Project description:Integrative analysis of primary estrogen receptor-positive (ER+) breast cancer, triple-negative breast cancer (TNBC), and metaplastic breast cancer (MBC) tumors using Starfysh.
Project description:In this study we report the neoantigen landscape, tumor mutational burden and tumor microenvironment of seven breast cancer patients, consisting of three Estrogen receptor (ER) positive and four Triple negative breast cancer (TNBC) subtypes.
Project description:We performed whole transcriptome sequencing of human monocytes that were co-cultured with estrogen receptor positive (ER+) or triple-negative (TNBC) breast cancer cell lines and studied the biological responses related to the differential gene activation in both cell types to understand how different cancer cells educate host cells to support tumor growth To characterize the differences in macrophage activation under the influence of either ER+ or TNBC breast cancer cells, we cultured freshly isolated human peripheral monocytes with two breast cancer cell lines (T47D, ER+ and MDA-MB-231, TNBC) in an in vitro transwell co-culture assay. The transwell setting allowed us to investigate the effect of soluble mediators on macrophage activation since direct cell contact of these cells was inhibited by a (PET) membrane (pore size 0.4â μm).
Project description:RNA-seq was performed on breast cancer cell lines and primary tumors RNA-seq was performed on 28 breast cancer cell lines, 42 Triple Negative Breast Cancer (TNBC) primary tumors, and 42 Estrogen Receptor Positive (ER+) and HER2 Negative Breast Cancer primary tumors, 30 uninovlved breast tissue samples that were adjacent to ER+ primary tumors, 5 breast tissue samples from reduction mammoplasty procedures performed on patients with no known cancer, and 21 uninvolved breast tissue samples that were adjacent to TNBC primary tumors.
Project description:Goal of this study was to investigate gene expression profiling across different molecular subtypes of breast cancers, such as Estrogen Receptor (ER) positive, HER2 amplified, Triple negative Basal A, Triple negative Basal B.
Project description:Comparison between Estrogen receptor positive and Estrogen receptor negative breast cancer samples Keywords: breast cancer type comparison
Project description:Purpose: To characterize the expression of phosphatases in estrogen receptor negative breast cancer Little is known about the role of phosphatases in the major estrogen receptor negative breast cancer phenotypes (i.e. those overexpressing ERBB2 and the triple negative). We carried out microarray phosphatome profiling in 41 estrogen receptor negative (ER-) breast cancer patients (as determined by immunohistochemistry (IHC)) containing both ERBB2+ and ERBB2- in order to characterize the differences between these groups by Statistical Analysis of Microarrays (SAM). Our findings point to the importance of the MAPK and PI3K pathways in ER- BCs as some of the most differentially expressed phosphatases (like DUSP4 and DUSP6) share ERK as substrate, or regulate the PI3K pathway (INPP4B, PTEN). These observations are also confirmed by pathway and GSEA analysis. It is shown that both ER- ERBB2+ and triple negative breast cancers have a distinctive pattern of phosphatase RNA expression. Surgical specimens from primary breast cancers that were estrogen receptor negative according to immunohistochemistry
Project description:Analysis of 143 formalin-fixed, paraffin-embedded (FFPE) primary breast tumors using a Custom Breast Cancer Panel and Human Cancer Panel for the DASL platform. Molecular markers between the pathology defined subtypes of breast cancer were assessed to hypothesize potential therapeutic targets specific to the subtypes Molecular Characterization of 143 primary breast carcinomas including 101 triple negative (TN: ER-, PR-, HER2-), 3 HER2-positive (HER2+: ER-, PR-, HER2+), and 39 hormone receptor-positive (HR+: ER+ and/or PR+)
Project description:In recent years, there has been an emphasis on personalizing breast cancer treatment in order to avoid the debilitating side effects caused by broad-spectrum chemotherapeutic drug treatment. Development of personalized medicine requires the identification of proteins that are expressed by individual tumors. Herein, we reveal the identity of plasma membrane proteins that are overexpressed in estrogen receptor α-positive, HER2-positive, and triple negative breast cancer cells. The proteins we identified are involved in maintaining protein structure, intracellular homeostasis, and cellular architecture; enhancing cell proliferation and invasion; and influencing cell migration. These proteins may be useful for breast cancer detection and/or treatment.
