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RNA-seq performed on either wild-type, p53 null, or p21 null MMTV-Wnt1 mouse mammary tumors treated with or without doxorubicin.

ABSTRACT: RNA-seq performed on either wild-type, p53 null, or p21 null MMTV-Wnt1 mouse mammary tumors treated with or without doxorubicin.

PROVIDER: PRJNA552227 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9624800_1.fastq.gz	Fastqsanger.gz
	SRR9624800_2.fastq.gz	Fastqsanger.gz
	SRR9624810_1.fastq.gz	Fastqsanger.gz
	SRR9624810_2.fastq.gz	Fastqsanger.gz
	SRR9624820_1.fastq.gz	Fastqsanger.gz

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RNA-seq performed on either wild-type, p53 null, or p21 null MMTV-Wnt1 mouse mammary tumors treated with or without doxorubicin.

Project description:The effects of doxorubicin on mammary tumors

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Gene expression profiling using RNA-Seq data of MMTV-Wnt1 tumor tissue from mice treated with E7386

Project description:We conducted an RNA-Seq analysis using total RNA extracted from MMTV-Wnt1 tumor tissues resected from mice orally administered E7386 at 25 or 50 mg/kg twice daily, or vehicle, for 3 days (Day 4) or 7 days (Day 8) and examined the differentially expressed gene levels compared with vehicle at days 4 and 8.

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The MMTV-Wnt1 murine model produces two phenotypically distinct subtypes of mammary tumors with unique therapeutic responses to an EGFR inhibitor (RNA-seq)

Project description:The Wnt gene family is an evolutionarily conserved group of proteins that regulate cell growth, differentiation, and stem cell self-renewal. Aberrant Wnt signaling in human breast tumors has been proposed to be an attractive drug target, especially in the basal-like subtype where canonical Wnt signaling is both enriched and predictive of poor clinical outcomes. The development of effective Wnt based therapeutics, however, has been slowed in part by a limited understanding of the context dependent nature with which these aberrations influence breast tumorigenesis. We recently reported that MMTV-Wnt1 mice, which are an established model for studying Wnt signaling in breast tumors, develop two subtypes of tumors by gene expression classification: Wnt1-EarlyEx and Wnt1-LateEx. Here, we extend this initial observation and show that Wnt1-EarlyEx tumors had high expression of canonical Wnt, non-canonical Wnt, and EGFR signaling pathway signatures. Therapeutically, Wnt1-EarlyEx tumors had a dynamic reduction in tumor volume when treated with an EGFR inhibitor. Wnt1-EarlyEx tumors also had primarily Cd49fpos/Epcamneg FACS profiles, but were unable to be serially transplanted into wild-type FVB female mice. Wnt1-LateEx tumors, conversely, had a bloody gross pathology, which was highlighted by the presence of ‘blood lakes’ by H&E staining. These tumors had primarily Cd49fpos/Epcampos FACS profiles, but also contained a secondary Cd49fpos/Epcamneg subpopulation. Wnt1-LateEx tumors were enriched for activating Hras1 mutations and were capable of reproducing tumors when serially transplanted into wild-type FVB female mice. This study definitely shows that the MMTV-Wnt1 mouse model produces two phenotypically distinct subtypes of mammary tumors. Importantly, these subtypes differ in their therapeutic response to an EGFR inhibitor, suggesting that a subset of human tumors with aberrant Wnt signaling may also respond to erlotinib.

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The MMTV-Wnt1 murine model produces two phenotypically distinct subtypes of mammary tumors with unique therapeutic responses to an EGFR inhibitor (Agilent CGH)

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Whole-genome expression profiling of metastatic versus non-metastatic mammary tumors in MMTV-Wnt1 transgenic mice

Project description:To identify genes that mediate lung metastasis in breast cancer, we compared expression profiles of metastatic versus non-metastatic mammary tumors in MMTV-Wnt1 transgenic mice. A subset of biologically relevant genes with statistically significant changes was selected for validation. These genes include Alox15, Ptn, Ror2, Sox9, Jag2 and Runx2. These genes encode proteins that play important roles in the immune and inflammatory responses as well as osteogenesis and skeletal morphogenesis.

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The MMTV-Wnt1 murine model produces two phenotypically distinct subtypes of mammary tumors with unique therapeutic responses to an EGFR inhibitor (Agilent gene expression)

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Suppressed cytokine and chemokine transcriptional signatures in mammary stem/progenitor cells are associated with dietary protection against Wnt1-driven mammary tumorigenesis

Project description:Maintenance and propagation of breast cancer stem cells (BCSCs) is mediated via cytokine and growth factor networks. Direct in vivo linkage between dietary regulation of mammary stem (MaSC)/progenitor cell numbers and protection from breast cancer has not been reported. Here, we investigated the effect of post-weaning intake of soy protein isolate (SPI) relative to the control casein (CAS) diet on the stem/progenitor population and tumor formation in MMTV-Wnt1-Transgenic (Wnt1-Tg) female mice. Gene expression profile of the basal (MaSC-enriched) sub-population in preneoplastic Wnt1-Tg mice demonstrated a stem cell-like expression pattern and markedly suppressed expression of inflammatory cytokines, C-X-C family chemokines, and metastasis-associated genes with dietary SPI exposure. four Samples: two CAS diet, two SPI diet

2014-06-30 | E-GEOD-37849 | biostudies-arrayexpress

Suppressed cytokine and chemokine transcriptional signatures in mammary stem/progenitor cells are associated with dietary protection against Wnt1-driven mammary tumorigenesis

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RNA-seq of murine macrophages (J774A.1 and Raw264.7) grown for 48 hours in conditioned media collected from primary murine Triple Negative Breast Cancer cells

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