Project description:In the current pilot study we aimed to identify differentially expressed miRNAs in two types of single hormone receptor-positive breast cancer [ER(+)/PgR(-) and ER(-)/PgR(+)] with further distinction into HER2-overexpressing/amplified and HER2-negative tumors in a well-established cohort collected at Medical University of Gdańsk.
Project description:Core needle biopsy (Cx) primary cancer specimens were collected at Okayama University Hospital in Japan from hormone receptor positive /HER2 negative patients that subsequently received two weeks of neoadjuvant hormone therapy. Thirty clinical TNM stage I and II women were enrolled in this study. The study was approved by the Institutional Review Board and all patients signed informed consent forms. Patients received preoperative hormone therapy daily for two weeks before surgery. Premenopausal patients received tamoxifen (40 mg) and postmenopausal patients received letrozole (2.5 mg). All patients underwent a mastectomy or breast-conserving surgery. Surgical samples after treatment were also collected. Hormone and HER2 receptor statuses were determined in the diagnostic Cx specimens before hormone therapy. Cases with ≥1% positive nuclear staining for estrogen receptors (ER) or progesterone receptors (PgR) with IHC were considered hormone receptor-positive. Cases with either 0 or 1 positive IHC staining for HER2 or with an HER2 gene copy number < 2.0 by fluorescent in situ hybridization (FISH) analysis were considered HER2−. Specimens for gene expression analysis were collected into RNA and later stored at -80°C. Gene expression profiling was performed using Affymetrix U133A gene chips. Expression data were normalized using the MAS5 algorithm, mean centered to 600, and log2 transformed before further analysis.
Project description:Transcriptomics analyses to study the effect of the imidazopyridine X15695 on proliferation of estrogen receptor positive (ER+) breast and androgen receptor positive (AR+) prostate cancer cells. The effect of X15695 was analyzed on vehicle or steroid hormone-treated breast and prostate cancer cells.
Project description:Hyperactivation of phosphatidylinositol-3 kinase (PI3K) promotes escape from hormone dependence in estrogen receptor-positive breast cancer. A significant fraction of breast cancers exhibit de novo or acquired resistance to estrogen deprivation. We used gene expression microarrays to identify genes and pathways that are commonly dysregulated in ER+ cell lines with acquired hormone-independent growth. MCF-7, ZR75-1, MDA-361, and HCC-1428 ER+, estrogen-responsive breast cancer cells were cultured under hormone-depleted conditions (10% DCC-FBS) for several months until sustainable hormone-independent cell populations emerged.
Project description:HCI-13 patient-derived xenograft was treated with vehicle or a tissue-selective androgen receptor modulator (SARM), enobosarm. RNA was extracted from the tumors and microarray was performed. Objective: The objective of the study is to determine the effect of an androgen receptor (AR) agonist or a selective AR modulator (SARM) on hormone receptor-positive breast cancer growth in preclinical models and to determine the underlying mechanism of action.
Project description:Androgen Receptor is a Backdoor Inhibitor of Wildtype and Mutant Estrogen Receptors in Refractory Hormone Receptor-Positive Breast Cancers