Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA173369 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Molecular subtyping plays a vital role in the treatment of breast cancer, however, current clinical outcomes remain unsatisfactory despite having multiple molecular subtypes available, particularly for triple-negative breast cancers. Henceforth, our research primarily focuses on traditional molecular subtyping by utilizing transcriptome sequencing and ATAC-seq sequencing techniques to classify both tumor tissues and adjacent tissues from patients with breasts cancers into distinct groups. Through this process, we aim to identify key gene expressions involved in the development of breasts cancers as well as epigenetic characteristics influenced by alterations in chromatin accessibility patterns. Subsequently, employing conventional methods used for classifying breasts cancers into different molecular types enables us to further investigate significant variations observed specifically within triple-negative breasts cancers regarding their gene expression profiles and chromatin accessibility patterns. Lastly, utilizing data from TCGA database pertaining exclusively to cases involving triple-negative breasts cancers allows us to conduct regression analyses concerning our aforementioned findings while simultaneously selecting relevant molecular models closely associated with this particular subtype of breasts malignancy. Additionally evaluating how these differentially expressed genes influence prognosis through prognostic modeling analysis tailored towards predicting outcomes solely within cases involving individuals diagnosed with triple negative-breast malignancies will enable us ultimately construct an innovative model incorporating both gene expressions along with chromatin accessibility patterns as distinguishing features providing more substantial guidance towards improving clinical treatments targeting individuals afflicted by such conditions.
2025-01-01 | GSE254212 | GEO
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
2014-06-30 | E-GEOD-51999 | biostudies-arrayexpress
Project description:This microarray dataset contains 51 triple-negative breast cancers with clinical and recurrence information for at least 3 years of follow-up and 106 luminal breast cancers (reanalyzed data from Series GSE24124, GSE9309, and GSE17040). A novel set of 45-gene signature that was statistically predictive of distant metastasis recurrence for triple-negative breast cancer was identified in this study.
2012-11-01 | GSE33926 | GEO
Project description:The dire need for more effective treatments for clinically aggressive breast cancers has motivated intensive investigations into their cellular and molecular etiology. Breast cancers that are “triple-negative” for the clinical markers, ESR1, PGR, and HER2, typically belong to the Basal-like molecular subtype. Defective Rb, p53, and Brca1 pathways are each associated with triple-negative and Basal-like subtypes. Our mouse genetic studies demonstrate that concomitant inactivation of all three pathways in mammary epithelium has an additive effect on tumor latency, and predisposes highly penetrant, metastatic, adenocarcinomas. These tumors are poorly differentiated with histologic features that are common among human Brca1-mutated tumors, including heterogeneous morphology, metaplasia, and necrosis. Transcriptomic analyses demonstrated that the tumors shared attributes of both Basal-like and Claudin-low signatures, two molecular subtypes encompassed by the broader triple-negative category defined by clinical markers. Ex vivo tumorsphere formation, which was suppressed by Notch and Wnt pathway inhibition, and tumor antigen profiles and are consistent with enrichment of stem-like and luminal progenitor cells among these tumors. These studies establish a novel mouse model of malignant breast cancer based on events in the human disease and underscore the non-reciprocal requirements of three canonical tumor suppressor pathways in breast cancer evolution. Morphogenetic pathways may provide additional avenues for targeted therapeutic intervention. Gene expression analysis of mouse mammary tumors with perturbation of Rb family pathways, p53, and/or Brca1 are compared to other mouse model tumors (n=152)
2011-12-17 | E-GEOD-34479 | biostudies-arrayexpress
Project description:The goal of the second gene expression analysis (samples 17-83) was to determine the molecular subtypes of human breast cancers of a triple-negative breast cancer (TNBC) biobank.
2021-10-05 | GSE182021 | GEO
Project description:When making treatment decisions, oncologists often stratify breast cancers into a low-risk group (ER+, low grade); an intermediate-risk group (ER+, high grade); and a high-risk group that includes Her2+ and triple-negative (ER-/PR-/Her2-) tumors. None of the currently available gene signatures correlates to this clinical classification. We aimed to develop a test that is practical for the oncologists, that offers both molecular characterization of BCs, and improved prediction of prognosis and treatment response. We investigated the molecular basis of such clinical practice by grouping Her2+ and triple-negative breast cancers together during clustering analyses on the genome-wide gene expression profiles of our training cohort, mostly derived from fine needle aspiration biopsies (FNABs) of 149 consecutive evaluable Breast cancers. The analyses consistently divided these tumors into a three-cluster pattern, similar to clinical risk-stratification groups, that was reproducible in published microarray databases (n=2487) annotated with clinical outcomes. The clinicopathologic parameters of each of these three molecular groups were also similar to clinical classification. The low-risk group had good outcomes and benefited from endocrine therapy. Both intermediate- and high-risk groups had poor outcomes and were resistant to endocrine therapy. The latter demonstrated the highest rate of complete pathological response to neoadjuvant chemotherapy; the highest activities in MYC, E2F1, Ras, β-Catenin and IFN-γ pathways; and poor prognosis predicted by 14 independent prognostic signatures. Based on a multivariate analysis, this new gene signature, termed ClinicoMolecular Triad Classification, predicted recurrence and treatment response better than all pathologic parameters and other prognostic signatures. 149 invasive breast cancers from the 172 specimens contained 161 tumors were used in this study. Expression data of the 11 tumors with replicate was separately combined before analysis.
2011-09-28 | E-GEOD-16987 | biostudies-arrayexpress
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.
2022-08-29 | GSE212143 | GEO
Project description:About 15-20% of all breast cancers are triple negative breast cancers, which are often highly aggressive. We performed global quantitative phosphotyrosine profiling of a large panel of triple negative breast cancer cell lines using high resolution Fourier transform mass spectrometry. Our study identified 1,903 tyrosine-phosphorylated peptides derived from 969 proteins. Heterogeneous activation of tyrosine kinases was observed in triple negative breast cancer derived cell lines.
2016-07-06 | PXD001222 | Pride
Project description:Triple-negative breast cancer (TNBC) is characterized by its aggressive behavior, with trend to early relapse and metastasis as well as poor survival. Limited therapies and lack of effective therapeutic targets are one of the main challenges in clinical management of TNBC. Histone post-translational modifications (hPTMs) have been implicated in breast cancer. However, rare information on the association between hPTMs and molecular subtypes of breast cancer can be found so far.
2024-02-01 | PXD049101 |
Project description:Specific Breast Cncer (BC) subtypes are associated with a bad prognosis due to the absence of successful treatment plans. Moreover, the triple negative breast cancer (TNBC) subtype, with estrogen (ER), progesterone (PR) and human epidermal growth factor-2 (HER2) negative receptors status, were characterized by unsuccessful therapies, makes it a clinical challenge for oncologists. In addition, Proton RadioTherapy (PRT) represents an effective treatment also against conventional radiotherapy (RT) resistant cancers, and a promising therapeutically choice for TNBC. Our study aimed at analyze the in vivo molecular response induced by PRT in a MDA-MB-231 triple negative Breast Cancer xenograft model, focusing on gene expression profile (GEP) analyses. Our results demonstrate the multiple advantages of xenograft tissue microarrays for preclinical signature characterization of PRT to understand the molecular mechanism activated and to discover new molecular targets.
2020-10-02 | GSE149023 | GEO