Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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?
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PMID:Somatic hybridization and oncogenesis; (Mechanism of formation of malignant tumors and metastases by the action of antilymphocytic serum). 16 99

In vivo and in vitro studies bearing on tumor-specific and viral-associated antigenicity of human breast carcinomas were reviewed with particular attention to the following clinical considerations: (a) breast carcinomas arise in a nonrandom fashion; (b) in situ carcinomas precede invasive breast carcinomas; (c) invasive breast carcinomas behave in a heterogeneous fashion. Microscopically demonstrable lymphoreticuloendothelial responses, skin window tests, and leukocyte migration tests all indicate that tumor-specific antigenicity develops in assoication with the early phases of mammary carcinogenesis. Such antigenicity is maximally expressed in in situ carcinomas without associated invasive breast cancer and minimally in invasive breast cancers with metastases. Immunogenic breast cancer tissues commonly contain a protein component the antigenic and physicochemical properties of which are similar to those of a protein component of murine mammary tumor virus. Advances in our understanding and control of human mammary carcinogenesis and biological behavior are dependent on the clinicopathological characterization of individual patients and their breast tissues as well as on the analytical procedures used.
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PMID:Biological considerations of tumor-specific and virus-associated antigens of human breast cancers. 17 36

The role of the kidneys in hepatic carcinogenesis was studied in inbred Buffalo strain male rats ingesting 0.04% N-4-(4'-flourobiphenyl) acetamide in the diet. Experimental groups were made up of male rats with both kidneys intact and male rats with the left kidney removed. The incidence of carcinomas of the liver and the number of rats with large carcinomas, multiple carcinomas, poorly differentiated and undifferentiated carcinomas, and metastases were greater in rats with a uninephrectomy. Apparently the animals with one kidney removed were unable to secrete the metabolites of N-4-(4'-fluorobiphenyl) acetamide as readily as the rats with both kidneys.
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PMID:Increased susceptibility to carcinoma of the liver in rats with one kidney ingesting N-4-(4'-fluorobiphenyl) acetamide. 18 8

Outbred Osborne Mendel, Japanese, Wistar, NIH Black, and Sorague-Dawley male rats 12 weeks of age ingested 0.025% N-2-fluorenyldiacetamide in a semisynthetic diet Sprague-Daeley and NIH Black male rats were most susceptible to the development of carcinomas and cirrhosis of the liver and also had the highest incidence of metastases. More and larger carcinomas per liver and more poorly differentiated and undifferentiated carcinomas were found, as well as more advanced cirrhosis, Japanese and Wistar male rats were susceptible, but less so, to hepatic carcinogenesis and cirrhosis. These rats had fewer and smaller hepatic carcinomas per liver, and the neoplasms were well differentiated. By contrast, Osborne Mendel male rats were least susceptible to hepatic carcinogenesis and cirrhosis.
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PMID:Various degrees of susceptibility of different stocks of rats to N-2-fluorenyldiacetamide hepatic carcinogenesis. 18 58

The ESR method was employed to study the distribution of the coordinative paramegnetic centers on the energy chain of electron transport and on the detoxifying system during carcinogenesis caused by a disturbance of the normal hormonal balance in the organism and at the tumour regression stage achieved with estrogen - in tumours of the ovary, spleen, liver and adrenals. At various stages of the hormonal carcinogenesis and under hormonal control both quantitative and qualitative changes on the paramagnetic centers were found. The tumour growth on liver and adrenals lowers the level of the catalytic form of the cytochrome P-450 and of the non-heme iron complexes. In metastases of ovarian tumours the kinetics of the triplet signal development is registered. In the tumour and on the liver an antibate change of the intensities of the signal was observed with g-factors of 2,1 and 2,15. At the tumour tissues a shift of the g-factor of free radicals was found - from g=2.005 to g=2.000. When a complete regression of tumours occured under hormonal balance control, the characteristics of the ESR spectra on the liver and adrenals restores to their values on intact tissues.
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PMID:[Coordinative paramagnetic enzyme centers during hormonal carcinogenesis and tumor regression under conditions of hormonal regulation]. 19 Oct 93

The lesions that appear during hepatocarcinogenesis can be separated into morphologically distinct entities, which have been arranged into sequences believed to represent stages in carcinogenesis. Similarly, the primary and transplantable hepato-cellular carcinomas (HCC) can be arranged into a sequence of stages believed to represent the progression toward the ultimate cancer cell. Separation of morphological entities has been most successful in rat liver. Ultrastructural studies differentiate between lesions derived from hepatocytes and those originating in other cellular components of the liver. They show that there is variability and divergence in the structure of cellular organelles in the early stages of carcinogenesis, that there is simplification of cellular structure and of organelles during the progression of HCC, and that qualitative changes specific for cancer cells do not exist. Toxic changes associated with the process of carcinogenesis are loss of stacks; wrapping of cisternae around mitochondria; dilation, denudation, and vesiculation of cisternae; increase of autophagy; depletion of glycogen, and enlargement of nuclei and nucleoli. Early changes are storage of glycogen and hyperplasia of smooth endoplasmic reticulum. Subsequent alterations are increased variability in the size, shape, and structure of mitochondria and in the structure of endoplasmic reticulum, including the appearance of fingerprints. A transient stage recognizable by storage of lipid may represent a degenerative process. Ultrastructural characteristics of basophilic cells such as abundance of free ribosomes and absence of glycogen and of smooth endoplasmic reticulum suggest that they may be a stage in the formation of HCC. Progression of HCC is associated with a decrease in the number and size of mitochondria, reduction of mitochondrial cristae, decrease in the number and complexity of microbodies, reduction of the tubulovesicular form of smooth reticulum, accumulation of free ribosomes, and increase of the granular component and condensation of the fibrillar component of nucleoli. Various types of nuclear inclusions reflect the increased mitotic rate of the neoplastic tissue. Changes of the cellular surface are believed to be associated with the ability of the cells to invade and metastasize. Future investigations will require the use of single doses of potent carcinogens, application of morphometric methods at the ultrastructural level, and acceptance of primates as models for human hepatocarcinogenesis.
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PMID:Ultrastructure of hepatocellular tumors. 22 4

Saccharin is carcinogenic for the urinary bladder in rats and mice, and most likely is carcinogenic in human beings. The neoplasms of the urinary bladder are malignant and invade and metastasize. Male rats are more susceptible to urinary bladder carcinogenesis than female rats. Rats exposed as fetuses develop neoplasms more readily than rats exposed as weanlings. The lesions in the urinary bladder go through the stages of hyperplasia, hyperplastic nodules, and later carcinomas. The male of the human species ingesting saccharin, as for rats, is more susceptible to carcinogenesis of the urinary bladder than the female. Neoplasms of the urinary bladder in rats were not caused by stones, parasites, sodium, or impurities. There is a cocarcinogenic effect between saccharin and methylnitrosurea for the urinary bladder. Even through carcinomas of the urinary bladder are present in rats given the higher doses of saccharin, one was observed in a female rat given 0.5%. Chronic renal disease develops in rats ingesting saccharin. The disease is more advanced at the lower doses than at the higher doses, suggesting that saccharin at the lower doses does not reach the urinary bladder. Early neoplasms are seen in the renal pelvis of rats given the higher doses of saccharin. The risk ratios for urinary bladder carcinomas in human beings increase with both frequency andduration of saccharin usage. Benign and malignant neoplasms at all sites are significantly increased in mice and rats ingesting the higher doses of saccharin. These neoplasms are present in the reproductive and hematopoietic systems, and to a lesser extent in the lungs, vascular system and squamous epithelium. Neoplasms in some organs develop with the lower doses of saccharin. Lymphosarcomas of the lung are significantly increased in rats given 0.01% saccharin. Chronic renal disease in rats given saccharin interferes with the health and life span and consequently with development of neoplasms. Saccharin initiates neoplasms of the skin when its application is followed by croton oil. Epidemiological studies have not been done for neoplasms other than the urinary bladder in human beings.
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PMID:Carcinogenicity of saccharin. 36 8

A series of studies pertaining to perinatal carcinogenesis have been reviewed. Their main objective was development and definition of a sensitivity biologic model for carcinogenicity screening. Data were summarized on factors modifying the carcinogenic response of various tissues following transplacental, neonatal-infant, or adult exposure of (B57BL/6J X C3HeB/FeJ)F1 mice to a single administration of ENU. In addition, tumor response of mice treated during specific perinatal age periods with DEN, BP, aflatoxin B1, benzidine . 2HCl, DDT, dieldrin, and safrole were analyzed. The results revealed that the age of the animals at the time of carcinogenic exposure has been the most effective modulator of carcinogenesis in liver, lung, stomach, ovary, and lymphoreticular tissues. Infancy proved to be the most susceptible period to carcinogenesis as demonstrated by a great variety of tissues that responded to treatment and the incidence of tumors which developed. Depending on the nature of carcinogen, variation in organ sites undergoing carcinogenesis was considerable, apparently due to difference in their enzymatic competence to activate and metabolize the agent. Thus a single treatment with ENU, a spontaneously activated type of procarcinogen, induced 59 primary types of tumors in 22 tissues. In contrast, treatment of infants by procarcinogens requiring enzymatic activation led to development of tumors only at a limited number of tissue sites. However, regardless of the type of carcinogen used, the liver consistently responded with development of tumors. Detailed morphologic and biologic evaluations of the induced liver tumors demonstrated in addition to the benign neoplastic variety, the presence of the frank malignant tumors. The character of tumors was dependent not only on carcinogenicity of the agent used but also on the age of mice at the time of carcinogenic treatment. Perinatally induced primary liver tumors showed greater tendency to metastasize and were more readily transplantable into an isogeneic host than those induced at later age periods. Data showed the advantage of prenatal and/or postnatal treatment in combination of life-long exposures to test agents as a more sensitive bioassay system in comparison with solely postweaning treatment. Because the early age period is the most sensitivity life phase to carcinogenesis, it appears to be a good model for prescreening various potential carcinogens, especially when only small amounts of test substances are available. The importance of the proper relationship of such bioassay to the other test systems regarding assessment of potential human risk has been emphasized.
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PMID:Neoplastic response of mouse tissues during perinatal age periods and its significance in chemical carcinogenesis. 38 63

We find that colonic adenocarcinoma, which is an extremely rare neoplasm of all animals except man and carcinogen-treated rodents, occurs spontaneously in some marmosets. The cotton-topped Saguinus oedipus oedipus is particularly prone to develop it, but we have found it also at necropsy in Callimico goeldii (Goeldi's marmoset). Numerous metastases to regional lymph nodes develop. The cancers arise de novo in the mucosa and early invade the submucosa and lymphatic apparatus and paracolonic lymph nodes. These findings and the continuing occurrence of this cancer in our colony suggests that the marmoset may be the long-sought primate model for experimental intestinal carcinogenesis.
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PMID:Spontaneous colonic adenocarcinoma in marmosets. 41 16

Six hundred patients with primary differentiated thyroid carcinoma had follow-up studies for a minimum of 15 years and a maximum of 45 years. Recurrence rate and death rate were significantly different in defined high-risk and low-risk groups of patients. These basic risk groups were defined by age and sex alone; low risk consisted of men 40 years of age and younger and women 50 years of age and younger whereas the high-risk group were older patients. Recurrence and death rates in patients at high risk were 33% and 27% while respective figures for patients at low risk were 11% and 4%. In more recent years these results have shown significant improvement. Basic risk group definition outweighed the effect of pathologic type, local disease extension, type of treatment, and site of recurrence or metastasis. For instance, radioactive iodine cured 70% of patients at low risk with metastatic disease but only 10% of patients at high risk. Less aggressive biologic behavior of thyroid cancer before the age of menopause implies that an estrogen-rich milieu may alter the effects of initiating and promoting factors in carcinogenesis. It also suggests that therapeutic trials of estrogen be undertaken in progressive metastatic differentiated thyroid cancer.
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PMID:Risk factor analysis in differentiated thyroid cancer. 42 22


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