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1. Roger P, Daures JP, Maudelonde T, Pignodel C, Gleizes M, Chapelle J, Marty-Double C, Baldet P, Mares P, Laffargue F, Rochefort H: Dissociated overexpression of cathepsin D and estrogen receptor alpha in preinvasive mammary tumors. Hum Pathol; 2000 May;31(5):593-600
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  • The role of estrogen as a promoter agent of sporadic breast cancer has been considered by assaying, in benign breast disease (BBD) and in situ carcinomas (CIS), 2 markers, the estrogen receptor alpha (ERalpha) and cathepsin D (cath-D) involved in estrogen action on mammary tissue.
  • ERalpha and cath-D were assayed by quantitative immunohistochemistry using an image analyzer in 170 lesions of varying histological risk (94 BBD and 76 CIS), and in "normal" glands close to these lesions.
  • The ERalpha level increased significantly in proliferative BBD with atypia (P < .001), in non-high-grade CIS (P < .001), and in adjacent "normal" glands.
  • ERalpha level was decreased in high-grade ductal CIS (DCIS) and also in adjacent "normal" glands.
  • Cath-D level increased in ductal proliferative BBD (P < or = .01) and in high-grade DCIS (P < or = .003), but not in the other lesions.
  • According to Mac Neman test, the high-grade DCIS were predominantly ERalpha negative and cath-D positive (P = .0017), and the other CIS were predominantly ERalpha positive and cath-D negative (P = .0002).
  • We propose that ERalpha-negative breast cancers may develop directly from high-grade DCIS and that ERalpha assay in preinvasive lesions should be considered in prevention trials with antiestrogens.
  • [MeSH-major] Breast Neoplasms / metabolism. Carcinoma in Situ / metabolism. Carcinoma, Ductal, Breast / metabolism. Carcinoma, Lobular / metabolism. Cathepsin D / metabolism. Receptors, Estrogen / metabolism

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  • (PMID = 10836299.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Estrogen Receptor alpha; 0 / Receptors, Estrogen; EC 3.4.23.5 / Cathepsin D
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2. Foote MR, Giesy SL, Bernal-Santos G, Bauman DE, Boisclair YR: t10,c12-CLA decreases adiposity in peripubertal mice without dose-related detrimental effects on mammary development, inflammation status, and metabolism. Am J Physiol Regul Integr Comp Physiol; 2010 Dec;299(6):R1521-8
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  • The trans 10, cis 12-conjugated linoleic acid (10,12-CLA) isomer reduces adiposity in several animal models.
  • Moreover, 10,12-CLA was recently shown to promote mammary ductal hyperplasia and ErbB2/Her2-driven mammary cancer in the mouse.
  • The 0.5% dose reduced ductal elongation and caused premature alveolar budding.
  • [MeSH-major] Adiposity / drug effects. Basal Metabolism / drug effects. Inflammation / chemically induced. Linoleic Acids, Conjugated / pharmacology. Mammary Glands, Animal / drug effects
  • [MeSH-minor] Adipose Tissue / drug effects. Adipose Tissue / metabolism. Administration, Oral. Animals. Biomarkers / metabolism. Dose-Response Relationship, Drug. Female. Hyperinsulinism / chemically induced. Hyperinsulinism / metabolism. Liver / drug effects. Liver / metabolism. Mice. NF-kappa B / metabolism. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 20844263.001).
  • [ISSN] 1522-1490
  • [Journal-full-title] American journal of physiology. Regulatory, integrative and comparative physiology
  • [ISO-abbreviation] Am. J. Physiol. Regul. Integr. Comp. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Linoleic Acids, Conjugated; 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha; 0 / trans-10,cis-12-conjugated linoleic acid
  • [Other-IDs] NLM/ PMC3007182
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3. Tu Y, Jerry DJ, Pazik B, Smith Schneider S: Sensitivity to DNA damage is a common component of hormone-based strategies for protection of the mammary gland. Mol Cancer Res; 2005 Aug;3(8):435-42
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  • An early full-term pregnancy significantly reduces the risk of getting breast cancer in women.
  • In animals, this protection can be mimicked by a short-term exposure to physiologic doses of estrogen plus progesterone.
  • Little is known, however, about the use of this pathway in response to other chemopreventive agents.
  • In this article, we investigated the ability of retinoids, such as 9-cis retinoic acid, all-trans retinoic acid, and N-4-hydroxyphenylretinamide (4-HPR), to sensitize the ductal epithelial cells of virgin mammary glands to DNA damage responses.
  • [MeSH-major] DNA Damage. Mammary Glands, Animal / drug effects
  • [MeSH-minor] Animals. Apoptosis. Cell Death. Dose-Response Relationship, Drug. Estrogens / metabolism. Female. Fenretinide / pharmacology. Gamma Rays. Genes, p53. Immunohistochemistry. In Situ Nick-End Labeling. Mice. Mice, Inbred BALB C. Ovary / pathology. Progesterone / metabolism. Retinoid X Receptors / metabolism. Risk Factors. Sensitivity and Specificity. Transforming Growth Factor beta / metabolism. Tretinoin / metabolism. Tumor Suppressor Protein p53 / metabolism. Up-Regulation

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  • (PMID = 16123139.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogens; 0 / Retinoid X Receptors; 0 / Transforming Growth Factor beta; 0 / Tumor Suppressor Protein p53; 187EJ7QEXL / Fenretinide; 4G7DS2Q64Y / Progesterone; 5300-03-8 / alitretinoin; 5688UTC01R / Tretinoin
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4. Howell A, Bundred NJ, Cuzick J, Allred DC, Clarke R: Response and resistance to the endocrine prevention of breast cancer. Adv Exp Med Biol; 2008;617:201-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Response and resistance to the endocrine prevention of breast cancer.
  • The data from the Ral trials also suggests that this agent appears less effective than Tam in preventing DCIS.
  • Equally surprising is the effectiveness of oophorectomy and Tam in mutation carriers, particularly BRCA1, which is associated with ERalpha+ tumors.
  • Data summarised in Table 1 indicate that TDLU are responsive to estrogen, ED, and SERMs/SERDs in premenopausal women and there may be the targets for the preventative effect of early oophorectomy particularly in BRCA1 carriers where we have demonstrated endocrine responsiveness of TDLU, which at this heterozygote stage are ERalpha+.
  • The decline in numbers of atypical lobules in breasts without invasive cancer suggests that these are targets for the 'preventive' effect of the menopause, as suggested by Wellings.
  • The data also suggest that ERalpha+ DCIS is responsive to estrogen and ED supporting premalignant lesions is a target as does the data from the NSABP P1 trial indicating a marked preventive effect of Tam in women previously diagnosed with atypical ductal hyperplasia and a preventative effect on CIS.
  • [MeSH-major] Breast Neoplasms / prevention & control. Drug Resistance, Neoplasm. Hormone Replacement Therapy


5. Moorman PG, Grubber JM, Millikan RC, Newman B: Antidepressant medications and their association with invasive breast cancer and carcinoma in situ of the breast. Epidemiology; 2003 May;14(3):307-14
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  • [Title] Antidepressant medications and their association with invasive breast cancer and carcinoma in situ of the breast.
  • BACKGROUND: Experimental studies in animals have suggested that antidepressants may promote the growth of mammary tumors, but epidemiologic data have not shown consistent associations between antidepressant use and breast cancer.
  • METHODS: We analyzed data from a population-based, case-control study conducted in North Carolina from 1996 to 2000 to examine the association between antidepressant use and breast cancer.
  • Logistic regression models were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) separately for invasive breast cancer and carcinoma in situ.
  • Overall, women with invasive breast cancer did not report antidepressant use more frequently than controls (OR = 1.0; CI = 0.7-1.2).
  • There was a suggestion that use of selective serotonin reuptake inhibitor antidepressants for 36 months or more was more common among the breast cancer cases (OR = 2.7; CI = 0.9-7.9).
  • CONCLUSIONS: Antidepressant use in general was not related to an increased risk of breast cancer.
  • Continued monitoring of this relation is warranted, given the high prevalence of use of these drugs in the general population.
  • [MeSH-major] Antidepressive Agents / adverse effects. Breast Neoplasms / epidemiology. Carcinoma in Situ / epidemiology. Carcinoma, Ductal, Breast / epidemiology. Serotonin Uptake Inhibitors / adverse effects

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  • (PMID = 12859031.001).
  • [ISSN] 1044-3983
  • [Journal-full-title] Epidemiology (Cambridge, Mass.)
  • [ISO-abbreviation] Epidemiology
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50-CA58223; United States / NCI NIH HHS / CA / R29-CA67385
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antidepressive Agents; 0 / Serotonin Uptake Inhibitors
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6. Newcomb PA, Titus-Ernstoff L, Egan KM, Trentham-Dietz A, Baron JA, Storer BE, Willett WC, Stampfer MJ: Postmenopausal estrogen and progestin use in relation to breast cancer risk. Cancer Epidemiol Biomarkers Prev; 2002 Jul;11(7):593-600
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  • [Title] Postmenopausal estrogen and progestin use in relation to breast cancer risk.
  • Epidemiological evidence now consistently supports a modest increase in breast cancer risk among women using postmenopausal hormones, usually estrogens.
  • Less is known regarding how the addition of progestin affects breast cancer risk.
  • The objective of this study was to investigate the type and duration of postmenopausal therapy and breast cancer risk.
  • The subjects were 5298 postmenopausal women (age range, 50-79 years) with a new diagnosis of invasive breast cancer from statewide tumor registries.
  • Participants completed a structured telephone interview covering hormone use and breast cancer risk factors.
  • Multivariable regression models were used to estimate relative risks (RRs) and 95% confidence intervals (CIs).
  • The RR for breast cancer increased with longer durations of hormone use, about 2%/year for estrogen alone (RR, 1.02; 95% CI, 1.01-1.03) and 4%/year for estrogen-progestin use (RR, 1.04; 95% CI, 1.01-1.08).
  • Estrogen-progestin use that was both recent and long term (>5 years in duration) was more strongly associated with breast cancer risk (RR, 1.57; 95% CI, 1.15-2.14) than similar use of estrogen alone (RR, 1.39; 95% CI, 1.17-1.65).
  • In estrogen-progestin users, risks were similar for sequential and continuous use regimens but perhaps stronger for lobular than ductal breast cancer.
  • Estrogen-progestin use, both sequential and continuous, appears to be more strongly associated with risk of breast cancer than use of estrogen alone.
  • [MeSH-major] Breast Neoplasms / chemically induced. Breast Neoplasms / epidemiology. Hormone Replacement Therapy / adverse effects. Progestins / adverse effects
  • [MeSH-minor] Age Distribution. Aged. Case-Control Studies. Cohort Studies. Confidence Intervals. Drug Combinations. Estrogen Replacement Therapy / adverse effects. Estrogen Replacement Therapy / methods. Female. Humans. Massachusetts / epidemiology. Middle Aged. Odds Ratio. Postmenopause. Probability. Reference Values. Reproducibility of Results. Risk Assessment. Risk Factors. Time Factors. Wisconsin / epidemiology

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  • (PMID = 12101105.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA47147; United States / NCI NIH HHS / CA / CA47305; United States / NCI NIH HHS / CA / CA69664
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Progestins
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7. Zujewski J, Vaughn-Cooke A, Flanders KC, Eckhaus MA, Lubet RA, Wakefield LM: Transforming growth factors-beta are not good biomarkers of chemopreventive efficacy in a preclinical breast cancer model system. Breast Cancer Res; 2001;3(1):66-75
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  • [Title] Transforming growth factors-beta are not good biomarkers of chemopreventive efficacy in a preclinical breast cancer model system.
  • Using a carcinogen-initiated rat model of mammary tumorigenesis, we tested the hypothesis that transforming growth factor (TGF)-betas are useful biomarkers of chemopreventive efficacy in the breast.
  • The chemopreventive agents tested were tamoxifen and the retinoids 9-cis-retinoic acid (9cRA) and N-(4-hydroxyphenyl)retinamide (4-HPR), because both antiestrogens and retinoids have previously been shown to upregulate TGF-betas in vitro.
  • Despite demonstrable chemopreventive efficacy in this model, none of these agents, alone or in combination, had any significant impact on the expression of TGF-betas in the mammary ductal epithelium or periductal stroma as determined by immunohistochemistry.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Chemoprevention. Mammary Neoplasms, Experimental / chemically induced. Mammary Neoplasms, Experimental / prevention & control. Transforming Growth Factor beta / metabolism
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Genetic Markers / physiology. Immunoenzyme Techniques. Models, Molecular. Progestins / therapeutic use. Rats. Rats, Sprague-Dawley. Retinoids / therapeutic use. Tamoxifen / therapeutic use. Time Factors

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  • (PMID = 11250748.001).
  • [ISSN] 1465-5411
  • [Journal-full-title] Breast cancer research : BCR
  • [ISO-abbreviation] Breast Cancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Genetic Markers; 0 / Progestins; 0 / Retinoids; 0 / Transforming Growth Factor beta; 094ZI81Y45 / Tamoxifen
  • [Other-IDs] NLM/ PMC13902
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8. Albright CD, Klem E, Shah AA, Gallagher P: Breast cancer cell-targeted oxidative stress: enhancement of cancer cell uptake of conjugated linoleic acid, activation of p53, and inhibition of proliferation. Exp Mol Pathol; 2005 Oct;79(2):118-25
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  • [Title] Breast cancer cell-targeted oxidative stress: enhancement of cancer cell uptake of conjugated linoleic acid, activation of p53, and inhibition of proliferation.
  • We investigated the mechanism of inhibition of cell proliferation by mixed isomers of CLA (9-cis, 11-trans CLA; 10-trans, 12-cis CLA) on human, non-tumorigenic MCF10A cells that were derived from mammary ductal epithelial cells and MCF7 cells that were derived from a well differentiation mammary adenocarcinoma.
  • CLA caused tumor cell-targeted increased expression of 4-hydroxy-2-nonenal (4HNE), a product of lipid peroxidation, and decreased proliferation in MCF7 cells, as measured by the incorporation of bromodeoxyuridine (BrdU) and expression of phosphorylated histone H3, and the effects of CLA in combination with HPO on mitosis were greater than the effects of either agent alone.
  • These studies suggest that tumor cell-targeted increased sensitivity to oxidative stress and activation of p53 play important roles in the regulation of human breast cancer cell proliferation by CLA.
  • [MeSH-major] Breast Neoplasms / metabolism. Linoleic Acids, Conjugated / metabolism. Linoleic Acids, Conjugated / pharmacology. Oxidative Stress / physiology. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation / drug effects. DNA-Binding Proteins / drug effects. Electrophoresis, Polyacrylamide Gel. Female. Fluorescent Antibody Technique. Forkhead Transcription Factors. Humans. Immunoblotting. Lipid Peroxidation / drug effects. Transcription Factors / drug effects

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  • (PMID = 15992797.001).
  • [ISSN] 0014-4800
  • [Journal-full-title] Experimental and molecular pathology
  • [ISO-abbreviation] Exp. Mol. Pathol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK56350
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / FOXO1 protein, human; 0 / Forkhead Transcription Factors; 0 / Linoleic Acids, Conjugated; 0 / Transcription Factors; 0 / Tumor Suppressor Protein p53
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9. Nakamura H, Bai J, Nishinaka Y, Ueda S, Sasada T, Ohshio G, Imamura M, Takabayashi A, Yamaoka Y, Yodoi J: Expression of thioredoxin and glutaredoxin, redox-regulating proteins, in pancreatic cancer. Cancer Detect Prev; 2000;24(1):53-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of thioredoxin and glutaredoxin, redox-regulating proteins, in pancreatic cancer.
  • Pancreatic cancer (pancreatic ductal carcinoma) is one of the most malignant solid tumors with poor prognosis.
  • There is accumulating evidence that cellular reduction/oxidation (redox) status is deeply involved in the growth promotion and drug resistance of cancer cells.
  • We therefore investigated the expression of redox-regulating proteins, such as thioredoxin (TRX) and glutaredoxin (GRX) in surgically resected pancreatic tissues and cis-diamminedichloroplatinum (CDDP)-resistant cells.
  • Pancreatic ductal carcinoma tissues were immunohistochemically more positive for TRX (24/32 cases) and GRX (29/32 cases) than pancreatic cystadenocarcinoma or normal pancreas tissues.
  • Plasma levels of TRX (mean +/- SD) measured by ELISA were significantly higher in patients with pancreatic ductal carcinoma (54.8 +/- 37.6 ng/ml, n = 60) than in healthy controls (24.4 +/- 12.9 ng/ml, n = 81).
  • These results indicate the possible association of TRX and GRX with malignant potential of pancreatic ductal carcinoma.
  • [MeSH-major] Carcinoma, Ductal, Breast / metabolism. Cystadenocarcinoma / metabolism. Oxidoreductases. Pancreatic Neoplasms / metabolism. Protein Biosynthesis. Thioredoxins / biosynthesis
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents / pharmacology. Biomarkers, Tumor / biosynthesis. Biomarkers, Tumor / blood. Cisplatin / pharmacology. Drug Resistance, Neoplasm. Enzyme-Linked Immunosorbent Assay. Glutaredoxins. Humans. Immunoblotting. Middle Aged. Oxidation-Reduction. Prognosis. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / metabolism

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  • (PMID = 10757123.001).
  • [ISSN] 0361-090X
  • [Journal-full-title] Cancer detection and prevention
  • [ISO-abbreviation] Cancer Detect. Prev.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / GLRX protein, human; 0 / Glutaredoxins; 52500-60-4 / Thioredoxins; EC 1.- / Oxidoreductases; Q20Q21Q62J / Cisplatin
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