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Akt inhibition with MK-2206 is associated with favorable immune profile changes within the tumor microenvironment of hormone receptor positive, HER2 negative breast cancer [PI3K panel]

ABSTRACT: Akt inhibition with MK-2206 is associated with favorable immune profile changes within the tumor microenvironment of hormone receptor positive, HER2 negative breast cancer [PI3K panel]

PROVIDER: PRJNA632733 | ENA |

REPOSITORIES: ENA

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Akt inhibition with MK-2206 is associated with favorable immune profile changes within the tumor microenvironment of hormone receptor positive, HER2 negative breast cancer [PI3K panel]

Project description:Gene expression was assessed with Nanostring in the surgical specimens obtained from a Window of Opportunity trial with MK-2206 in early stage breast cancer. Tumor biopsies and surgical specimens were compared for patients who received MK-2206 along with a prospective untreated control group of patients. Greater expression of interferon related genes was seen in surgical specimens following MK-2206 and compared to untreated controls.

2020-05-25 | GSE150509 | GEO

Akt inhibition with MK-2206 is associated with favorable immune profile changes within the tumor microenvironment of hormone receptor positive, HER2 negative breast cancer [IO360 panel]

2020-05-25 | GSE150458 | GEO

A phase 1b study of the Akt-inhibitor MK-2206 in combination with weekly paclitaxel and trastuzumab in patients with advanced HER2-overexpressing solid tumor malignancies

Project description:16 patients with HER2+ tumors were enrolled (12 breast, 3 gastric, 1 esophageal). 27 samples (12 primary + 15 metastatic) from the 16 unique patients were assayed on Agilent 60K expression microarrays, and association between expression and response data were evaluated to identify potential biomarker of MK2206 response We conducted a phase 1b study of MK-2206 in combination with weekly paclitaxel 80 mg/m2 and trastuzumab 2 mg/kg in patients with HER2+ malignancies. Dose escalation was performed using a modified toxicity probability interval method. Molecular profiling of archived tissue samples and limited PK analyses were performed.

2016-07-31 | E-GEOD-75087 | biostudies-arrayexpress

Akt inhibition with MK-2206 is associated with favorable immune profile changes within the tumor microenvironment of hormone receptor positive, HER2 negative breast cancer [IO360 panel]

Project description:Akt inhibition with MK-2206 is associated with favorable immune profile changes within the tumor microenvironment of hormone receptor positive, HER2 negative breast cancer [IO360 panel]

| PRJNA632489 | ENA

Akt inhibition with MK-2206 is associated with favorable immune profile changes within the tumor microenvironment of hormone receptor positive, HER2 negative breast cancer

Project description:Akt inhibition with MK-2206 is associated with favorable immune profile changes within the tumor microenvironment of hormone receptor positive, HER2 negative breast cancer

| PRJNA632732 | ENA

Selective Akt inhibition by MK-2206 eleminates colorectal cancer-initiating stem cells

Project description:To identify the regulatory mechanisms and signalling pathways involved in colorectal cancer (CRC) development, we compared the transcriptome of patient-derived tumor-initiating cells (TICs) with their normal stem cell counterparts of the same patient. This study demonstrates the relevance of AKT-signalling in colonic TIC proliferation and survival. Functional testing uncovered the selective AKT-inhibitor MK-2206 as a potential therapeutic for TIC-directed therapy in CRC. Gene expression profiling of tumor and normal tissues from 5 patients.

2016-07-06 | E-GEOD-70018 | biostudies-arrayexpress

Selective Akt inhibition by MK-2206 eleminates colorectal cancer-initiating stem cells

2016-07-06 | GSE70018 | GEO

Spatial proteomics of selinexor, MK-2206 and combination response in AML cells

Project description:In order to characterize the dynamics of proteins between different cellular compartments in response to selinexor (XPO1 inhibitor), MK-2206 (Akt inhibitor) an the combination i AML cells, we treated MV4-11 and PL-21 cells for 6 hours with DMSO, 1 uM selinexor, 1 uM MK-2206 or the combination. Each condition was performed in 4 biological bio-reps.

2022-08-07 | PXD033527 | Pride

FOXO3a Is A Major Target Of Inactivation By PI3K/AKT Signaling In Aggressive Neuroblastoma

Project description:Neuroblastoma is a pediatric tumor of the peripheral sympathetic nervous system with a highly variable prognosis. Activation of the PI3K/AKT pathway in neuroblastoma is correlated with poor patient prognosis, but the precise downstream effectors mediating this effect have not been determined. Here, we identify the forkhead transcription factor FOXO3a as a key target of the PI3K/AKT pathway in neuroblastoma. FOXO3a expression was elevated in low stage neuroblastoma tumors and normal embryonal neuroblasts, but reduced in late stage neuroblastoma. Inactivation of FOXO3a by AKT was essential for neuroblastoma cell survival. Treatment of neuroblastoma cells with the dual PI3K/mTOR inhibitor PI-103 activated FOXO3a and triggered apoptosis. This effect was rescued by FOXO3a silencing. Conversely, apoptosis induced by PI-103 or the AKT inhibitor MK-2206 was potentiated by FOXO3a overexpression. Further, levels of total or phosphorylated FOXO3a correlated closely with apoptotic sensitivity to MK-2206. In clinical specimens, there was an inverse relationship between gene expression signatures regulated by PI3K signaling and FOXO3a transcriptional activity. Moreover, high PI3K activity and low FOXO3a activity were each associated with an extremely poor prognosis. Our work indicates that expression of FOXO3a and its targets offer useful prognostic markers as well as biomarkers for PI3K/AKT inhibitor efficacy in neuroblastoma. Affymetrix U133 Plus 2.0 profiling of SY5Y-TetR-FOXO3A cells treated with doxycycline and/or the PI3K/mTOR inhibitor PI-103. Each condition profiled in triplicate.

2013-05-01 | E-GEOD-42762 | biostudies-arrayexpress

FOXO3a Is A Major Target Of Inactivation By PI3K/AKT Signaling In Aggressive Neuroblastoma

2013-05-01 | GSE42762 | GEO

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