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Query: UMLS:C0006142 (breast cancer)
 160,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intermittent implantation of 600--1,300 microgram estriol subcutaneously beginning 48 h before oral administration of 7,12-dimethylbenz(a)anthracene or procarbazine prevents development of 80--90% of carcinomas of the breast occurring during the natural life span of the intact female Sprague-Dawley rat. Some estriol precursors were less inhibitory of breast cancer development among 23 other estrogens and androgens, progestins and glucocorticoids tested. More frequent or lower estriol doses than 100--200 microgram/kg/24 h every 2 months were less inhibitory of breast carcinogenesis. No other types of neoplasms were reduced in incidence by estriol implants, which also reduced uterine weights by 20--25%. Intermittent substitution of estriol for estrone or estradiol in the nuclear receptor complexes of target cells probably accounts for these observations, which resemble the effect of castration in reducing breast cancer incidence. Human studies indicate excellent tolerance for oral estriol doses of 10--200 microgram/kg/24 h, which may correct subnormal estriol/estrone + estradiol urinary quotients associated with elevated risk of breast carcinogenesis in epidemiologic investigations.
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PMID:Clinical and experimental aspects of the anti-mammary carinogenic activity of estriol. 9

A leukocyte migration procedure was utilized to test cellular hypersensitivity of breast cancer patients' leukocytes to autologous and homologous breast cancer tissues and to murine milk containing murine mammary tumor virus (MuMTV). The in vitro responsiveness of the leukocytes and the antigenicity of breast cancer tissues were compared with in vivo prognostically favorable lymphoreticuloendothelial (L-RE) responses seen microscopically at the time of mastectomy and with the results of skin window tests of cellular hypersensitivity. The data suggest that immunogens appear in the in situ phase of the disease and provoke prognostically favorable L-RE responses. These immunogens possess antigenic similarity to some component(s) of MuMTV. Progression of the disease is associated with or preceded by a loss of tissue immunogenicity and/or diminished specific cellular hypersensitivity. The findings are pertinent to investigations of human mammary carcinogenesis and immunoprophylaxis.
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PMID:Prognostically favorable immunogens of human breast cancer tissue: antigenic similarity to murine mammary tumor virus. 16 50

Breast cancer is the result of a multistage carcinogenic process. Initiation, promotion, dependency and autonomy make up a sequence of experimentally distinguishable phases of this process. Progression--the transition from dependency on hormonal support to autonomy--is demonstrable clinically. High-affinity saturatable estrogen binding by breast cancer cytosols distinguishes endocrine-responsive mammary neoplasms from autonomous breast cancers. Approximately 70% of neoplasms containing estrogen-recepor protein at a level of 2.5 femtomoles per mg. protein or higher regress after endocrine ablation (ovariectomy in premenopausal women; adrenalectomy or hypophysectomy in postmenopausal women). Only about 5% of neoplasms lacking the receptor will respond to these maneuvers. Estrogen-receptor content also predicts clinically for estrogen and androgen responsiveness, and experimentally for prolactin dependency. Fifty per cent of primary breast cancers in women are receptor-positive. Normal breast tissue and benign breast lesions characteristically lack receptor protein. The receptor proteins appear to be induced in neoplastic cells during mammary carcinogenesis in endocrinologic settings where non-cancerous breast cells do not contain free receptor in large amounts and fail to manifest endocrinologic growth stimulation. Implications of these findings for endocrinologic management of disseminated mammary cancer, adjuvant therapy, and breast cancer prevention are discussed.
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PMID:Endocrinology in cancer of the breast. Status and prospects. 17 80

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

Cryostat sections of clinicopathologically characterized breast cancer tissues were eluted with phosphate-buffered 0.9% sodium chloride solution, pH 7.2. The proteins were then characterized by polyacrylamide gel electrophoresis with and without prior treatment with sodium dodecyl sulfate. Approximately 65% of the brease cancer tissue eluates contained a prominent protein fraction with a molecular weight of 47,000 to 55,000 (p50). No such component was found in 15 of 17 eluates of benign breast tissue. Charge density studies disclosed that the p50 component included three populations of proteins that could be characterized according to the migration relative to gp55 derived from RIII murine mammary tumor virus, namely, fast (F-p50), intermediate (I-p50), and slow (S-p50). Prognostically favorable pathological characteristics, i.e., stage, nuclear grade, and lymphoreticuloendothelial responses, were proportionately most frequently found among S-p50 bbreast cancers and were least frequently found among F-p50 breast cancers. It appears that the S-p50 component acts in vivo as a prognostically significant immunogen. Further knowledge of the relationship between protein characteristics and clinicopathological features of human breast cancers would contribute to our understanding of mammary carcinogenesis and biological behavior.
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PMID:Prognostically significant protein components of human breast cancer tissues. 18 41

The etiology of cancer resembles that of many other diseases in that multiple factors may be required. Because of this, the role or viruses in the etiology of human cancers is especially difficult to assess. When animal tumor systems were used as models, the roles of various predisposing characteristics in virus oncogenesis were elucidated. Extrapolation of these findings to the human diseases suggests the importance of genetics, age, hormones, immune competence, and stress in determining susceptibility to tumor development in individuals infected with an oncogenic virus. The importance of cofactors in induction of those human tumors most strongly associated with virus infection, including Burkitt's lymphoma, nasopharyngeal carcinoma, cerviccal carcinoma, acute myelogenous leukemia, and breast cancer, is reviewed. Understanding of the role of these cofactors in virus carcinogenesis may lead to disease prevention through elimination of one or more of the cofactors.
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PMID:The viral etiology of cancer: a realistic approach. 19 10

Several pre-malignant diseases are known to have a genetic etiology. This study focuses attention upon precancerous disorders wherein the mode of inheritance is either well established or wherein it remains unclear even though familial aggregation of the particular diseases have been amply documented. These conditions will be discussed as useful models for systematic investigations of the host etiologic component in carcinogenesis. Our survey of hereditary precancerous syndromes includes multiple polyposis of the coli, the multiple mucosal neuroma syndrome, the Cancer Family Syndrome, Sipple's syndrome, Von Recklinghausen's neurofibromatosus, the multiple nevoid basal cell carcinoma syndrome, tuberous sclerosis, familial cutaneous malignant melanoma, and carcinoma of the breast. We have emphasized the heterogeneous character of many forms of familial cancer. Familial breast cancer associations clearly show such heterogeneity, as do colon cancer syndromes. Certain of these precancerous states are characterized by phenotypes which are clinically apparent, polyposis coli being the classic example. Others, such as Sipple's syndrome are amenable to routine screening for biochemical markers. The bulk of putative genetic cancer-predisposing problems require further basic investigation of modes of inheritance. Cancer control may be enhanced through communication of useful genetic and diagnostic information to primary care physicians. Referral of cancer clusters of possible genetic etiology from clinicians to human geneticists facilitates the necessary basic research.
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PMID:Familial cancer syndromes: a survey. 40 22

The effect of Danazol, a synthetic gonadotropin inhibitor, on two groups of Sprague-Dawley rats with dimethylbenze (a) anthracine (DMBA) induced mammary carcinoma was studied. Twenty-four (83%) of 29 control animals developed mammary tumors. Forty-four rats in one treatment group received Danazol after tumor reached 0.5 cm in diameter. Twenty-nine (66%) demonstrated tumor regression (p less than 0.005) and in 16 (36%) tumor disappeared (p less than 0.005). In a second treatment group (given Danazol daily after administration of DMBA), only seven of 50 rats (14%) developed palpable mammary carcinoma (p less than 0.0005). Danazol therapy resulted in regression of established mammary carcinoma in rats, and produced a striking inhibition of carcinogenesis in those animals treated from the time DMBA was administered. Danazol is clinically safe; studies using it in the treatment of breast cancer in women who are candidates for hormonal ablative therapy seem warranted.
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PMID:Danazol therapy in hormone-sensitive mammary carcinoma. 41 78

Two nuclear families showing characteristics of the SBLA syndrome are described wherein progeny of breast cancer-affected mothers manifested early childhood malignant neoplasms. These observations have led us to postulate a novel type genetic-environmental interactive model which incorporates Knudsen's "two-hit" hypothesis as a partial explanation for the exceedingly early onset of cancer in the subject progeny. Given the assumption that the first hit was germinal with transfer of the deleterious SBLA gene at conception, we postulate that the second or somatic-hit occurred early on in utero. This may have involved a complex mechanism of one or more factors including tumor cell products, tumor specific antigens, immunosuppression, de-repressed oncogene, or an activated oncogenic virus via a transplacental communicable phenomenon. The testing of this new hypothesis dealing with carcinogenesis in the SBLA syndrome should employ immunologicalgenetic parameters concurrently in fetuses and mothers.
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PMID:Childhood cancer and the SBLA syndrome. 45 66

The problem of a relationship between nutrition and cancer has to be approached from two different points of view: 1. Direct effect of carcinogens present in foods or in food additives (direct carcinogenesis), 2. In-vivo synthesis of carcinogens caused by changes in metabolism due to altered dietary habits (indirect carcinogenesis). For the second mechanism, we have to make a distinction between the effects of nutritional deficiency and of nutritional excess. Some examples from animal experiments are presented. In man, possible relationships between nutrition and cancer are postulated mainly for tumors of the gastrointestinal tract and recently also for hormone-dependent cancers. Epidemiological evidence points to the major importance of the indirect way of carcinogenesis caused by specific nutritional deficiencies and excesses. Experimental studies in man are difficult to perform. Therefore, most hypotheses are based on statistical associations, and great caution is required in drawing inferences on causal relationships. Cancers of the upper and lower gastrointestinal tract epidemiologically behave in a different way, the former showing a marked decrease in most western countries, the latter a slight increase. The etiology of the cancers of the esophagus and stomach has still to be determined in spite of many hypotheses. Migrant studies show a major effect of environmental rather than genetic factors. Substantial differences in dietary habits between countries with high and low incidence of stomach cancer (Japan and United States) point to the importance of nutrition as an etiological factor with a high probability, but no specific dietary components have been identified so far. The same is true for cancer of the large bowel. Recent hypotheses suggest that dietary factors may relate to cancer of the colon by their effect on bile production and on the bacterial makeup of faeces which in turn might be transforming bile acids into active carcinogens. There is, however, disagreement about the specific dietary component responsible for this model of carcinogenesis. BURKITT stresses the importance of the lower consumption of dietary fiber, resulting in retarded bowel function and additional time for bacterial proliferation and degradation by bacteria of bile acids. WYNDER, on the other hand, explains the increased bile acid and neutral sterol excretion and microbial modification of these compounds with the high content of animal fat in the western diet. With hormone-dependent cancers (breast, endometrium, ovary, prostate), a correlation has been shown between body weight and height and breast cancer as well as between overweight and cancer of the endometrium. Which aspect of diet, if any, is responsible for changes in hormone metabolism, resulting in an increased risk of these cancers, is still to be proved. On the basis of current knowledge, it is extremely difficult to draw inferences for preventive action. Certainly, a cancer-preventing diet cannot be established...
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PMID:[Nutrition and cancer (author's transl)]. 101 38


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