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Molecular signatures of in-situ to invasive progression for basal-like breast cancers: An integrated mouse model and human tumor study [human]

ABSTRACT: Molecular signatures of in-situ to invasive progression for basal-like breast cancers: An integrated mouse model and human tumor study [human]

PROVIDER: PRJNA756990 | ENA |

REPOSITORIES: ENA

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Molecular signatures of in-situ to invasive progression for basal-like breast cancers: An integrated mouse model and human tumor study

Project description:Molecular signatures of in-situ to invasive progression for basal-like breast cancers: An integrated mouse model and human tumor study

| PRJNA756989 | ENA

Molecular signatures of in-situ to invasive progression for basal-like breast cancers: An integrated mouse model and human tumor study [CGH]

Project description:Molecular signatures of in-situ to invasive progression for basal-like breast cancers: An integrated mouse model and human tumor study [CGH]

| PRJNA756993 | ENA

Molecular signatures of in-situ to invasive progression for basal-like breast cancers: An integrated mouse model and human tumor study [mouse]

Project description:Molecular signatures of in-situ to invasive progression for basal-like breast cancers: An integrated mouse model and human tumor study [mouse]

| PRJNA756991 | ENA

Molecular signatures of in-situ to invasive progression for basal-like breast cancers: An integrated mouse model and human tumor study [CGH]

Project description:This study identifies progression in breast ductal carcinoma in situ (DCIS) as it progresses towards triple negative invasive breast cancer (TNBC). Bulk DNA arrayCGH was performed on the C3Tag genetically engineered mouse model that forms human breast-like DCIS and TNBC.

2022-06-01 | GSE182599 | GEO

Molecular signatures of in-situ to invasive progression for basal-like breast cancers: An integrated mouse model and human tumor study [human]

Project description:This study identifies progression in breast ductal carcinoma in situ (DCIS) as it progresses towards triple negative invasive breast cancer (TNBC).

2022-06-01 | GSE182387 | GEO

Molecular signatures of in-situ to invasive progression for basal-like breast cancers: An integrated mouse model and human tumor study [mouse]

Project description:This study identifies progression in breast ductal carcinoma in situ (DCIS) as it progresses towards triple negative invasive breast cancer (TNBC).

2022-06-01 | GSE182388 | GEO

Molecular signatures of in situ to invasive progression for basal-like breast cancers: An integrated mouse model and human DCIS study.

Project description:Ductal carcinoma in situ (DCIS) of the breast is a non-obligate precursor of Invasive Ductal Carcinoma (IDC) and thus the identification of features that may predict DCIS progression would be of potential clinical value. Experimental mouse models can be used to address this challenge by studying DCIS-to-IDC biology. Here we utilize single cell RNA sequencing (scRNAseq) on the C3Tag genetically engineered mouse model that forms DCIS-like precursor lesions and for which many lesions progress into end-stage basal-like molecular subtype IDC. We also perform bulk RNAseq analysis on 10 human synchronous DCIS-IDC pairs comprised of estrogen receptor (ER) positive and ER-negative subsets and utilize 2 additional public human DCIS data sets for comparison to our mouse model. By identifying malignant cells using inferred DNA copy number changes from the murine C3Tag scRNAseq data, we show the existence of cancer cells within the C3Tag pre-DCIS, DCIS, and IDC-like tumor specimens. These cancer cells were further classified into proliferative, hypoxic, and inflammatory subpopulations, which change in frequency in DCIS versus IDC. The C3Tag tumor progression model was also associated with increase in Cancer-Associated Fibroblasts and decrease in activated T cells in IDC. Importantly, we translate the C3Tag murine genomic findings into human DCIS where we find common features only with human basal-like DCIS, suggesting there are intrinsic subtype unique DCIS features. This study identifies several tumor and microenvironmental features associated with DCIS progression and may also provide genomic signatures that can identify progression-prone DCIS within the context of human basal-like breast cancers.

| S-EPMC9293914 | biostudies-literature

Molecular signatures of DCIS to invasive progression for basal-like breast cancers: An integrated mouse model and human tumor study

Project description:Molecular signatures of DCIS to invasive progression for basal-like breast cancers: An integrated mouse model and human tumor study

| PRJNA732953 | ENA

Molecular signatures of DCIS to invasive progression for basal-like breast cancers: An integrated mouse model and human tumor study

Project description:Molecular signatures of DCIS to invasive progression for basal-like breast cancers: An integrated mouse model and human tumor study

| PRJNA732952 | ENA

18F-fluorodeoxy-glucose positron emission tomography marks MYC-overexpressing human basal-like breast cancers.

Project description:Fluorine-18-fluoro-2-deoxy-D-glucose (FDG) is widely used as positron-emission-tomography (PET) radiotracer for the detection and staging of human cancer. Tumor uptake of FDG varies substantially between different cancer types and between patients with the same tumor type. The molecular basis for this heterogeneity is unknown. Using cancer cell lines and primary human tumors of distinct histologic origins, we here show that increased FDG uptake is universally associated with coordinate upregulation of genes within the glycolysis, pentose-phosphate, and other related metabolic pathways. In primary human breast cancers, this FDG signature shows significant overlap with established breast cancer signatures for the “basal-like” disease subtype and “poor prognosis”. FDG high breast cancer showed significantly more gene copy number alterations genome wide than FDG low cancers. About 50 % of primary breast cancers with high FDG uptake and FDG gene expression signature show DNA copy gain encompassing the c-myc gene locus and express gene sets regulated by the transcription factor MYC. Our data shows that FDG-PET marks a distinct subset of “basal-like” human breast cancer which is characterized by MYC and prognostically unfavorable gene expression signatures, suggesting that FDG-PET imaging may be useful to risk-stratify patients with locally advanced breast cancer.

2011-11-01 | GSE21217 | GEO

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