Diseases : DID06582 - breast neoplasm

ZScoreRScoreEntity TypeIDNameSynonyms
13.7966588225 140 - [0, 0, 3, 13] Diseases DID06582 breast neoplasm breast neoplasm; Breast tumour; Neoplasm of breast; Breast Neoplasm; Tumors, Breast; Breast Tumor; Tumor of the Breast; Tumor, Breast; mammary tumor; Breast Neoplasms; Tumor of breast; Tumour of breast; Neoplasm of the Breast; Mammary Neoplasms; Breast Tumors; NEOPLASM BREAST; Neoplasm, Breast; Breast cancer; Breast cancer; Ca breast - nos; Malignant neoplasm of breast; Malignant tumor of the breast; Mammary cancer; Primary breast cancer
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45 - [0, 0, 1, 4] Urban Endocrine Disruptors Targeting Breast Cancer Proteins.
[MEDLINE : 26700111]
(2016) Urban Endocrine Disruptors Targeting Breast Cancer Proteins. Chemical research in toxicology;Chem. Res. Toxicol.;2016 Feb;29(2):150-61

- Urban Endocrine Disruptors Targeting Breast Cancer Proteins.

- Some of the chemicals that exhibited the best affinity scores for breast cancer proteins in each category were 1,3,7,8-tetrachlorodibenzo-p-dioxin, bisphenol A derivatives, perfluorooctanesulfonic acid, and benzo (a) pyrene, for catalase, several proteins, sex hormone-binding globulin, and cytochrome P450 1A2, respectively.

- Many of these compounds have been associated with a broad range of diseases including the development or increased susceptibility to breast cancer, the most prevalent cancer in women worldwide, according to the World Health Organization.

- Thus, this article presents a virtual high-throughput screening (vHTS) to evaluate the affinity of proteins related to breast cancer, such as ESR1, ERBB2, PGR, BCRA1, and SHBG, among others, with EDCs from urban sources.

- In short, this work shows the potential of several EDCs to bind breast cancer associated proteins as a tool to prioritize compounds to perform in vitro analysis to benefit the regulation or exposure prevention by the general population.

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30 - [0, 0, 1, 1] Editor's Highlight: Transcriptome Profiling Reveals Bisphenol A Alternatives Activate Estrogen Receptor Alpha in Human Breast Cancer Cells.
[MEDLINE : 28591870]
(2017) Editor's Highlight: Transcriptome Profiling Reveals Bisphenol A Alternatives Activate Estrogen Receptor Alpha in Human Breast Cancer Cells. Toxicological sciences : an official journal of the Society of Toxicology;Toxicol. Sci.;2017 08;158(2):431-443

- These findings point to the importance of better understanding the risk of adverse effects from exposure to BPA alternatives, including hormone-dependent breast cancer.

- Editor 's Highlight: Transcriptome Profiling Reveals Bisphenol A Alternatives Activate Estrogen Receptor Alpha in Human Breast Cancer Cells.

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25 - [0, 0, 0, 5] Bisphenol S induced epigenetic and transcriptional changes in human breast cancer cell line MCF-7.
[MEDLINE : 30616060]
(2019) Bisphenol S induced epigenetic and transcriptional changes in human breast cancer cell line MCF-7. Environmental pollution (Barking, Essex : 1987);Environ. Pollut.;2019 Mar;246:697-703

- These results illustrated that BPS exposure might play roles in the progression of breast cancer.

- Besides, methylation status in promoter of breast cancer related genes CDH1, SFN, TNFRSF10C were also changed, which implied that BPS might play a role in the development of breast cancer.

- Gene expression profiling showed that some genes related to breast cancer progression were upregulated, including THBS4, PPARGC1A, CREB5, COL5A3.

- Gene ontology (GO) analysis of the differentially expressed genes revealed the significantly changes in PI3K-Akt signaling pathway and extracellular matrix, which were related to the proliferation, migration and invasion of breast cancer cells.

- Bisphenol S induced epigenetic and transcriptional changes in human breast cancer cell line MCF-7.

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25 - [0, 0, 1, 0] DNA Methylation Targets Influenced by Bisphenol A and/or Genistein Are Associated with Survival Outcomes in Breast Cancer Patients.
[MEDLINE : 28505145]
(2017) DNA Methylation Targets Influenced by Bisphenol A and/or Genistein Are Associated with Survival Outcomes in Breast Cancer Patients. Genes;Genes (Basel);2017 May;8(5):

- DNA Methylation Targets Influenced by Bisphenol A and/or Genistein Are Associated with Survival Outcomes in Breast Cancer Patients.

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5 - [0, 0, 0, 1] Bisphenol AF as an Inducer of Estrogen Receptor β (ERβ): Evidence for Anti-estrogenic Effects at Higher Concentrations in Human Breast Cancer Cells.
[MEDLINE : 29093337]
(2017) Bisphenol AF as an Inducer of Estrogen Receptor β (ERβ): Evidence for Anti-estrogenic Effects at Higher Concentrations in Human Breast Cancer Cells. Biological & pharmaceutical bulletin;Biol. Pharm. Bull.;2017 ;40(11):1909-1916

- Bisphenol AF as an Inducer of Estrogen Receptor β (ERβ): Evidence for Anti-estrogenic Effects at Higher Concentrations in Human Breast Cancer Cells.

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5 - [0, 0, 0, 1] Bisphenol A (BPA) Exposure In Utero Leads to Immunoregulatory Cytokine Dysregulation in the Mouse Mammary Gland: A Potential Mechanism Programming Breast Cancer Risk.
[MEDLINE : 26911702]
(2016) Bisphenol A (BPA) Exposure In Utero Leads to Immunoregulatory Cytokine Dysregulation in the Mouse Mammary Gland: A Potential Mechanism Programming Breast Cancer Risk. Hormones & cancer;Horm Cancer;2016 08;7(4):241-51

- The recent rise in incidence of human breast cancer and decreased age of first detection suggests a possible environmental etiology.

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5 - [0, 0, 0, 1] Synthesis of Triphenylethylene Bisphenols as Aromatase Inhibitors That Also Modulate Estrogen Receptors.
[MEDLINE : 26704594]
(2016) Synthesis of Triphenylethylene Bisphenols as Aromatase Inhibitors That Also Modulate Estrogen Receptors. Journal of medicinal chemistry;J. Med. Chem.;2016 Jan;59(1):157-70

- The hypothesis is that in normal tissue the estrogenic SERM activity of a dual AI/SERM could attenuate the undesired effects stemming from global estrogen depletion caused by the AI activity of a dual AI/SERM, while in breast cancer tissue the antiestrogenic SERM activity of a dual AI/SERM could act synergistically with AI activity to enhance the antiproliferative effect.

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This project is supported by the Canadian Institutes of Health Research (award #111062), Alberta Innovates - Health Solutions, and by The Metabolomics Innovation Centre (TMIC), a nationally-funded research and core facility that supports a wide range of cutting-edge metabolomic studies. TMIC is funded by Genome Alberta, Genome British Columbia, and Genome Canada, a not-for-profit organization that is leading Canada's national genomics strategy with $900 million in funding from the federal government.