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:Triple negative breast cancers lack targeted therapies with little side effects and contain higher percentage of cancer stem cells than the other breast cancer subtypes. Genes capturing the features of cancer stem cells of such diseases may serve as potential subtyping marker or therapeutic targets for triple negative breast cancer management. This data descriptor presents a set of transcriptome data from 3 cohorts of cancer stem cells as represented as CD44+/CD24-/low and 2 cohorts of non-cancer stem cells isolated from triple negative breast cancer cells, each having 3 replicates.
Project description:Breast cancer (BC) is the most prevalent and lethal tumor among women worldwide.
Although the antitumor effects of melatonin are well documented, its precise molecular
mechanisms in specific breast cancer subtypes remain unclear. This dataset provides
proteomic data from total protein extracts of two breast cancer cell lines [MCF-7
(ER+and PR+) and MDA-MB-468 (triple negative) treated with melatonin. The aim of
the study was to identify melatonin-induced changes in global protein expression and to
assess its potential as a therapeutic modulator in hormone-responsive and triple-negative
breast cancer.
Project description:Plasticity delineates cancer subtypes with more or less favourable outcomes. In breast cancer, triple-negative is the subtype that lacks the expression of major differentiation markers (i.e. estrogen receptor [ER]), ant its high cellular plasticity results in higher aggressiveness and poor prognosis compared to other subtypes. Whether plasticity poses a vulnerability to cancer cells remains elusive. Here, we show that cancer cell plasticity can be exploited to differentiate triple-negative breast cancer. Using a high-throughput reporter drug screen with 9,501 compounds, we identify three polo-like kinase 1 (PLK1) inhibitors as major inducers of ER protein expression and downstream activity in triple-negative breast cancer cells via the transcription factor BATF. PLK1 inhibition upregulates a cell differentiation program characterized by increased DNA damage, mitotic arrest and ultimately cell death. Notably, cells surviving PLK1 inhibition have decreased tumorigenic potential, and targeting PLK1 in already established tumours reduces tumour growth both in cell line and patient-derived xenograft models. In addition, genes upregulated upon PLK1 inhibition are correlated with expression in normal breast tissue and confer better overall survival in breast cancer patients. Our results indicate that differentiation therapy based on PLK1 inhibition might be an alternative strategy to treat triple-negative breast cancer.
Project description:Breast cancer is one of the most common cancers in women. Of the different subtypes of breast cancer, the triple negative breast cancer subtype of breast cancer is the most aggressive. A proteomic screen of nucleolar content across breast cancer subtypes found that triple negative breast cancer cell lines have a distinct nucleolar proteome signature in comparison to non-TNBC breast cancer cell lines.
Project description:Analysis of 97 formalin-fixed, paraffin-embedded (FFPE) primary breast tumors using Illumina DASL microarray technology on a Custom Breast Cancer Panel and the Illumina Human Cancer Panel. Molecular markers between the pathology defined subtypes of breast cancer were assessed to hypothesize potential therapeutic targets specific to the subtypes Molecular Characterization of 97 primary breast tumor formalin-fixed, paraffin-embedded (FFPE) specimens including 24 triple negative (TN: ER-, PR-, HER2-), 9 HER2-positive (HER2+: ER-, PR-, HER2+), and 64 hormone receptor-positive (HR+: ER+ and/or PR+). 91 of the 97 specimens were characterized on the Illumina Human Cancer DASL Panel and 86 of 97 specimens were characterized on a custom Breast Cancer DASL Panel, 80 of these specimens were common to both the Human Cancer DASL Panel and the custom Breast Cancer DASL Panel.
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:To discover individual genes with potential diagnostic and therapeutic utilities, we use gene expression profiling from real patient tissues to identify significantly regulated genes out of a broad coverage of human transcriptome. We use Agilent gene expression microarray technologies to measure gene expressions of 32 cancerous and normal tissues from breast cancer patients. Total RNAs were extracted and analyzed using Agilent microarray technologies. The whole genome expression profiling has been proformed and several significantly differently expressed genes (such as HS3ST4, MMP1, MMP11) were quatified by qPCR to verify their up/down-regulations, leading to discovery of important genes related to breast cancer metastasis. We examined 32 human breast tissues of three different breast cancer subtypes (including Luminal A, Luminal B, Triple Negative) and normal controls to perform microarray gene expression profiling.
Project description:Addressing tumor heterogeneity in breast cancer research is crucial, given the distinct subtypes like triple-negative, luminal A/B, and HER2, requiring precise differentiation for effective treatment. This study introduces a non-invasive method by analyzing post-translationally modified proteins in plasma extracellular vesicles (EVs), which play a role in immune regulation and intercellular communication. Examining modifications like phosphorylation, acetylation, and glycosylation in EVs provides insights into breast cancer dynamics. One hundred one plasma samples from luminal A/B, triple-negative breast cancer, and healthy individuals underwent discovery and validation experiments. The study identified over 28,000 unique non-modified peptides, 5,000 phosphopeptides, 680 acetyl peptides, and 1,300 glycopeptides that were successfully characterized. Bioinformatics analyses revealed significant overexpression of 815 non-modified proteins, 3,958 phosphopeptides, 352 acetyl peptides, and 895 glycopeptides in luminal A/B or triple-negative breast cancer subtypes. Phosphorylated and glycosylated PD-L1 peptides emerged as potential markers for breast cancer, regardless of subtype. Aligning findings with literature and PAM50 gene signatures highlighted markers correlated with lower survival rates. The study also conducted 123 scheduled parallel reaction monitoring (PRM) analyses, leveraging machine learning to pinpoint a panel of specific modification sites with high accuracy in subtype differentiation. This research reveals diagnostic markers and enhances understanding of the molecular landscape, contributing to more effective and personalized breast cancer diagnostics and treatments.
Project description:Triple negative breast cancer is a heterogeneous disease with distinct molecular subtypes that differentially respond to chemotherapy and targeted agents. The purpose of this study was to explore the clinical relevance of Lehmann triple negative breast cancer subtypes by identifying any differences in response to neoadjuvant chemotherapy among them.