Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Crebbp loss drives small cell lung cancer and increases sensitivity to HDAC inhibition [preSC cell line]

ABSTRACT: Crebbp loss drives small cell lung cancer and increases sensitivity to HDAC inhibition [preSC cell line]

PROVIDER: PRJNA482448 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Crebbp loss drives small cell lung cancer and increases sensitivity to HDAC inhibition

Project description:Crebbp loss drives small cell lung cancer and increases sensitivity to HDAC inhibition

| PRJNA482442 | ENA

Crebbp loss drives small cell lung cancer and increases sensitivity to HDAC inhibition [thyroid]

Project description:Crebbp loss drives small cell lung cancer and increases sensitivity to HDAC inhibition [thyroid]

| PRJNA482447 | ENA

Crebbp loss drives small cell lung cancer and increases sensitivity to HDAC inhibition [SCLC]

Project description:Crebbp loss drives small cell lung cancer and increases sensitivity to HDAC inhibition [SCLC]

| PRJNA482450 | ENA

Crebbp loss drives small cell lung cancer and increases sensitivity to HDAC inhibition [pituitary tumor]

Project description:Crebbp loss drives small cell lung cancer and increases sensitivity to HDAC inhibition [pituitary tumor]

| PRJNA482449 | ENA

Crebbp loss drives small cell lung cancer and increases sensitivity to HDAC inhibition [thyroid]

Project description:This study assessed tumor suppressor roles of CREBBP in SCLC and other neuroendocrine tumors. Genetically engineered mouse models were used to determine the tumor suppressor role of Crebbp in SCLC and other neuroendocrine tumors.

2018-10-17 | GSE117551 | GEO

Crebbp loss drives small cell lung cancer and increases sensitivity to HDAC inhibition [SCLC]

2018-10-17 | GSE117547 | GEO

Crebbp loss drives small cell lung cancer and increases sensitivity to HDAC inhibition [pituitary tumor]

2018-10-17 | GSE117549 | GEO

Crebbp loss drives small cell lung cancer and increases sensitivity to HDAC inhibition [preSC cell line]

2018-10-17 | GSE117550 | GEO

CREBBP cooperates with cell cycle machinery to attenuate chidamide sensitivity in relapsed/refractory DLBCL

Project description:Frequent inactivating mutations of histone acetyltransferase CREBBP is a characteristic feature of diffuse large B-cell lymphoma (DLBCL), highlighting the attractiveness of targeting the CREBBP deficiency as a therapeutic strategy. In this study, we demonstrate that chidamide, a novel histone deacetylase (HDAC) inhibitor, is effective in treating a subgroup of relapsed/refractory DLBCL patients, achieving an overall response rate (ORR) of 25.0% and a complete response (CR) rate of 15.0%. However, the clinical response to chidamide remains poor as most patients exhibit resistance, hampering the clinical utility of the drug. Functional studies in both in vitro and in vivo models showed that CREBBP loss of function is correlated with chidamide sensitivity, which is associated with modulating cell cycle machinery. A combinatorial drug screening of 130 kinase inhibitors targeting cell cycle regulators identified AURKA inhibitors, which inhibited G2/M transition during cell cycling, as top candidates that synergistically enhanced antitumor effects of chidamide in CREBBP-proficient DLBCL cells. Our study demonstrated that CREBBP inactivation can serve as a potential biomarker to predict chidamide sensitivity, while a combination of AURKA inhibitor and chidamide provides a novel therapeutic strategy for the treatment of relapsed/refractory DLBCL.

2024-02-24 | GSE167383 | GEO