p53 is a potential mediator of pregnancy and hormone-induced resistance to mammary carcinogenesis - Wikidata - awgldk - TriplyDB

p53 is a potential mediator of pregnancy and hormone-induced resistance to mammary carcinogenesis

p53 is a potential mediator of pregnancy and hormone-induced resistance to mammary carcinogenesis

http://www.wikidata.org/entity/Q33947714

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Skp2B attenuates p53 function by inhibiting prohibitin Carcinogen inducibility in vivo and down-regulation of DMBT1 during breast carcinogenesis Physical interaction and mutual transrepression between CCAAT/enhancer-binding protein beta and the p53 tumor suppressor Progesterone receptor knockout mice have an improved glucose homeostasis secondary to beta -cell proliferation A noncoding RNA is a potential marker of cell fate during mammary gland development.Hormonal control of p53 and chemoprevention Progesterone's role in mammary gland development and tumorigenesis as disclosed by experimental mouse genetics Pregnancy-induced changes in cell-fate in the mammary gland Activation of p53, inhibition of telomerase activity and induction of estrogen receptor beta are associated with the anti-growth effects of combination of ovarian hormones and retinoids in immortalized human mammary epithelial cells The protective role of pregnancy in breast cancer The p53-estrogen receptor loop in cancer The p53 tumor suppressor gene is regulated in vivo by nuclear factor 1-C2 in the mouse mammary gland during pregnancy Induction of a novel histone deacetylase 1/c-Myc/Mnt/Max complex formation is implicated in parity-induced refractoriness to mammary carcinogenesis Lack of effects of postnatal exposure to a mixture of aryl hydrocarbon-receptor agonists on the development of methylnitrosourea-induced mammary tumors in sprague-dawley rats.Parity-induced decrease in systemic growth hormone alters mammary gland signaling: a potential role in pregnancy protection from breast cancer.Prognostic interaction between expression of p53 and estrogen receptor in patients with node-negative breast cancer: results from IBCSG Trials VIII and IX Effect of the p53-tristetraprolin-stathmin-1 pathway on trophoblasts at maternal-fetal interface.Deregulated estrogen receptor alpha and p53 heterozygosity collaborate in the development of mammary hyperplasia.Stress signaling and the shaping of the mammary tissue in development and cancer.Effects of parity and serum prolactin levels on the incidence and regression of DMBA-induced tumors in OFA hr/hr rats.Mitochondrial Hep27 is a c-Myb target gene that inhibits Mdm2 and stabilizes p53.Mechanisms of estrogen receptor antagonism toward p53 and its implications in breast cancer therapeutic response and stem cell regulation.The complex relationship between pregnancy and breast cancer.Transcriptional responses to estrogen and progesterone in mammary gland identify networks regulating p53 activity.Transcriptional regulation of estrogen receptor-alpha by p53 in human breast cancer cells.TP53 and breast cancer.Proliferation of estrogen receptor-alpha-positive mammary epithelial cells is restrained by transforming growth factor-beta1 in adult mice.P53 genotype as a determinant of ER expression and tamoxifen response in the MMTV-Wnt-1 model of mammary carcinogenesis Mammary epithelial stem cells: transplantation and self-renewal analysis.p53 codon 72 polymorphism and recurrent pregnancy loss: a meta-analysis.Hormones and progeny of breast tumor cells.Estrogen and progesterone induce persistent increases in p53-dependent apoptosis and suppress mammary tumors in BALB/c-Trp53+/- mice Parity induces differentiation and reduces Wnt/Notch signaling ratio and proliferation potential of basal stem/progenitor cells isolated from mouse mammary epithelium Evidence that an early pregnancy causes a persistent decrease in the number of functional mammary epithelial stem cells--implications for pregnancy-induced protection against breast cancer.The in vivo Therapeutic Effect of Free Wanderer Powder ( xiāo yáo sǎn, Xiaoyaosan) on Mice with 4T1 Cell Induced Breast Cancer Model.New biological insights on the link between radiation exposure and breast cancer risk.ICRP Publication 131: Stem Cell Biology with Respect to Carcinogenesis Aspects of Radiological Protection.Functional significance of Aurora kinase A regulatory interactions with p53-ERα complex in human breast cancer cells.Estrogen receptor-alpha binds p53 tumor suppressor protein directly and represses its function.Antiestrogens are pro-apoptotic in normal human breast epithelial cells.

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P2860

p53 is a potential mediator of pregnancy and hormone-induced resistance to mammary carcinogenesis

http://www.wikidata.org/entity/Q33947714

description

2001 nî lūn-bûn

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2001 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

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2001 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2001年の論文

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2001年論文

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2001年論文

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2001年論文

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2001年論文

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2001年論文

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2001年论文

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name

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p53 is a potential mediator of ...... ance to mammary carcinogenesis

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P1433

Proceedings of the National Academy of Sciences of the United States of America

P1476

p53 is a potential mediator of ...... ance to mammary carcinogenesis

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P2093

B W O'Malley

http://www.w3.org/2001/XMLSchema#string

D Medina

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L Sivaraman

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O M Conneely

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P2860

Interaction of the p53-regulated protein Gadd45 with proliferating cell nuclear antigen

Susceptibility of the mammary gland to carcinogenesis. II. Pregnancy interruption as a risk factor in tumor incidence

WAF1, a potential mediator of p53 tumor suppression

Tumor suppressor p53 is a regulator of bcl-2 and bax gene expression in vitro and in vivo

p53 mutations in human cancers

A mammalian cell cycle checkpoint pathway utilizing p53 and GADD45 is defective in ataxia-telangiectasia

p53: puzzle and paradigm

Germ line p53 mutations in a familial syndrome of breast cancer, sarcomas, and other neoplasms

Wild-type p53 induces apoptosis of myeloid leukaemic cells that is inhibited by interleukin-6

Progesterone facilitates chromosome instability (aneuploidy) in p53 null normal mammary epithelial cells.

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10.1073/PNAS.221459098

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22

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98

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2001-10-16T00:00:00Z

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11743350

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11606748

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60062

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