Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA122289 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Distinct molecular subtypes of breast carcinomas have been identified, but translation into clinical use has been limited. We have developed two platform independent algorithms to explore genomic architectural distortion using array comparative genomic hybridization (aCGH) data to measure 1) whole arm gains and losses (WAAI) and 2) complex rearrangements (CAAI). By applying CAAI and WAAI to data from 595 breast cancer patients we were able to separate the cases into eight subgroups with different distribution of genomic distortion. Within each subgroup data from expression analyses, sequencing and ploidy indicated that progression occurs along separate paths into more complex genotypes. Histological grade had prognostic impact only in the Luminal related groups while the complexity identified by CAAI had an overall independent prognostic power. This study emphasizes the relationship between structural genomic alterations, molecular subtype and clinical behavior, and provides a score of genomic complexity as a new tool for prognostication in breast cancer. Array CGH of 255 breast tumor samples vs a male skin fibroblast reference sample, in color reversal.
2009-12-15 | E-GEOD-19425 | biostudies-arrayexpress
Project description:Chromatin architecture plays a key role in development and cancer, yet most studies lack mechanistic depth due to widespread epigenomic remodeling. To address this, we tracked chromatin structure dynamics during the progression of endocrine resistance in ER+ breast cancer using Hi-C, chromatin accessibility, epigenomic, and transcriptomic pro_iling. We uncovered a critical role for H3K9 methylation and the demethylase KDM4C association with SWI/SNF in driving proliferation of cells fated to become resistant through a non-genomic estrogen-mediated mechanism. These _indings highlight the mechanistic contribution of chromatin regulation in therapy resistance and offer a blueprint for studying similar processes in cancer, development, and cell fate decisions.
2025-11-05 | PXD070354 | Pride
Project description:Identifying drivers of cancer progression to guide treatment selection is hindered by limited abilities to understand tumor heterogeneity’s impact on evolution. Here, we delineated the phenotypic variability across ~300,000 prostate tumor cells collected from multi-loci in primary and matched locoregional metastases. We found inter-patient heterogeneity to be confined to malignant populations. While malignant populations exhibit intra-locus heterogeneity, they maintain inter-loci phenotypic similarity within a patient’s prostate gland. Furthermore, the inter-loci malignant population similarity is paired with a shared clonal architecture. Lastly, we show that malignant populations disseminating to locoregional lymph nodes mirror the clonal architecture and phenotypic heterogeneity observed across primary tumor loci while showcasing cell state transition to inflammatory phenotypes. These findings provide insights into four distinct measures of tumor heterogeneity, revealing diverse evolutionary paths across patients converging to common phenotypic adaptations in early prostate cancer progression.
2025-12-01 | GSE271675 | GEO
Project description:Distinct molecular subtypes of breast carcinomas have been identified, but translation into clinical use has been limited. We have developed two platform independent algorithms to explore genomic architectural distortion using array comparative genomic hybridization (aCGH) data to measure 1) whole arm gains and losses (WAAI) and 2) complex rearrangements (CAAI). By applying CAAI and WAAI to data from 595 breast cancer patients we were able to separate the cases into eight subgroups with different distribution of genomic distortion. Within each subgroup data from expression analyses, sequencing and ploidy indicated that progression occurs along separate paths into more complex genotypes. Histological grade had prognostic impact only in the Luminal related groups while the complexity identified by CAAI had an overall independent prognostic power. This study emphasizes the relationship between structural genomic alterations, molecular subtype and clinical behavior, and provides a score of genomic complexity as a new tool for prognostication in breast cancer.
2009-12-16 | GSE19425 | GEO
Project description:Genomic Profiling in Cancer Patients (Breast Cancer Paired Tumor Samples)
| PRJNA487831 | ENA
Project description:Genomic Profiling in Cancer Patients (Breast Cancer Paired Tumor Samples)
| PRJNA487832 | ENA
Project description:Chromatin architecture plays a key role in development and cancer, yet most studies lack mechanistic depth due to widespread epigenomic remodeling. To address this, we tracked chromatin structure dynamics during the progression of endocrine resistance in ER+ breast cancer using Hi-C, chromatin accessibility, epigenomic, and transcriptomic profiling. We uncovered a critical role for H3K9 methylation and the demethylase KDM4C in driving proliferation of cells fated to become resistant through a non-genomic estrogen-mediated mechanism. These findings highlight the mechanistic contribution of chromatin regulation in therapy resistance and offer a blueprint for studying similar processes in cancer, development, and cell fate decisions.
2026-04-24 | GSE296424 | GEO
Project description:Chromatin architecture plays a key role in development and cancer, yet most studies lack mechanistic depth due to widespread epigenomic remodeling. To address this, we tracked chromatin structure dynamics during the progression of endocrine resistance in ER+ breast cancer using Hi-C, chromatin accessibility, epigenomic, and transcriptomic profiling. We uncovered a critical role for H3K9 methylation and the demethylase KDM4C in driving proliferation of cells fated to become resistant through a non-genomic estrogen-mediated mechanism. These findings highlight the mechanistic contribution of chromatin regulation in therapy resistance and offer a blueprint for studying similar processes in cancer, development, and cell fate decisions.
2026-04-24 | GSE296423 | GEO
Project description:Chromatin architecture plays a key role in development and cancer, yet most studies lack mechanistic depth due to widespread epigenomic remodeling. To address this, we tracked chromatin structure dynamics during the progression of endocrine resistance in ER+ breast cancer using Hi-C, chromatin accessibility, epigenomic, and transcriptomic profiling. We uncovered a critical role for H3K9 methylation and the demethylase KDM4C in driving proliferation of cells fated to become resistant through a non-genomic estrogen-mediated mechanism. These findings highlight the mechanistic contribution of chromatin regulation in therapy resistance and offer a blueprint for studying similar processes in cancer, development, and cell fate decisions.
2026-04-24 | GSE296422 | GEO
Project description:Chromatin architecture plays a key role in development and cancer, yet most studies lack mechanistic depth due to widespread epigenomic remodeling. To address this, we tracked chromatin structure dynamics during the progression of endocrine resistance in ER+ breast cancer using Hi-C, chromatin accessibility, epigenomic, and transcriptomic profiling. We uncovered a critical role for H3K9 methylation and the demethylase KDM4C in driving proliferation of cells fated to become resistant through a non-genomic estrogen-mediated mechanism. These findings highlight the mechanistic contribution of chromatin regulation in therapy resistance and offer a blueprint for studying similar processes in cancer, development, and cell fate decisions.
2026-03-12 | GSE296426 | GEO