Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MDA-MB-468 cells treated with docetaxel or EZH2i+AKTi

ABSTRACT: MDA-MB-468 cells treated with docetaxel or EZH2i+AKTi

PROVIDER: PRJNA1055096 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR27290500_1.fastq.gz	Fastqsanger.gz
	SRR27290500_2.fastq.gz	Fastqsanger.gz
	SRR27290489_1.fastq.gz	Fastqsanger.gz
	SRR27290489_2.fastq.gz	Fastqsanger.gz
	SRR27290490_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 72

Similar Datasets

MDA-MB-468 cell line treated with AKTi (ipatasertib) and EZH2i (tazemetostat)

Project description:MDA-MB-468 cell line treated with AKTi (ipatasertib) and EZH2i (tazemetostat).

2024-01-01 | GSE205729 | GEO

MDA-MB-468 cells treated with docetaxel or EZH2i+AKTi I

Project description:MDA-MB-468 cells treated with docetaxel or EZH2i+AKTi I

| PRJNA1054653 | ENA

MDA-MB-468 cells treated with docetaxel or EZH2i+AKTi II

Project description:MDA-MB-468 cells treated with docetaxel or EZH2i+AKTi II

| PRJNA1055097 | ENA

MDA-MB-468 cell line treated with AKTi (ipatasertib) and EZH2i (tazemetostat)

Project description:MDA-MB-468 cell line treated with AKTi (ipatasertib) and EZH2i (tazemetostat)

| PRJNA847253 | ENA

MDA-MB-468 and SUM149PT cell lines treated with AKTi (ipatasertib) and EZH2i (tazemetostat)

Project description:MDA-MB-468 and SUM149PT cell lines treated with AKTi (ipatasertib) and EZH2i (tazemetostat)

| PRJNA847247 | ENA

MDA-MB-468 cells treated with docetaxel or EZH2i+AKTi

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-07-08 | GSE251710 | GEO

MDA-MB-468 cells treated with docetaxel or EZH2i+AKTi I

Project description:Triple negative breast cancer (TNBC) is the most aggressive breast cancer subtype and has the highest rate of recurrence1. The predominant standard of care for advanced TNBC is systemic chemotherapy with or without immunotherapy, however responses are typically short-lived1,2. Thus, there is an urgent need to develop more effective treatments. PI3K pathway components represent plausible therapeutic targets, as approximately 70% of TNBCs have PIK3CA/AKT1/PTEN alterations3–6. However, unlike hormone receptor-positive tumors, it is still unclear if or how PI3K pathway inhibitors will be effective in triple-negative disease7. Here we identify a promising AKT inhibitor-based therapeutic combination for TNBC. Specifically, we show that AKT inhibitors potently synergize with agents that suppress the histone methyltransferase, EZH2, and promote robust tumor regression in multiple TNBC models in vivo. AKT and EZH2 inhibitors exert these effects by first cooperatively driving basal-like TNBC cells into a more differentiated, luminal-like state, which cannot be effectively induced by either agent alone. Once differentiated, these agents kill TNBCs by hijacking signals that normally drive mammary gland involution. Finally, using machine learning approach, we developed a classifier that can be used for patient selection. Together these findings identify a promising therapeutic strategy for this highly aggressive tumor type and illustrate how deregulated epigenetic enzymes can insulate tumors from oncogenic vulnerabilities. These studies also reveal how developmental tissue-specific cell death pathways may be co-opted for therapeutic benefit.

2024-07-08 | GSE250632 | GEO

MDA-MB-468 cells treated with docetaxel or EZH2i+AKTi II

2024-07-08 | GSE251708 | GEO

SUM149PT cell line treated with AKTi (ipatasertib) and EZH2i (tazemetostat)

Project description:SUM149PT cell line treated with AKTi (ipatasertib) and EZH2i (tazemetostat).

2024-01-01 | GSE205730 | GEO

MDA-MB-468 and SUM149PT cell lines treated with AKTi (ipatasertib) and EZH2i (tazemetostat)

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-01-01 | GSE205731 | GEO