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BT474 tumors in the presence or absence of SHP2

ABSTRACT: The first bona fide PTP proto-oncogene was the Src-homology 2 domain-containing phosphatase SHP2 (encoded by PTPN11), an ubiquitously expressed PTP that transduces mitogenic, pro-survival, cell fate and/or pro-migratory signals from numerous growth factor-, cytokine- and extracellular matrix receptors. In malignancies, SHP2 is hyperactivated either downstream of oncoproteins or by mutations.We provide analysis of the breast cancer cells BT474 grown as xenografts in the presence or absence of SHP2 for 30 days.

ORGANISM(S): Homo sapiens

PROVIDER: GSE34523 | GEO | 2011/12/20

SECONDARY ACCESSION(S): PRJNA156319

REPOSITORIES: GEO

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BT474 tumors in the presence or absence of SHP2

Project description:The first bona fide PTP proto-oncogene was the Src-homology 2 domain-containing phosphatase SHP2 (encoded by PTPN11), an ubiquitously expressed PTP that transduces mitogenic, pro-survival, cell fate and/or pro-migratory signals from numerous growth factor-, cytokine- and extracellular matrix receptors. In malignancies, SHP2 is hyperactivated either downstream of oncoproteins or by mutations.We provide analysis of the breast cancer cells BT474 grown as xenografts in the presence or absence of SHP2 for 30 days. The HER2-postive breast cancer cell line BT474 was transduced with a doxycycline-inducible lentiviral vector expressing a CTRL miR or SHP2 miR1 or SHP2 miR2. Cells from each group were injected in imuunodeficinet mice and after tumor development, the knockdown of SHP2 was induced for 30 days in vivo. At day 30, tumors were dissected and RNA isolated for gene expression analysis.

2011-12-20 | E-GEOD-34523 | biostudies-arrayexpress

Primary TNBC tumor in the presence or absence of SHP2

2012-01-16 | GSE35118 | GEO

SUM159 cells grown in 2D cultures in the presence or absence of SHP2

2022-06-23 | GSE182033 | GEO

Primary TNBC tumor in the presence or absence of SHP2

Project description:The first bona fide PTP proto-oncogene was the Src-homology 2 domain-containing phosphatase SHP2 (encoded by PTPN11), an ubiquitously expressed PTP that transduces mitogenic, pro-survival, cell fate and/or pro-migratory signals from numerous growth factor-, cytokine- and extracellular matrix receptors. In malignancies, SHP2 is hyperactivated either downstream of oncoproteins or by mutations.We provide analysis of a primary triple-negative breast tumor grown as xenografts in the presence or absence of SHP2 for 30 days. A primary triple-negative breast tumor (BT8) was transduced with a doxycycline-inducible lentiviral vector expressing a CTRL miR or SHP2 miR1 or SHP2 miR2. Cells from each group were injected in immunodeficient mice and after tumor development, the knockdown of SHP2 was induced for 30 days in vivo. At day 30, tumors were dissected and RNA isolated for gene expression analysis.

2012-01-16 | E-GEOD-35118 | biostudies-arrayexpress

MCF10A-HER2/3 cells grown in 3D cultures in the presence or absence of SHP2

2011-12-20 | GSE34524 | GEO

MCF10A-HER2/3 cells grown in 3D cultures in the presence or absence of SHP2

Project description:The first bona fide PTP proto-oncogene was the Src-homology 2 domain-containing phosphatase SHP2 (encoded by PTPN11), an ubiquitously expressed PTP that transduces mitogenic, pro-survival, cell fate and/or pro-migratory signals from numerous growth factor-, cytokine- and extracellular matrix receptors. In malignancies, SHP2 is hyperactivated either downstream of oncoproteins or by mutations.We provide analysis of the mammary epithelial cells MCF10A overexpressing human HER2 and HER3 and grown in 3D cultures for 15 days in the presence or absence of SHP2. The human mammary epithelial cells MCF10A were transduced with a doxycycline-inducible lentiviral vector expressing a CTRL miR or SHP2 miR1 or SHP2 miR2. Cells from each group were grown in 3D cultures, and the knockdown of SHP2 was induced for 15 days. RNA was extracted for gene expression analysis.

2011-12-20 | E-GEOD-34524 | biostudies-arrayexpress

BT474 tumors and MCF10A-HER2/3 cells in the presence or absence of SHP2

Project description:This SuperSeries is composed of the following subset Series: GSE34523: BT474 tumors in the presence or absence of SHP2 GSE34524: MCF10A-HER2/3 cells grown in 3D cultures in the presence or absence of SHP2 Refer to individual Series

2011-12-20 | E-GEOD-34525 | biostudies-arrayexpress

Shp2 transcriptome in melanoma

Project description:1205Lu Metastatic Human melanoma cell lines with knockdown of Shp2 (PTPN11) were grown as xenograft tumors in NSG mice. RNA was extracted from the tumors and analyzed on [HuGene-2_0-st] Affymetrix Human Gene 2.0 ST Array [transcript (gene) version] Shp2 knockdown compared with non-target controls

2016-07-03 | E-GEOD-53282 | biostudies-arrayexpress

SHP2 Is Required for BCR-ABL1-Induced Hematologic Neoplasms

Project description:BCR-ABL1-targeting tyrosine kinase inhibitors (TKIs) have revolutionized treatment of Philadelphia chromosome-positive (Ph+) hematologic neoplasms. Nevertheless, acquired TKI resistance remains a major problem in chronic myeloid leukemia (CML), and TKIs are less effective against Ph+ B-cell acute lymphoblastic leukemia (B-ALL). GAB2, a scaffolding adaptor that binds and activates SHP2, is essential for leukemogenesis by BCR-ABL1, and a GAB2 mutant lacking SHP2 binding cannot mediate leukemogenesis. Using a genetic loss-of-function approach and bone marrow transplantation (BMT) models for CML and BCR-ABL1+ B-ALL, we show that SHP2 is required for BCR-ABL1-evoked myeloid and lymphoid neoplasia. Ptpn11 deletion impairs initiation and maintenance of CML-like myeloproliferative neoplasm, and compromises induction of BCR-ABL1+ B-ALL. SHP2, and specifically, its SH2 domains, PTP activity and C-terminal tyrosines, is essential for BCR-ABL1+, but not WT, pre-B cell proliferation. The MEK/ERK pathway is regulated by SHP2 in WT and BCR-ABL1+ pre-B cells, but is only required for the proliferation of BCR-ABL1+ cells. SHP2 is required for SRC family kinase (SFK) activation only in BCR-ABL1+ pre-B cells. RNAseq reveals distinct SHP2-dependent transcriptional programs in BCR-ABL1+ and WT pre-B cells. Our results suggest that SHP2, via SFKs and ERK, represses MXD3/4 to facilitate a MYC-dependent proliferation program in BCR-ABL1-transformed pre-B cells.

2017-06-06 | GSE99656 | GEO

Shp2 transcriptome in melanoma

2016-01-01 | GSE53282 | GEO

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