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MYC Amplification as a Predictive Factor of Complete Pathologic Response to Docetaxel-based Neoadjuvant Chemotherapy for Breast Cancer.MYC基因扩增作为乳腺癌多西他赛新辅助化疗完全病理缓解的预测因素
Clin Breast Cancer. 2017 Jun;17(3):188-194. doi: 10.1016/j.clbc.2016.12.005. Epub 2016 Dec 24.
2
The role of HER2, EGFR, and other receptor tyrosine kinases in breast cancer.HER2、表皮生长因子受体(EGFR)及其他受体酪氨酸激酶在乳腺癌中的作用。
Cancer Metastasis Rev. 2016 Dec;35(4):575-588. doi: 10.1007/s10555-016-9649-6.
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The Quest for Targets Executing MYC-Dependent Cell Transformation.对执行MYC依赖性细胞转化的靶点的探索。
Front Oncol. 2016 Jun 2;6:132. doi: 10.3389/fonc.2016.00132. eCollection 2016.
4
MYC copy gain, chromosomal instability and PI3K activation as potential markers of unfavourable outcome in trastuzumab-treated patients with metastatic breast cancer.MYC基因拷贝数增加、染色体不稳定和PI3K激活作为曲妥珠单抗治疗的转移性乳腺癌患者不良预后的潜在标志物。
J Transl Med. 2016 May 17;14(1):136. doi: 10.1186/s12967-016-0883-z.
5
MiR-16 mediates trastuzumab and lapatinib response in ErbB-2-positive breast and gastric cancer via its novel targets CCNJ and FUBP1.微小RNA-16通过其新靶点细胞周期蛋白J(CCNJ)和远上游元件结合蛋白1(FUBP1)介导曲妥珠单抗和拉帕替尼对表皮生长因子受体2(ErbB-2)阳性乳腺癌和胃癌的反应。
Oncogene. 2016 Dec 1;35(48):6189-6202. doi: 10.1038/onc.2016.151. Epub 2016 May 9.
6
Inhibition of fatty acid oxidation as a therapy for MYC-overexpressing triple-negative breast cancer.抑制脂肪酸氧化作为治疗MYC过表达三阴性乳腺癌的一种方法。
Nat Med. 2016 Apr;22(4):427-32. doi: 10.1038/nm.4055. Epub 2016 Mar 7.
7
Parabens and Human Epidermal Growth Factor Receptor Ligand Cross-Talk in Breast Cancer Cells.对羟基苯甲酸酯与乳腺癌细胞中人类表皮生长因子受体配体的相互作用
Environ Health Perspect. 2016 May;124(5):563-9. doi: 10.1289/ehp.1409200. Epub 2015 Oct 27.
8
Metabolic reprogramming in triple-negative breast cancer through Myc suppression of TXNIP.通过Myc抑制TXNIP实现三阴性乳腺癌中的代谢重编程
Proc Natl Acad Sci U S A. 2015 Apr 28;112(17):5425-30. doi: 10.1073/pnas.1501555112. Epub 2015 Apr 13.
9
Cross-talk between ER and HER2 regulates c-MYC-mediated glutamine metabolism in aromatase inhibitor resistant breast cancer cells.雌激素受体(ER)与人类表皮生长因子受体2(HER2)之间的相互作用调控芳香化酶抑制剂耐药乳腺癌细胞中c-MYC介导的谷氨酰胺代谢。
J Steroid Biochem Mol Biol. 2015 May;149:118-27. doi: 10.1016/j.jsbmb.2015.02.004. Epub 2015 Feb 12.
10
RB loss contributes to aggressive tumor phenotypes in MYC-driven triple negative breast cancer.RB缺失促成了MYC驱动的三阴性乳腺癌中的侵袭性肿瘤表型。
Cell Cycle. 2015;14(1):109-22. doi: 10.4161/15384101.2014.967118.

乳腺癌亚型中由MYC驱动的信号通路。

MYC-Driven Pathways in Breast Cancer Subtypes.

作者信息

Fallah Yassi, Brundage Janetta, Allegakoen Paul, Shajahan-Haq Ayesha N

机构信息

Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC 20057, USA.

出版信息

Biomolecules. 2017 Jul 11;7(3):53. doi: 10.3390/biom7030053.

DOI:10.3390/biom7030053
PMID:28696357
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5618234/
Abstract

The transcription factor MYC (MYC proto-oncogene, bHLH transcription factor) is an essential signaling hub in multiple cellular processes that sustain growth of many types of cancers. MYC regulates expression of RNA, both protein and non-coding, that control central metabolic pathways, cell death, proliferation, differentiation, stress pathways, and mechanisms of drug resistance. Activation of MYC has been widely reported in breast cancer progression. Breast cancer is a complex heterogeneous disease and treatment options are primarily guided by histological and biochemical evaluations of the tumors. Based on biochemical markers, three main breast cancer categories are ER+ (estrogen receptor alpha positive), HER2+ (human epidermal growth factor receptor 2 positive), and TNBC (triple-negative breast cancer; estrogen receptor negative, progesterone receptor negative, HER2 negative). MYC is elevated in TNBC compared with other cancer subtypes. Interestingly, MYC-driven pathways are further elevated in aggressive breast cancer cells and tumors that display drug resistant phenotype. Identification of MYC target genes is essential in isolating signaling pathways that drive tumor development. In this review, we address the role of MYC in the three major breast cancer subtypes and highlight the most promising leads to target MYC functions.

摘要

转录因子MYC(MYC原癌基因,bHLH转录因子)是多种细胞过程中的关键信号枢纽,维持多种癌症的生长。MYC调节RNA的表达,包括蛋白质编码和非编码RNA,这些RNA控制着中心代谢途径、细胞死亡、增殖、分化、应激途径和耐药机制。MYC的激活在乳腺癌进展中已被广泛报道。乳腺癌是一种复杂的异质性疾病,治疗方案主要由肿瘤的组织学和生化评估指导。基于生化标志物,乳腺癌主要分为三类:ER+(雌激素受体α阳性)、HER2+(人表皮生长因子受体2阳性)和TNBC(三阴性乳腺癌;雌激素受体阴性、孕激素受体阴性、HER2阴性)。与其他癌症亚型相比,TNBC中MYC水平升高。有趣的是,在具有耐药表型的侵袭性乳腺癌细胞和肿瘤中,MYC驱动的途径进一步升高。鉴定MYC靶基因对于分离驱动肿瘤发展的信号通路至关重要。在本综述中,我们阐述了MYC在三种主要乳腺癌亚型中的作用,并突出了针对MYC功能最有前景的线索。