oncogenic and cytotoxic) to polycyclic aromatic hydrocarbon oncogens, were studied with respect to their drug-metabolizing enzymes. The 10T1/2CL8 cells (a C3H mouse embryo fibroblastic cell line) were much more effective in converting 3-methylcholanthrene (3-MC) to 3-MC water-soluble metabolites, 3-MC phenols, and 3-MC-bound cellular macromolecules than were CVP3SC6 cells (a new line of C3H mouse adult ventral prostate fibroblasts). Basal aryl hydrocarbon hydroxylase activity was higher in 10T1/2CL8 cells than in CVP3SC6 cells, while the reverse was found for epoxide hydrase activity (using 3-methylcholanthrene-11, 12-oxide as substrate. 3-MC or benz(a)anthracene induced epoxide hydrase activity in both cell lines to about the same extent. 3-MC did not induce aryl hydrocarbon hydroxylase activity in CVP3SC6 cells. Aryl hydrocarbon hydroxylase activity was markedly induced in both cell lines by benz(a)anthracene and was slightly induced in 10T1/2CL8 cells by 3-MC. In a chemical oncogenesis cell culture system, transformation of 10T1/2CL8 cells mediated by 3-MC could be increased two- to threefold by treating the cell cultures with: either benz(a)anthracene, styrene oxide, cyclohexene oxide, or 1,2,3,4-tetrahydrona=phthalene-1,2-oxide; or with cyclohexene or 1,2-dihydrona-phthalene, alkene precursors of cyclohexene oxide and 1,2,3,4-tetrahydronaphthalene-1,2-oxide, respectively. When 10T1/2CL8 cells were treated with a combination of benz(a)anthracene and cyclohexene, 3-MC-mediated transformation was increased 7.8-fold. CVP3SC6 cells that were not transformed by 3-MC or other hydrocarbon oncogens were transformed by a combined treatment with benz(a)anthracene, 1,2-dihydronaphthalene, and 3-MC.

Aryl Hydrocarbon Hydroxylases↗

PubMed1975

Somatic hybridization and oncogenesis; (Mechanism of formation of malignant tumors and metastases by the action of antilymphocytic serum).

The results of experiments carried out to test some of the consequences of the earlier general theory of oncogenesis, according to which the malignant tumor cell can arise as a result of somatic hybridization of cells of different organ- and tissue-specificity, are described. In the first series a tumor induced by cellophane film, was grafted into syngeneic and allogeneic mice, and antilymphocytic serum (ALS) was then injected. Metastases occurred only in allogeneic recipients receiving ALS. It was thus shown that the ability of cells of this particular tumor to metastasize is not a property inherent in its cells but is acquired by them as a result of interaction with the recipient organism. In the second series it was shown by two immunological methods that the cells of metastases arising under these conditions contain tissue compatibility antigens of donor and recipient origin, i. e., that they are somatic hybridsmin the third series skin from individuals of another strain was grafted on to mice and ALS was injected; hepatomas developed in 74% of these mice. The theory is used to explain several phenomena of carcinogenesis not explicable by other theories: the phenotypic nature of cell transformation, the causes and nature of the duration of the latent period of tumor development, the mechanism responsible for the ability of tumors to overcome the system of immunological defense, the mechanism of activation of endogeneous oncogenic viruses, etc. Finally an answer is given to the question: what is a tumor?

Animals↗

PubMed1975

The influence of pinealectomy and of pinealectomy combined with thymectomy oncogenesis caused by polyoma virus in rats.

The inoculation of Polyoma virus suspension to neonatal pinealectomized rats did not provoke a growth of neoplasia. However, if the pinealectomy was combined with neonatal thymectomy, renal tumors occured in a rate of 50 of animals. An incidence of renal tumors was observed also in 57.6% of thymectomized rats, but not in non operated control group. The stimulating effect of pinealectomy on the growth of transplantable tumors has already been described several times (2, 3, 6, 8). The question of a possible change in the viral oncogenesis after pinealectomy was raised. For this reason Polyoma virus was used and its oncogenic effect was studied on the neonatally pinealectomized rats, on rats neonatally thymectomized and on neonatally pinealectomized rats which were simultaneously thymectomized.

Animals↗

PubMed1976

[Somatic hybridization and oncogenesis: induction of tumors in mice by administration of mixtures of cells of the homologous organs and their hybrids].

The 2 months old C57BL/6J mice were injected with the mixtures of kidney and spleen cells from mice of the same strain or of the same cells following the hybridization induced by Sendai virus. The tumours of liver, kidney and lymphoid system appeared in 25% of recipients within 12--14 months. The result obtained is predicted by the general theory of oncogenesis proposed early by L. B. Mekler.

Animals↗

PubMed1978

Suppressive effects on simian virus 40-induced oncogenesis of several immunosuppressive agents and hormonal modifications applied during the latent period.

The long latent period required for tumor induction with Simian virus 40 (SV40) in the subcutis of hamsters can be used to investigate whether host factor(s) participate in oncogenesis. Several treatments were applied during this period, and the results were compared with those of the same treatment applied in another series of experiments, homologous SV40 tumor grafting in hamsters. The results obtained were as follows: (a) the latent period for SV40 tumor induction in the female was shorter than that in the male; tumor development was delayed significantly by oophorectomy but was little affected by orchiectomy. Tumor development was markedly delayed in animals of both sexes by estrone given at birth but was accelerated by testosterone given in the adult male; (b) by each of these hormonal modifications, growth of transplanted SV40 tumors was influenced in a different way from that of tumor induction; (c) immunosuppressive treatments, such as thymectomy, administration of antilymphocyte sera, cyclophosphamide, or cortisone acetate delayed and decreased tumor development when applied in the latent period, and the degree or pattern of this effect varied from one procedure to another, depending on the sex and age of the animals; (d) in contrast, tumor growth was markedly accelerated in thymectomized or cortisone-treated hosts irrespective of sex. The different and almost reverse effect of the same procedure in the two phases of tumorigenesis may indicate two discriminating mechanisms operating in the host during these phases. This different effect may be due to virtual absence of any "mature" neoplastic cell in the latent period, except for a few weeks before the appearance of a palpable tumor. These results suggest that the long period of latency may be spent to complete SV40-induced neoplastic conversion of cells, receiving some help by host factors.

Age Factors↗