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The protein profile of mammary gland and tumors between Brca1-WT and MT miece by DIA-MS(DDA data)

ABSTRACT: WT mammary gland(WTMG),mutant-MG(MTMG),WT breast tumors(WTBT),MTBT and MTBT-adjacent MG were collected to do data-independent acquisiton(DIA)mass to find the intrinsic factors that is associated with Brca1-deficiency induced breast cancer.

INSTRUMENT(S): Orbitrap Eclipse

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Epithelial Cell, Mammary Gland

DISEASE(S): Breast Cancer

SUBMITTER: jianjie li

LAB HEAD: Xiaoling Xu&Chuxia Deng

PROVIDER: PXD030355 | Pride | 2022-02-20

REPOSITORIES: Pride

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			Action	DRS
	1.raw	Raw
	10.raw	Raw
	11.raw	Raw
	12_raw.msf	Msf
	2.raw	Raw

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The protein profile of mammary gland and tumors between Brca1-WT and MT miece by DIA-MS(DIA-data)

Project description:WT mammary gland(WTMG),mutant-MG(MTMG),WT breast tumors(WTBT),MTBT and MTBT-adjacent MG were collected to do data-independent acquisiton(DIA)mass to find the intrinsic factors that is associated with Brca1-deficiency induced breast cancer.

2022-02-20 | PXD030328 | Pride

RNAseq of Brca1-deficient mouse mammary tumors

Project description:Brca1 mutation predisposes women to early onset of breast and ovarian cancers.Through its diverse functions in DNA damage repair, cell cycle control, transcription regulation, ubiquitination and so on, BRCA1 acts as a very significant tumor suppressor and genomic safeguard. Brca1 deficiency induces severe cellular stress, when occurring in the mammary glands, it impairs the regular developmental process and eventually causes tumorigenesis due to accumulation of genome instability and other mechanisms. The Brca1-defiencient mouse mammary tumor were characterized with great tumoral heterogeneity, which is in line with the human breast cancers carrying BRCA1 mutations. Here we studied the molecular complexicity of Brca1-deficient mouse mammary tumors vie RNA sequencing.

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Project description:Microarrays were used to determine relative global gene expression changes in WT and BRCA1-mutation carrier breast epithelium as well as tumors created from WT and BRCA1-mutation carrier breast epithelial cells.

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Normal human mammary tissues from BRCA1 mutation carriers, non-BRCA1/2 mutation carriers and normal women

Project description:Gene expression profiles of normal human mammary tissue from BRCA1 mutation carriers, non-BRCA1/2 mutation carriers and normal women. RNA was prepared from normal breast tissue (confirmed by pathology) from reduction mammoplasties (n=5) and prophylactic mastectomies of known BRCA1 (n=7) and non-BRCA1/2 mutation carriers (n=8). non-BRCA1/2 carriers were individuals with a strong family history of breast cancer (kConFab Category 1 (http://www.kconfab.org/Collection/Eligibility.shtml) where no mutation in BRCA1 or BRCA2 has been identified in the family by high sensitivity testing (http://www.kconfab.org/Progress/Sensitivity.shtml) of any individual affected by breast or ovarian cancer. Normal breast samples refer to reduction mammoplasty specimens, where family history is generally not known. Microarray expression profiles were obtained from whole pre-neoplastic breast tissue from three categories of patient, as described in the summary. Samples were checked for keratin gene expression levels as a marker for epithelium tissue, and a number of samples were removed because two or more keratin genes lacked detectable expression (BeadStudio detection p-value 0.01). One other sample was removed because its expression profile appeared abnormal. Out of 36 samples initially profiled, 20 passed the quality filters and were used for the final analysis.

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Project description:One of the major hurdles for the early detection of cancer is our poor understanding of tumour initiating events. Historically, cancer research has focused on histological and molecular characterisation of established tumours, which has led to the identification of hundreds of putative driver mutations. It is currently unclear how these genetic aberrations impact the cell state of nascent tumour cells and their microenvironment. BRCA1 driven triple negative breast cancer (TNBC) for example has been shown to arise from luminal progenitor cells1,2 yet little is known about how BRCA1 loss-of-function (LOF) and concomitant mutations affect the luminal progenitor cell state. Here we demonstrate how time-resolved single-cell profiling of genetically engineered mouse models before tumour formation can address this challenge. We found that the perturbation of Brca1/p53 in luminal progenitors induces an aberrant alveolar differentiation pre-malignancy. Unlike alveolar differentiation occurring during gestation, this process is cell autonomous and characterised by the dysregulation of transcription factors driving alveologenesis. Our experimental approach has allowed us to further identify responses in the stromal and immune cell compartments during the early steps of tumourigenesis. Based on our data we propose a model where transcriptional and epigenetic changes driven by Brca1/p53 inadvertently promote a differentiation program hardwired in luminal progenitors, highlighting the deterministic role of the cell of origin and offering a potential explanation for the tissue specificity of BRCA1 tumours. Moving forward, the phenotype identified herein should be evaluated as a target for early detection and treatment of TNBC.

2021-02-02 | E-MTAB-10043 | biostudies-arrayexpress

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