Resistance to Aromatase Inhibitors in Breast Cancer

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Endocrine resistance in breast cancer—an overview and update. Mol Cell Endocrinol. Mechanisms of aromatase inhibitor resistance. Approaches towards expression profiling the response to treatment. A candidate molecular signature associated with tamoxifen failure in primary breast cancer. Accurate prediction and validation of response to endocrine therapy in breast cancer.

J Clin Oncol. Molecular profiling of aromatase inhibitor-treated postmenopausal breast tumors identifies immune-related correlates of resistance.

More about research at Mayo Clinic

Clin Cancer Res. Differences in the transcriptional response to fulvestrant and estrogen deprivation in ER-positive breast cancer. Molecular changes in lobular breast cancers in response to endocrine therapy. Cancer Res. Direct integration of intensity-level data from Affymetrix and Illumina microarrays improves statistical power for robust reanalysis.

BMC Med Genet. Yu G, He QY. Mol BioSyst. RankProd: a bioconductor package for detecting differentially expressed genes in meta-analysis.

Background

Likhite N, Warawdekar UM. A unique method for isolation and solubilization of proteins after extraction of RNA from tumor tissue using trizol. J Biomol Tech. Methods Mol Biol. Anal Chem. Cox J, Mann M. MaxQuant enables high peptide identification rates, individualized p. Nat Biotechnol. Nucleic Acids Res. Molecular portraits of human breast tumours. A comparison of PAM50 intrinsic subtyping with immunohistochemistry and clinical prognostic factors in tamoxifen-treated estrogen receptor-positive breast cancer.

Role of the androgen receptor in breast cancer and preclinical analysis of enzalutamide. Enrichr: interactive and collaborative HTML5 gene list enrichment analysis tool. BMC Bioinformatics. Ki67 proliferation index as a tool for chemotherapy decisions during and after neoadjuvant aromatase inhibitor treatment of breast cancer: results from the American College of Surgeons Oncology group Z trial Alliance. New strategies in metastatic hormone receptor-positive breast cancer: searching for biomarkers to tailor endocrine and other targeted therapies. Miller WR, Larionov A.

Changes in expression of oestrogen regulated and proliferation genes with neoadjuvant treatment highlight heterogeneity of clinical resistance to the aromatase inhibitor, letrozole. Metastasis dormancy in estrogen receptor-positive breast cancer. Bartosh TJ. Cancer cell cannibalism and the SASP: ripples in the murky waters of tumor dormancy. Mol Cell Oncol. Extracellular matrix: a gatekeeper in the transition from dormancy to metastatic growth. Eur J Cancer. Induction of metastasis by SP in a rat mammary model and its association with poor survival of breast cancer patients.

The life and works of SP—from conception to cancer. Am J Cancer Res.


  • Study sheds new light on mechanism of breast cancer treatment resistance.
  • Acquired resistance to aromatase inhibitors: where we stand!.
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The association between breast cancer and SP methylation in peripheral blood by multicenter case- control studies. Plasma SP level as a novel prognostic marker of metastatic breast cancer. SP antibody-mediated therapy as a new promising strategy for the treatment of pancreatic cancer. Basse C, Arock M. The increasing roles of epigenetics in breast cancer: implications for pathogenicity, biomarkers, prevention and treatment.

Background

Int J Cancer. Trends Mol Med. Breast cancer methylomes establish an epigenomic foundation for metastasis. Sci Transl Med. Global DNA methylation is altered by neoadjuvant chemoradiotherapy in rectal cancer and may predict response to treatment—a pilot study. Eur J Surg Oncol. De Smet C, Loriot A. DNA hypomethylation in cancer: epigenetic scars of a neoplastic journey. Estrogen deprivation results in altered DNA methylation profile in breast cancer cells—role in endocrine resistance?

Regulation of histone mRNA in the unperturbed cell cycle: evidence suggesting control at two posttranscriptional steps. Mol Cell Biol. Downregulation of histone H2A and H2B pathways is associated with anthracycline sensitivity in breast cancer.

Acquired resistance to aromatase inhibitors: where we stand!

Increased expression of histone proteins during estrogen-mediated cell proliferation. Environ Health Perspect.


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  • Cytoplasmic cyclin E mediates resistance to aromatase inhibitors in breast cancer?
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Anticancer Res. Histone deacetylase inhibitor induces DNA damage, which normal but not transformed cells can repair. HDAC inhibitors induce tumor-cell-selective pro-apoptotic transcriptional responses.

Cell Death Dis. Ceccacci E, Minucci S. Inhibition of histone deacetylases in cancer therapy: lessons from leukaemia. Br J Cancer. Characterization of the weak estrogen receptor alpha agonistic activity of exemestane. Biological reprogramming in acquired resistance to endocrine therapy of breast cancer.

Clinical instability of breast cancer markers is reflected in long-term in vitro estrogen deprivation studies. Cholesterol biosynthesis pathway as a novel mechanism of resistance to estrogen deprivation in estrogen receptor-positive breast cancer. Antiestrogen-resistant subclones of MCF-7 human breast cancer cells are derived from a common monoclonal drug-resistant progenitor.

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"CYTOPLASMIC CYCLIN E MEDIATES RESISTANCE TO AROMATASE INHIBITORS IN BR" by Iman Doostan

High CDK6 protects cells from fulvestrant-mediated apoptosis and is a predictor of resistance to fulvestrant in estrogen receptor-positive metastatic breast cancer. Download references. CS and AKT generated the transcriptome dataset. JW conducted proteomics and supported proteomics data analysis.

AF and LR provided technical support with tissue collection and processing. CS analysed and interpreted the data and drafted the manuscript.

Dr. Judy Garber and aromatase inhibitors for breast cancer prevention - Dana-Farber Cancer Institute

AHS supervised the project and helped to write and edit the manuscript. All authors read and approved the final manuscript. Correspondence to Andrew H. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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