Showing papers on "Carcinogenesis published in 1972"
TL;DR: Leukocytes were active in LAI when taken from animals bearing tumours and after tumour removal, and when the specific tumour antigen was added in the form of a soluble extract.
Abstract: A proportion of peritoneal leukocytes from CBA mice adhered to glass haemacytometer surfaces and withstood a gentle washing. This proportion was reduced with cells taken from mice sensitized to a methylcholanthrene‐induced tumour, when the specific tumour antigen was added in the form of a soluble extract. The reaction of leukocyte adherence inhibition (LAI) may have an immunological basis similar to that of macrophage migration inhibition, but LAI is a much simpler procedure. Leukocytes were active in LAI when taken from animals bearing tumours and after tumour removal. When serum from mice bearing a particular tumour was added to sensitized leukocytes in the presence of the specific tumour antigen, the inhibition of adherence was substantially relieved or blocked. LAI could thus be used to demonstrate both cellmediated immunity to tumours and blocking factors in serum by a brief, simple procedure. A potential application to human tumour immunology is indicated. Copyright
253 citations
TL;DR: This chapter evaluates the available knowledge of simian virus 40 (SV40) oncogenesis and assesses the implications for carcinogenesis by DNA-tumor viruses as a whole and summarizes different tests that can be employed to detect virus-induced changes in SV40-transformed cells.
Abstract: Publisher Summary This chapter evaluates the available knowledge of simian virus 40 (SV40) oncogenesis and assesses the implications for carcinogenesis by DNA-tumor viruses as a whole. It summarizes different tests that can be employed to detect virus-induced changes in SV40-transformed cells. Inoculation of such cells into susceptible hosts usually results in the production of tumors, the ultimate criterion necessary to establish that malignant transformation has indeed occurred. Fusion or cocultivation of the transformed cell with normal susceptible cells may sometimes succeed in the rescue of infectious virus. The optimum conditions required to elicit the production of virus from a majority of the transformed cells have not yet been established. Transformed cells are usually immune to superinfection by the transforming virus. Nucleic acid hybridization experiments indicate that multiple copies of the SV40 genome is present, probably integrated into the host cell chromosome. Virus-specific mRNA is present in the transformed cells. The extent of the transcription of the viral genome seems to vary from one transformed cell line to the next. No relationships have been established between the extent of transcription in a given transformed cell line and the number and/or magnitude of virus-specific changes of that cell line. A series of in vitro tests may detect a variety of surface changes on the transformed cells. These tests include immunofluorescence, agglutination, cytotoxicity, colony inhibition, and mixed hemadsorption.
112 citations
TL;DR: Rats immunized with syngeneic urinary bladder papillomas, then challenged with a methylcholanthrene pellet inserted into the bladder, develop (4 to 6 months later) fewer primary bladder tumors than rats immunizing with normal bladder tissue.
Abstract: Human neoplasms derived from the same tissue have been previously shown to have tumor associated antigens characterizing that tissue type. Evidence is now presented for the existence of analogous antigens common to both rat bladder papillomas and carcinomas, and for antigens common to mouse bladder carcinomas. Rats immunized with syngeneic urinary bladder papillomas, then challenged with a methylcholanthrene pellet inserted into the bladder, develop (4 to 6 months later) fewer primary bladder tumors than rats immunized with normal bladder tissue.
91 citations
TL;DR: Although it remains to be shown whether DNA methylation is related to the initiation of cancer, the data presented are consistent with the hypothesis that cytoplasmic mutations are involved in carcinogenesis.
74 citations
TL;DR: Some of the proliferative properties of normal and malignant mammalian cell systems will be briefly discussed in relation to problems of tumour growth (including a few questions of cancer therapy and carcinogenesis).
Abstract: The molecular processes associated with DNA replication and cell division, the mechanisms responsible for the regulation of cell proliferation, and the kinetic analysis of cell proliferation in simple and complex systems are topical problems of current research in cell biology. Their fundamental importance for many aspects of cancer research need not be stressed. In the following, some of the proliferative properties of normal and malignant mammalian cell systems will be briefly discussed in relation to problems of tumour growth (including a few questions of cancer therapy) and carcinogenesis. General Aspects
72 citations
TL;DR: In his analysis of the literature on radiation cancerogenesis, the author suggests that all malignancies may be stimulated by irradiation and all types of radiation may be cancerogenic.
Abstract: In his analysis of the literature on radiation cancerogenesis, the author suggests (subject to further study) that (a) all malignancies may be stimulated by irradiation; (b) all types of radiation may be cancerogenic; (c) the risk is about 1-5 cases per million population per year per rad absorbed in relevant tissue for several sites; (d) the excess is manifested some limited number of years following a latent period (shorter for leukemia than for other malignancies; (e) chronic lymphatic leukemia is an apparent exception to the generality concerning all malignancies; and (j) fetal tissue may be several times more sensitive. Relatively high doses of radiation are either noncancerogenic or follow a different quantitative relationship from that seen at low doses.
36 citations
TL;DR: The data suggest that viral and non‐viral carcinogens induce malignancy by inducing chromosome re‐arrangements that result in a change in the balance between E and S.
Abstract: Malignant cell transformation and its reversion, in cells transformed after treatment with the chemical carcinogen dimethylnitrosamine, are controlled by the balance between chromosomes that determine the expression (E) of malignancy and those that determine its suppression (S). Malignancy is due to a change in chromosome balance so as to produce an excess of E over S. The chromosome groups that contain these two types of chromosomes have been identified as the same groups that determine the expression and suppression of malignancy in cells transformed by polyoma virus. The balance between these two types of chromosomes also controls the resistance of cells to treatment with 5-bromodeoxyuridine and visible light. The data suggest that viral and non-viral carcinogens induce malignancy by inducing chromosome re-arrangements that result in a change in the balance between E and S.
33 citations
TL;DR: The criteria usually accepted for a diagnosis of radiation cancer are: a history of previous irradiation, a cancer occurring within the irradiated area, gross tissue damage due to an excessive dose of radiation, and a long latent interval between irradiation and development of cancer.
Abstract: The criteria usually accepted for a diagnosis of radiation cancer are: (1) A history of previous irradiation. (2) A cancer occurring within the irradiated area. (3) Gross tissue damage due to an excessive dose of radiation. (4) A long latent interval between irradiation and development of cancer. The first two conditions are of course essential but the concept that radiation tumours develop only in tissues which have suffered gross radiation damage is open to dispute. It originated from the observation that radiation cancer of the skin typically occurs in an area of radiation dermatitis. It is true, for example, that in most cases of radiation-induced cancer of the pharynx the skin shows marked post-radiation damage as a result of treatment given many years ago for thyrotoxicosis or tuberculous glands. Yet the radiation dose delivered to the pharynx was probably considerably less than the dose to the skin and was therefore unlikely to have produced changes in the mucosa of the pharynx comparable to those ...
24 citations
TL;DR: Many resemblances exist between cell differentiation and neoplastic change: the importance of cytoplasmic factors is particularly evident, as the genotype appears to remain unmodified in the nuclei of differentiated as in malignant cells.
Abstract: Many resemblances exist between cell differentiation and neoplastic change: the importance of cytoplasmic factors is particularly evident, as the genotype appears to remain unmodified in the nuclei of differentiated as in malignant cells.
There is no opposition between malignancy and differentiation, highly malignant cells retaining in many cases a differentiation very close to normal. Loss of differentiation in malignancy is only an epiphenomenon.
While differentiation appears to be partially reversible, and in some models totally reversible, neoplastic changes are, with a very small number of exceptions, irreversible. Differentiation involves the gradual change of a group or a population of cells, malignancy of a single cell.
Further work on the molecular basis of differentiation would help to understand the nature of neoplasia, and vice versa.
17 citations
TL;DR: It is concluded that the liver-N-demethylating enzyme activity governs (a) the rate of methylation of liver DNA, and (b) the amount of systemic DMNA available for metabolic demethylation and DNA methylation in lung and kidney.
17 citations
Journal Article•
TL;DR: These studies confirm earlier findings, which suggested that the gs antigen expression induced in tumors is dependent on host-regulatory controls and that such controls of virogene and oncogene expressions of C-type RNA viral genome are independently affected by a carcinogen.
Abstract: The effect of various doses of 3-methylcholanthrene on s.c. tumor induction and the occurrence of the murine C-type RNA group specific ( gs ) viral antigen in tumor tissue were studied in weanling mice of 8 genotypically different strains. Tumor incidence was found to be related to the dose of 3-methylcholanthrene. On the other hand, the incidence of gs antigen in the induced tumors was independent of the dose of 3-methylcholanthrene and reflected the natural gs antigen expression of the mouse strain. Histopathological examination showed no relation of tumor type to carcinogen dosage or mouse strain. The majority of the tumors examined were sarcomas. These studies confirm earlier findings, which suggested that the gs antigen expression induced in tumors is dependent on host-regulatory controls and that such controls of virogene ( gs antigen) and oncogene (tumor induction) expressions of C-type RNA viral genome are independently affected by a carcinogen.
TL;DR: Liver tumors were induced in mice by neutron irradition followed by a dose of CCl4 and the relation between tumor induction and neutron dose was found to be linear at low doses.
Abstract: Liver tumors were induced in mice by neutron irradition followed by a dose of CCl4. The relation between tumor induction and neutron dose was found to be linear at low doses. This is interpreted to mean that although the tumor-induction process requires two or more independent events, only one of these can be considered a mutation. This result may or may not be applicable to other tumor systems.
TL;DR: The mechanism by which both donor and host alleles remain close to each other in the same genome and alternately are expressed may help to elucidate other problems in the areas of differentiation and oncogenesis.
Journal Article•
TL;DR: The attempt to review the extent to which drugs are known to induce cancer in humans focus is on radioactive drugs immunosuppressive drugs and chlornaphazine alkylating agents analgesic drugs containing phenacetin diphenylhydantoin (Dilantin) and coal tar and creosote preparations.
Abstract: In the attempt to review the extent to which drugs are known to induce cancer in humans focus is on radioactive drugs immunosuppressive drugs and chlornaphazine alkylating agents analgesic drugs containing phenacetin diphenylhydantoin (Dilantin) and coal tar and creosote preparations. Radioisotopes represent a special category of drugs in which carcinogenic properties are due to ionizing radiation at the site of deposition in the body. Although antilymphycyte serum antimetabolites and corticosteroids are not true carcinogens in that they are initiators of malignant disease these agents do seem to contribute to a high rate of cancer in patients receiving organ homografts by suppressing immune defenses that would ordinarily limit the progression of initiated cells. Chlornaphazine used in the treatment of polycythemia vera and Hodgkins disease was withdrawn in 1964 when high doses were found to cause bladder tumors. Alkylating agents also used primarily in the treatment of cancer are nearly always carcinogenic in laboratory animals. Far less conclusive is the evidence that other drugs are carcinogenic in humans. The evidence for occupational cancer is considerably more extensive than that in drug-induced cancer in humans. In contrast to animal studies it may be that in humans the doses are too small or too briefly given the latent period for carcinogenesis is longer than the interval of observation or confounding variables prevent easy recognition of relationships.
TL;DR: The relation of an oncogenic virus to breast cancer and the role of reverse transcriptase in tumor viruses were thoroughly discussed at the conference.
Abstract: An international conference on mammary neoplasia sponsored by the Institute for Medical Research and the National Institutes of Health was held in Cherry Hill New Jersey on November 11-13 1971. 2 reports given focused on the genetic aspects of breast cancer. Bulbrook reported on the urinary steroid excretion patterns in women while Brennan and Wolfe studied the usefulness of xeroradiography in detecting ductal hyperplasia. Paymaster reviewed the epidemiology of breast cancer in India while Ozzello suggested that human breast cancer cells may perform a variety of synthetic and secretory activities. Sarkar suggested that there may be a connection between human breast cancer and RNA viruses and Dalton presented the ultrastructural detail of the mouse feline and human RNA virus. Nandi discussed his recent studies which attempt to locate the mammary tumor virus activity in blood. Concerning tissue and organ culture Lasfargues outlined a new method of growing human breast cancer cells in suspension cultures. Concerning immunology and interferon Blair attempted to elucidate the observation that immunodepression depressed MTV-induced mammary tumor development. Studies have shown striking regression of spontaneous breast cancers in animals following the administration of interferon inducers. Although the role of specific RNA viruses in the oncogenesis of many animal tumors is widely accepted the exact genetic mechanisms by which the viral RNA is expressed causes malignant transformation in the intact animals are not clear. The recent discovery of the enzyme reverse transcriptase and the subsequent demonstration that it is an integral part of all RNA tumor virions has opened a new field of investigation. Spiegelman Schlom Gallo and Temin all reported on it. Muhlbock reported on the influence of prolactin and estrogen on breast cancer as did Meites and Pearson. Thus the relation of an oncogenic virus to breast cancer and the role of reverse transcriptase in tumor viruses were thoroughly discussed at the conference.