Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of alisertib and navitoclax on gene expression in B16 melanoma tumors

ABSTRACT: To investigate how tumor cells respond to alisertib and navitoclax single agents and combonation therapy in vivo, mice with melanoma were treated with these agents or vehicle-contol. RNAseq was used to investigate gene expression in tumors

ORGANISM(S): Mus musculus

PROVIDER: GSE212127 | GEO | 2022/10/26

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Effect of alisertib and navitoclax on gene expression in B16 melanoma tumors

Project description:Effect of alisertib and navitoclax on gene expression in B16 melanoma tumors

| PRJNA874062 | ENA

Modulation of Navitoclax Sensitivity by Dihydroarteminisin-Mediated MCL-1 Repression

Project description:Poor prognosis BCR-ABL+ B-ALL leukemic cells are highly dependent on the expression of endogenous anti-apoptotic MCL-1. However, the survival of most normal blood cells (e.g. progenitors, lymphocytes, and granulocytes) and other normal cell types (e.g. cardiomyocytes and neurons) are also exquisitely dependent on Mcl-1 gene expression, suggesting that effective therapeutic inhibition of MCL-1 could be acutely toxic, especially when combined with standard chemotherapy. Therefore, as an alternative to MCL-1 inhibition, we have identified dihydroarteminisin (DHA), a water-soluble metabolite of the anti-malarial arteminisin, which induces the down-modulation of MCL-1 protein expression by triggering an endoplasmic reticulum stress response. The DHA induced repression of MCL-1 expression renders leukemic cells highly sensitive to synergistic cell death induced by BH3-mimetic agents such as navitoclax (ABT-263) in a mouse model of BCR-ABL+ B-ALL. Furthermore, DHA also synergizes with navitoclax in human Ph+ ALL cell lines, and primary patient derived xenografts of Ph+ ALL. These data demonstrate that combining DHA with BH3-mimetic agents can improve therapeutic response in poor prognosis leukemia.

2018-02-14 | GSE95809 | GEO

Salinomycin treatment of Alisertib induced senescent A549 cells

Project description:Bulk RNA-seq data of alisertib induced senescent cells treated with Salinomycin vs. Untreated

2024-11-25 | GSE279184 | GEO

RNA Sequencing MDA-MB-231 Treared with TGFβ and Alisertib

Project description:RNA sequencing was performed on MDA-MB-231 samples treated with TGFβ nad Alisertib to obtaine the TGFβ-mediated gene expression profile which is regulated by AURKA activity.

2020-12-31 | GSE160990 | GEO

Effect of senolytics (Navitoclax, ABT263) on recovery following Myocardial Infarction

Project description:Ischemia reperfusion injury (IRI) following intervention for myocardial infarction remains an unmet clinical problem. Using an established mouse model, we demonstrated that IRI induces multiple cardiac cell linages to senescence. Senescence is is detrimental to recovery, as treatment with the senolytic navitoclax improves functional recovery.Here we are using SWATH-MS to investigate the molecular mechanisms responsible for the effect of navitoclax treatment.

2020-02-29 | MSV000085040 | MassIVE

Alisertib treatment in FANCA-deficient cell lines

Project description:Alisertib treatment in FANCA-deficient cell lines

| PRJEB113242 | ENA

Salinomycin treatment of Alisertib induced senescent A549 cells

Project description:Salinomycin treatment of Alisertib induced senescent A549 cells

| PRJNA1171320 | ENA

Cytokine Stimulation of ADAR-deleted B16 murine melanoma cells

Project description:ADAR was deleted from the B16 murine melanoma line using CRISPR/Cas9. The loss-of-function phenotype was assessed in vitro with cytokine stimulation or vehicle control.

2018-12-30 | GSE110708 | GEO

Irinotecan and Alisertib in Treating Patients With Advanced Solid Tumors or Colorectal Cancer

Project description:This phase I trial studies the side effects and best dose of alisertib when given together with irinotecan hydrochloride in treating patients with advanced solid tumors or colorectal cancer. Irinotecan hydrochloride and alisertib may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth.

| 2150139 | ecrin-mdr-crc

Dual BCL-xL and BCL-2 Inhibition for Advanced Myeloid Neoplasms: A phase 1 dose-escalation study of Navitoclax, Venetoclax, and Decitabine

Project description:Background: The BCL-2 inhibitor venetoclax in combination with a hypomethylating agent is effective against most acute myeloid leukemia (AML) subtypes, but less so against other high-risk myeloid neoplasms. One resistance mechanism to BCL-2 inhibition is increased dependence on alternate BH3-only anti-apoptotic proteins, such as BCL-xL. Navitoclax is a BCL-2/BCL-xL inhibitor that has been previously studied in hematologic malignancies. Patients and methods: We conducted a Phase 1 study of dose-escalated navitoclax added to venetoclax/decitabine for subjects with 1) secondary (s-AML) or therapy-related AML, 2) accelerated- or blast-phase myelofibrosis (AP/BP-MF), 3) myelodysplastic syndrome (MDS)/myeloproliferative neoplasm (MPN) overlap syndromes with excess blasts, or 4) relapsed/refractory (R/R) MDS with excess blasts. Results:Sixteen subjects were enrolled. Dose-escalation for BP-MF and s-AML was not completed due to discontinued navitoclax supply. Most common grade ≥3 treatment-emergent adverse events included neutropenia (69%), thrombocytopenia (69%), and febrile neutropenia (47%). No clinically significant bleeding was observed. One dose-limiting toxicity of delayed neutrophil recovery occurred. Among 15 evaluable subjects, the overall objective response rate was 60% (9/15). The recommended phase 2 dose was decitabine 20 mg/m2 days 1-5, venetoclax 400 mg/day days 1-14, and navitoclax 50 mg/day days 1-14 for AP-MF, MDS/MPN, and R/R MDS. Correlative studies indicate preserved immature platelet fractions despite on-target reduction of mature platelets, a reduction in disease-associated aberrant monocytes in subjects with monocytic disease, and higher baseline myeloblast dependence on BCL-2 and BCL-xL as predictive of response. Conclusion:Navitoclax added to venetoclax/decitabine is safely tolerable and is active in patients with high-risk myeloid malignancies.

2026-04-20 | GSE312447 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data