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

Incidence of breast cancers in Japanese women is increasing steadily. Mass screening of breast cancer was started in Japan under auspices of Adult Health Promotion Act of the Japanese Government from 1987. As the first screening method, the palpation of breasts is employed at present, but it is expected to be replaced by the mammography. In this report, the risk-benefit analysis is presented between risk of breast carcinogenesis due to radiation and benefit of mass screening of breast cancer. The benefit of mass screening is taken as the net elongation of average life expectancy of women due to survival from breast cancers. The risk of mammography is taken as the net loss of average life expectancy of women due to breast carcinogenesis. In the latter, the latency time and plateau period of radiation carcinogenesis were taken into consideration in the calculation. The results show that the ages at which the benefit and risk become equal are between 30 and 35 years old when dose equivalent of mammography is between 10 and 20 mSv, that are conventionally used. However, the critical age will be reduced to 20 years old if the dose equivalent becomes 1 mSv. Therefore, it is strongly recommended that a low dose mammographic system should be developed in order to achieve 1 mSv for the mass screening of breast cancer of Japanese women. In author's opinion, this is quite feasible by employing a new digital radiography with imaging plate.
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PMID:[Risk-benefit analysis for mass screening of breast cancer utilizing mammography as a screening test]. 258 91

The fatty acid composition of fractionated phospholipids and neutral lipids was analyzed in human breast cancer tissues and the surrounding, apparently healthy tissue. In the cancer tissues the relative amounts of unsaturated fatty acids were increased in all the phospholipid subclasses analyzed. The differences were more marked in phosphatidylethanolamine than in the other phospholipid fractions and, furthermore, the relative amount of phosphatidyl-ethanolamine was increased in cancerous tissue. In blood-erythrocyte phospholipids, no differences in fatty acid composition could be found between breast cancer and control patients. The present study suggests that the lipid composition of cancerous breast tissues differs from that of the surrounding tissue and may be involved in carcinogenesis.
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PMID:Phospholipids and fatty acids in breast cancer tissue. 260 32

int-2 is a proto-oncogene that is partially homologous to angiogenesis-inducing fibroblast growth factor and is believed to play a role in mouse mammary carcinogenesis. Recent evidence has suggested that this proto-oncogene may also play a role in human breast cancer. In the present study, we used Southern hybridization analysis to examine DNA from 79 primary and 11 recurrent human breast cancers for evidence of activation of int-2 through either gene rearrangement or amplification. A similar analysis was performed for two other proto-oncogenes, c-erbB-2 and c-myc, also suspected of playing a role in the development of human breast cancer. Proto-oncogene status was correlated with estrogen (ER) and progesterone (PR) receptor status, patient age, and lymph node (LN) status at the time of surgery. Gene rearrangement was not a frequent occurrence with any of the proto-oncogenes. However, amplification of int-2 occurred at a significantly higher frequency in recurrent breast cancers than in primary cancers and in patients with primary cancers who were less than or equal to 50 years of age versus greater than 50 years of age at surgery. Although amplification of all three proto-oncogenes occurred at a greater frequency in primary tumors from patients with lymph node metastases than from those without lymph node metastases, a significant difference was noted only in the case of c-myc amplification. These findings confirm and extend earlier results of studies of int-2, c-erbB-2 and c-myc amplification in human breast cancers and point to a role for int-2 activation in certain cases of recurrent breast malignant neoplasia.
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PMID:Amplification of the proto-oncogenes int-2, c-erb B-2 and c-myc in human breast cancer. 261 95

Pro-cathepsin D is overexpressed in breast cancer cells compared to normal mammary epithelial cells. Moreover, its processing and maturation are altered resulting in increased secretion. In estrogen-responsive breast cancer cell lines such as MCF7 cells and ZR75-1 cells, the 2.2-kb cathepsin D mRNA is accumulated specifically by estrogens and growth factors. Estrogen regulation is mostly transcriptional, while growth factors stabilize the mRNA and act indirectly. In estrogen-receptor-negative cell lines, there is a constitutive high production of cathepsin D mRNA. Moreover in uterine cells, progesterone is the inducer rather than estrogen, indicating the complexity of regulation by steroids, depending on the tissue. The increased production of cathepsin D appears to be correlated with the aggressiveness of the tumour, as shown by retrospective clinical studies, suggesting a role in mammary carcinogenesis.
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PMID:Overexpression and hormonal regulation of pro-cathepsin D in mammary and endometrial cancer. 262 16

The present study investigated the relation between the reproductive activity and the risk for cervical and endometrial cancers using both domestic and international materials. An association of increased risk for cervical cancer (C) with fertility at the levels of both an individual and a population was contrasted to another association of increased risk for endometrial cancer (E) with infertility at the same two levels. Both C and E patients experienced a delay of menstrual cycle (over 30 days) at high incidences (35-49%), whereas healthy controls and breast cancer patients were essentially free from such menstrual delay. The possible impact of the above hormonal characteristics of C and E patients on uterine carcinogenesis is discussed in the light of comparative endocrinology.
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PMID:Reproductive activity is a magic spell to connect the genesis of cancers of the uterine cervix and endometrium. 262 38

Despite extensive research, there is still uncertainty on the separate effects of parity and age at first birth on breast cancer risk. Thus, information on these variables from formal epidemiological articles published in English since 1970 is reviewed in the present article. Among 26 studies considered, one found no significant association with either variable, seven showed an association between age at first birth but not parity and breast cancer risk, six an association with parity but not age at first birth, and in twelve studies both variables appeared to be independently related with breast cancer risk. Various reasons for these apparent differences can be considered, including heterogeneity between various populations (for instance, the proportion of multiparous women in studies showing no association with parity tended to be higher than in studies finding an inverse relation with parity), criteria for selection of cases and controls, influence of age and other covariates (among which the interval between pregnancies is of particular interest) and, of course, the role of chance. The data reviewed suggest, from an aetiological viewpoint, that both parity and age at first birth have some independent effect on breast carcinogenesis. From a public health viewpoint, however, it appears that the importance of age at first birth is greater, since the trend is linear across subsequent age levels, while the protection of parity seems to be quantitatively relevant only for women with four or five births or more.
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PMID:Reproductive factors and breast cancer: an overview. 267 12

Although the important influence of a woman's reproductive history on her risk of breast cancer is widely recognized, it is not clear whether this is wholly accounted for by the age at her first full-term pregnancy, or whether there are additional, independent influences of breastfeeding or number of children. To examine the respective contributions to the risk of breast cancer of these reproductive factors, we used logistic regression methods to analyze data from a multicenter case-control study, the Cancer and Steroid Hormone Study. Included in the analysis were 4599 women, 20-55 years of age, identified as having an initial diagnosis of breast cancer by one of eight collaborating population-based cancer registries. The 4536 controls were women of similar ages selected by random dialing of households with telephones in the same eight areas. As expected, age at first full-term pregnancy exerted a strong influence on the risk of breast cancer. However, after it and other potentially confounding factors had been controlled for, parity and duration of breastfeeding also had a strong influence on the risk of breast cancer. Compared with women of parity one, women of parity seven or greater had an adjusted relative risk of breast cancer of 0.59 (95% CL, 0.44-0.79). Compared with parous women who never breastfed, women who had breastfed for 25 months or more had an adjusted relative risk of 0.67 (0.52-0.85). These results do not support the supposed preeminent importance of age at first full-term pregnancy among the reproductive determinants of breast carcinogenesis. Resolution of this issue may have important implications for elucidating hormonal influences on breast cancer and for projecting future trends in the disease.
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PMID:The independent associations of parity, age at first full term pregnancy, and duration of breastfeeding with the risk of breast cancer. Cancer and Steroid Hormone Study Group. 268 48

Experiments were carried out in mice demonstrating that dietary carotenoids (beta-carotene or canthaxanthin), starting before cancer initiation and continuing throughout the experiment, have a protective effect against indirect skin carcinogenesis induced by benzo[a]pyrene +/- UVA and breast cancer induced by 8-methoxypsoralen + UVA. Experiments in rats demonstrated that carotenoids also prevent the direct gastric carcinogenesis induced by N-methyl-N'-nitro-nitroso-guanidine. Recently, prevention by beta-carotene against colon cancer induced in mice by dimethylhydrazine, another indirect carcinogen, was confirmed by others. The prospects for carotenoid intervention with humans were based on their antitumorigenic effect, which is quite independent of pro-vitamin A activity, their lack of toxicity even after prolonged administration, and their immunostimulating activity. These facts helped to build up a rationale predicting that any epithelial cancer, after radical surgery, can be chemoprevented with supplemental carotenoids. Thus, it is expected that the remaining initiated epithelial tissue will be protected by quenching oxygen radical formation, against the onset of a second primary malignancy. This type of prevention can be envisaged in organs like the lung, urinary bladder, breast, stomach, and colon-rectum. At present, human intervention protocols with a randomized drug/placebo method are underway under the supervision of the Centro Tumori of Pavia to chemoprevent with beta-carotene second primary lung or bladder cancer after radical surgery. Preliminary observations regarding findings in humans without randomization (1980-1988) in Pavia are also reported here. This consisted of chemoprevention with beta-carotene plus canthaxanthin against recurrence of different epithelial malignancies after radical treatment (surgery +/- chemoradiotherapy). None of the 11 cases recruited, on the basis of radical nature of treatment and patient adherence, have shown any recurrence beyond their expected disease-free intervals.
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PMID:Cancer chemoprevention by supplemental carotenoids in animals and humans. 269 58

In this presentation we review information highlighting the multiple roles of both steroidal and polypeptide regulators of mammary epithelial cell growth with some additional emphasis on the work of our laboratory. The effects of both classes of hormones are complex and involve multiple interactions with epithelial components (malignant or normal) and the stromal compartment. Estrogens induce growth regulatory polypeptide growth factors which are responsible for many of the induced phenotypic effects in hormone-dependent breast cancer. Progression of hormone-dependent breast cancer to hormone independence probably involves multiple genetic mechanisms of oncogene activation, loss of the estrogen receptor, or loss of hormone responsivity of other gene products. Initial carcinogenesis and progression of mammary epithelium to cancer probably also requires both proliferative stimuli (estrogen, polypeptide growth factors) and genetic damage, leading to qualitatively different hormonal responses (hormone responsive cancer). New therapeutic strategies based on these biological considerations are emerging, including a variety of approaches which interfere at multiple points with ability of ligand to induce receptor signaling.
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PMID:Mechanisms of normal and malignant breast epithelial growth regulation. 269 41

Protein kinase C (PKC) is composed of a family of isozymes that transduce signals of certain hormones, growth factors, lectins, and neurotransmitters. This review addresses the role of PKC in the regulation of cellular proliferation and its disorders. PKC is directly activated in vivo by the second messenger diacylglycerol, a lipid produced by phospholipase C-catalyzed hydrolysis of phosphatidylinositol and polyphosphoinositides. Diacylglycerol activates PKC by reducing the enzyme's requirement for Ca2+. Phorbol ester tumor promoters and related agents potently activate PKC by a mechanism analogous to that of diacylglycerol, providing evidence that PKC activation is a critical event in tumor promotion. However, the role of PKC activation in tumor promotion is not entirely clear. For example, bryostatin is a potent PKC activator that antagonizes phorbol ester-mediated tumor promotion, and mezerein is a second-stage tumor promoter that potently activates PKC. In addition to studies concerned with tumor promotion, studies of oncogene action also indicate a role for PKC in carcinogenesis. A number of plasma membrane-associated oncogene products and related proteins are PKC substrates, and PKC activation leads to induction of the expression of oncogenes that code for nuclear proteins. PKC is implicated in human breast and colon carcinogenesis. Tumor-promoting bile acids activate PKC, and PKC expression studies in rat colonic epithelial cells and human breast cancer cells indicate a positive role for PKC in the proliferation of the cells. Altered expression of PKC in human colon and breast tumors indicates that PKC isozymes may be useful markers for these diseases.
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PMID:Biology of the protein kinase C family. 269 70


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