Browse
Submit Data
Databases
API
Help

Dataset Information

7 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Safety Study of the Drug MM-151 in Patients With Advanced Solid Tumors Resisting Ordinary Treatment

ABSTRACT: This study is a Phase 1 and pharmacologic open-labeled dose-escalation trial using a "3+3" design, evaluating MM-151 at varying dose levels and frequencies, and subsequently in combination with irinotecan.

DISEASE(S): Triple Negative Breast Neoplasms,Colorectal Cancer,Advanced Solid Tumors,Squamous Cell Head And Neck Cancer,Non Small Cell Lung Cancer,Triple Negative Breast Cancer,Solid Tumors,Cancer

PROVIDER: 2119391 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

ACCESS DATA

Json Xml

Similar Datasets

Phase 1 Combination Study of MM-151 With MM-121, MM-141, or Trametinib

Project description:This is a Phase 1 open-label, dose-escalation trial using "3+3" design, evaluating MM-151 co-administration with MM-121, MM-141, and trametinib at varying dose levels.

| 2197256 | ecrin-mdr-crc

Evaluation of MM-151 + Nal-IRI + 5-FU + Leucovorin in RAS/RAF Wild-type Metastatic Colorectal Cancer

Project description:A phase 1b/2a study evaluating the combination of MM-151 + nal-IRI + 5-FU + Leucovorin in RAS/RAF wild-type Metastatic Colorectal Cancer.

| 2216131 | ecrin-mdr-crc

Cellulosimicrobium sp. MM strain:MM

Project description:Cellulosimicrobium sp. MM strain:MM Genome sequencing and assembly

| PRJNA255748 | ENA

Emticicia sp. MM strain:MM

Project description:Emticicia sp. MM strain:MM Genome sequencing and assembly

| PRJNA316534 | ENA

Global proteomics in MM.1S treated with pomalidomide or dipeptides

Project description:Global proteomics of Multiple Myeloma cell line MM.1S treated with pomalidomide or cyclic imide dipeptides for 10 h. The samples were labeled with TMT-16pro.

2022-07-28 | PXD025336 | Pride

RNA-seq analysis after JQKD82 treatment in human multiple myeloma cell line MM.1S

Project description:Recent studies have highlighted the oncogenic roles of KDM5A; however, its molecular mechanism has not been fully delineated. Here we identifies KDM5A as a transcriptional activator of MYC target genes in multiple myeloma (MM). Genetic ablation of KDM5A or pharmacologic inhibition of KDM5 by novel inhibitor JQKD82 impairs MM cell growth. Gene expression profile reveals that JQKD82 decreases expression of MYC targets. Expression of MYC targets is similarly downregulated by KDM5A depletion, but little affected by KDM5B knockdown. Mechanistically, KDM5A co-localizes with MYC across the genome, and KDM5A and MYC coordinately promote MYC target gene transcription. The treatment with JQKD82 reduces phosphorylation level of RNA polymerase II (RNAPII), resulting in RNAPII pausing, accompanied by hyper-H3K4me3 status at the MYC loci. Finally, we shows that JQKD82 exerts anti-MM activity and prolongs overall survival in vivo mouse xenograft models. Our results delineate KDM5A function that reinforces MYC transcriptional program, and identify KDM5A as a potential therapeutic target in MM.

2021-03-22 | GSE148047 | GEO

Gene expression in glucose-grown P. putida KT2440 before and after 5 mM catechol addition

Project description:mRNA was sampled during exponential growth (OD600 = 2, Control), then an inhibitory dose of 5 mM catechol was added to the culture and samples were taken again after 1h (Stress)

2022-06-09 | GSE196571 | GEO

Chidamide effect on MM

Project description:Chidamide effect on MM

| PRJNA658123 | ENA

ChIP-seq and RNA-seq analyses in human multiple myeloma cell line MM.1S

2021-03-22 | GSE148048 | GEO

Clinical drug resistance linked to reversible phenotypic transition and epigenetic alteration in multiple myeloma

Project description:The development of proteasome inhibitors (PIs) for the treatment of multiple myeloma (MM) has dramatically increased treatment responses and improved survival. The first-in-class PI, bortezomib, was used in a twice-weekly intravenous as a sustained single or combinational regimen for relapsed and subsequently for newly diagnosed MM. The relatively rapid acquisition of drug resistance to PI treatment remains a crucial obstacle. Gradual familiarity with toxicity and optimizing dose schedules have formed the current use of PIs as key components in promoting response and eliminating resistance. Combination therapies and schedule adaptation to once-weekly use of PIs have meanwhile been shown to be both more tolerable and highly efficacious. Interestingly, patients may remain sensitive to PIs after relapse of initial therapy, implying that PI resistance is reversible and suggest a previously unrecognized drug resistance mechanism via epigenetic changes that may be intrinsic to PI treatment.

2021-02-24 | GSE136725 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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