Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Early measurable residual disease dynamics and B cell receptor reconstitution following venetoclax and obinutuzumab in chronic lymphocytic leukemia

ABSTRACT: Early measurable residual disease dynamics and B cell receptor reconstitution following venetoclax and obinutuzumab in chronic lymphocytic leukemia

PROVIDER: PRJNA933608 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR23400700_1.fastq.gz	Fastqsanger.gz
	SRR23400700_2.fastq.gz	Fastqsanger.gz
	SRR23400800_1.fastq.gz	Fastqsanger.gz
	SRR23400800_2.fastq.gz	Fastqsanger.gz
	SRR23400900_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 454

Similar Datasets

Early measurable residual disease dynamics and B cell receptor reconstitution following venetoclax and obinutuzumab in chronic lymphocytic leukemia

Project description:In chronic lymphocytic leukemia, measurable residual disease (MRD) depth following fixed-duration treatment is associated with progression-free survival (PFS). Often, MRD is reported as a static parameter, but successive MRD measurements may more accurately capture MRD dynamics and reveal valuable prognostic information. We used our recently developed IGHV leader-based NGS assay to measure MRD at four timepoints in 60 patients treated in the HOVON-139/GIVE trial, in which previously untreated patients received one year induction treatment with obinutuzumab and venetoclax, followed by randomization to consolidation treatment with venetoclax or MRD-conditional consolidation. Induction treatment resulted in MRD undetectability (<10-5) in 93% of assessed patients, with 85% and 74% of patients retaining MRD undetectability at six and twelve months after randomization. Uniquely, we measured MRD at a very early timepoint, during the fourth week of venetoclax ramp-up after obinutuzumab pre-induction. Here, MRD levels showed large interindividual variation, and, importantly, were associated with the probability of achieving MRD undetectability after induction treatment, MRD conversion after randomization and PFS. Additionally, the IGHV leader-based NGS assay allows characterization of the healthy background IGHV repertoire. Of note, venetoclax consolidation treatment, compared to no consolidation treatment, significantly impaired polyclonal IGHV repertoire reconstitution after induction treatment with venetoclax and obinituzumab.

2024-03-01 | GSE225043 | GEO

Immune recovery in tumor microenvironment of TP53-mutated AML following venetoclax combination therapy

Project description:The BCL-2 inhibitor venetoclax combined with the hypomethylating agent azacitidine or with low-dose cytarabine significantly improves response rates and overall survival (OS) for newly diagnosed unfit and relapsed / refractory (R/R) acute myeloid leukemia (AML) patients. We retrospectively analyzed our experience with venetoclax combination therapy in 41 unfit AML patients (23 untreated, 18 R/R). Overall response rates were 78.3% for untreated patients and 61.1% for R/R patients. TP53 alterations were observed in 13 patients (31.7%) and were identified as an independent predictor of poor outcome (p=0.0008). We further conducted single-cell RNA sequencing in bone marrow, sampled before and after venetoclax and azacitidine treatment, of three TP53-mutated AML patients who achieved complete remission (CR) or CR with incomplete hematologic recovery. After treatment, numbers of cells expressing anti-apoptotic genes such as BCL2 and MCL1 decreased. CD4 T cells, cytotoxic CD8 T cells, and NK cells significantly increased both in number and in levels of gene expression associated with cytotoxicity post-treatment, confirming immune recovery in the tumor microenvironment. Residual AML cells expressed CD47 and CLEC12A (CLL1). These results indicate that venetoclax combination therapy of AML is promising in real-world clinical practice and suggest a role for ancillary treatment targeting antigens expressed on residual AML cells as a therapeutic strategy in TP53-mutated AML.

2025-08-30 | GSE306339 | GEO

Single-Cell RNA-Seq Datasets of residual AML cells purifed from Patient Derived Xenograft bone marrow treated or not with venetoclax plus cytarabine [Patient TUH69]

Project description:The goal of this study is to compare single cell transcriptome of in vivo AML cells profiling before treatment and after venetoclax and cytarabine in single agent or after the duplet. This study uncovered transcriptionally different cell subpopulations that specifically emerge in VEN+AraC residual disease.

2021-06-26 | GSE178911 | GEO

Single-Cell RNA-Seq Datasets of residual AML cells purifed from Patient Derived Xenograft bone marrow treated or not with venetoclax plus cytarabine [Patient TUH07]

2021-06-26 | GSE178910 | GEO

Early-stage measurable residual disease dynamics and IGHV repertoire reconstitution during venetoclax and obinutuzumab treatment in chronic lymphocytic leukemia.

Project description: Not available

| S-EPMC10317999 | biostudies-literature

CLL-Venetoclax

Project description:Clonal dynamics towards the development of venetoclax resistance in chronic lymphocytic leukemia

| PRJEB24344 | ENA

Measuring Minimal Residual Disease beyond 10-5 through IGHV leader-based NGS increases Prognostic Discrimination in Chronic Lymphocytic Leukemia

Project description:The sensitivity of conventional techniques for the quantification of minimal/measurable residual disease (MRD) in chronic lymphocytic leukemia (CLL) is limited to MRD 10-4. Measuring MRD <10-4 could help to further distinguish between CLL patients with durable remission and those at risk of early relapse. We here present a novel, academically developed IGHV leader-based next-generation sequencing (NGS) assay for the quantification of MRD in CLL. We demonstrate, based on measurements in contrived MRD samples, that the linear range of detection and quantification of our novel assay reaches beyond MRD 10-5. If provided with sufficient DNA input, MRD can even be detected down to MRD 10-6. There was high inter-assay concordance between measurements of the IGHV leader-based NGS assay and allele-specific oligonucleotide quantitative PCR (r=0.92, [95%CI 0.86-0.96]) and droplet digital PCR (r=0.93, [95%CI 0.88-0.96]) on contrived MRD samples. In a cohort of 37 patients from the CLL11 trial, using MRD 10-5 as a cut-off, MRD undetectability was associated with superior progression-free survival (PFS) and time to next treatment. Importantly, deeper MRD measurement allowed for additional stratification of patients with MRD <10-4 but ≥10‑5. Whereas the PFS of these patients was significantly shorter, compared to patients with MRD <10-5 (HR 4.9, [95%CI 1.3-17.9], P=0.017), their PFS was superior to those with MRD ≥10‑4 (HR 0.18, [95%CI 0.06-0.46], P<0.001). These results clearly demonstrate the clinical utility of the novel IGHV-leader based NGS assay.

2021-11-13 | GSE188587 | GEO

High Expression Level of ROR1 and ROR1-signaling Associates With Venetoclax Resistance In Chronic Lymphocytic Leukemia

Project description:We examined the CLL cells transcriptome data of six patients who fail to clear their leukemia cells and develop progressive disease on venetoclax therapy. Methods: CLL cells were collected prior to venetoclax therapy (Sample Collection 1 (SC1)) and then more than 1 year later (Sample Collection 2 (SC2)). Negative isolation of CLL cells to ≥95% purity was performed prior to RNA isolation.

2022-06-23 | GSE192685 | GEO

High Expression Level of ROR1 and ROR1-signaling Associates With Venetoclax Resistance In Chronic Lymphocytic Leukemia

Project description:High Expression Level of ROR1 and ROR1-signaling Associates With Venetoclax Resistance In Chronic Lymphocytic Leukemia

| PRJNA792609 | ENA

IMPRINTS-CETSA Venetoclax in Kasumi-1 cells, 6h incubation

Project description:IMPRINTS-CETSA data acquisition of Kasumi-1 cells treated with Vehicle (DMSO), Venetoclax, Decitabine, Azacitidine and Azacitidine+Venetoclax using TMT 16 plex.

2024-10-23 | PXD056189 | Pride

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