Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MUC1-C DEPENDENCY IN DRUG RESISTANT HR+/HER2- BREAST CANCER IDENTIFIES A NEW TARGET FOR TREATMENT WITH AN ANTIBODY-DRUG CONJUGATE

ABSTRACT: MUC1-C DEPENDENCY IN DRUG RESISTANT HR+/HER2- BREAST CANCER IDENTIFIES A NEW TARGET FOR TREATMENT WITH AN ANTIBODY-DRUG CONJUGATE

PROVIDER: PRJNA1139759 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR29964000_1.fastq.gz	Fastqsanger.gz
	SRR29964000_2.fastq.gz	Fastqsanger.gz
	SRR29964001_1.fastq.gz	Fastqsanger.gz
	SRR29964001_2.fastq.gz	Fastqsanger.gz
	SRR29964002_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

MUC1-C DEPENDENCY IN DRUG RESISTANT HR+/HER2- BREAST CANCER IDENTIFIES A NEW TARGET FOR TREATMENT WITH AN ANTIBODY-DRUG CONJUGATE

Project description:MUC1-C is a common effector of treatment resistant HR+/HER2- BC cells and is a potential target for their treatment

2025-04-17 | GSE272989 | GEO

Identification of MUC1-C Dependence in Drug-Resistant Advanced Prostate Cancer Uncovers a New Target for Antibody-Drug Conjugate Therapy

Project description:Androgen receptor positive prostate cancer (PC), castration resistant prostate cancer (CRPC) and neuroendocrine prostate cancer (NEPC) represent a spectrum of malignancies that invariably become resistant to treatment with targeted and cytotoxic agents. There is no known common pathway responsible for these pleotropic mechanisms of resistance. The MUC1 gene is aberrantly expressed in CRPC and NEPC in association with poor clinical outcomes. The present results demonstrate that the oncogenic MUC1-C protein is necessary for resistance of (i) PC cells to enzalutamide (ENZ), and (ii) CRPC and NEPC cells to docetaxel (DTX). We show that MUC1-C-mediated ENZ and DTX resistance is conferred by upregulation of aerobic glycolysis and suppression of reactive oxygen species (ROS) necessary for self-renewal capacity. Common dependence of these drug-resistant phenotypes on MUC1-C for the cancer stem cell (CSC) state thus identified a potential new target for their treatment. cIn this context, we further demonstrate that targeting MUC1-C with an antibody-drug conjugate (ADC) is highly effective in suppressing (i) self-renewal of drug-resistant CRPC and NEPC CSCs and (ii) growth of t-NEPC tumor xenografts derived from drug-resistant cells and a patient with refractory disease. These findings reveal a shared MUC1-C-dependent pathway in drug-resistant CRPC and NEPC progression and identify MUC1-C as a target for their treatment with an ADC.

2025-01-02 | GSE276890 | GEO

Identification of MUC1-C Dependence in Drug-Resistant Advanced Prostate Cancer Uncovers a New Target for Antibody-Drug Conjugate Therapy

2025-01-02 | GSE276750 | GEO

Identification of MUC1-C Dependence in Drug-Resistant Advanced Prostate Cancer Uncovers a New Target for Antibody-Drug Conjugate Therapy

Project description:Identification of MUC1-C Dependence in Drug-Resistant Advanced Prostate Cancer Uncovers a New Target for Antibody-Drug Conjugate Therapy

| PRJNA1158796 | ENA

Identification of MUC1-C Dependence in Drug-Resistant Advanced Prostate Cancer Uncovers a New Target for Antibody-Drug Conjugate Therapy

Project description:Identification of MUC1-C Dependence in Drug-Resistant Advanced Prostate Cancer Uncovers a New Target for Antibody-Drug Conjugate Therapy

| PRJNA1159347 | ENA

MUC1-C IS ESSENTIAL FOR INFLAMMATORY MEMORY OF TYROSINE KINASE INHIBITOR RESISTANCE IN NSCLC CELLS

Project description:This study identifies the oncogenic protein MUC1-C as a key driver of resistance to the EGFR tyrosine kinase inhibitor osimertinib in non-small cell lung cancers (NSCLCs).MUC1-C promotes resistance by activating STAT1 and type I/II interferon pathways, creating an inflammatory memory of the resistant phenotype. This memory is maintained via MUC1-C/STAT1 interaction at one enhancer region (pELS-1) and MUC1-C/JUN/PBAF at another (pELS-2) in the MUC1 gene. MUC1-C also mediates resistance to combination EGFR/MET inhibitors and a fourth-generation EGFR TKI (TQB3804). Importantly, targeting MUC1-C with an antibody-drug conjugate (M1C ADC) is effective both in vitro and in a patient-derived xenograft model, making MUC1-C a promising therapeutic target for TKI-refractory NSCLC.

2025-04-22 | GSE294981 | GEO

Treatment-Resistant Prostate Cancer Stem Cell Plasticity Governed by MUC1-C Uncovers a Common target for ADC Treatment

2025-02-16 | GSE289308 | GEO

PANCREATIC DUCTAL ADENOCARCINOMAS RESISTANT TO KRAS INHIBITION ARE DRUGGABLE WITH AN ANTI-MUC1-C ADC

Project description:Treatment of pancreatic ductal carcinomas (PDACs) has been advanced by the development of KRAS mutant inhibitors. Despite this progress, PDACs invariably develop resistance to these agents by mechanisms that largely remain unclear. The MUC1 gene, which encodes an oncogenic MUC1-C protein, is upregulated in PDAC KRAS G12D tumors. We report that treatment of PDAC cells with the selective KRAS G12D MRTX1133 inhibitor is associated with induction of MUC1-C expression. We show that KRAS G12D inhibition activates a MUC1-C/NF-B p65 auto-inductive pathway. Our results further demonstrate that MUC1-C drives resistance to MRTX1133 by activating the inflammatory IFN type I and II pathways. Of clinical relevance, targeting MUC1-C genetically and pharmacologically reverses MRTX1133 resistance and is synergistic in combination with MRTX1133 treatment. In leveraging MRTX1133-induced upregulation of MUC1-C expression, an anti-MUC1-C (M1C) antibody-drug conjugate (ADC) is highly effective against MRTX1133-resistant PDAC KRAS G12D cell lines, patient-derived organoids and PDX tumor xenograft models. These findings demonstrate that MUC1-C confers resistance of PDAC KRAS G12D mutant cells to MRTX1133 and identify MUC1-C as a target for M1C ADC treatment of PDAC patients who are refractory to MRTX1133 treatment.

2025-04-08 | GSE293756 | GEO

A microbial-inspired antibody-drug conjugate for cancer immunotherapy

Project description:A microbial-inspired antibody-drug conjugate for cancer immunotherapy

| PRJNA1077275 | ENA

Sequencing the anti-MUC1 hybridoma antibody 139H2

Project description:Mucin 1 (MUC1) is a transmembrane mucin expressed at the apical surface of epithelial cells at different mucosal surfaces including breast and intestine. The MUC1 extracellular domain contains a variable number of tandem repeats (VNTR) of 20 amino acids, which are heavily O-linked glycosylated. Monoclonal antibodies against the MUC1 VNTR can be powerful tools because of their multiplicity of binding and possible applications in the diagnosis and treatment of MUC1-expressing cancers. One such antibody is the hybridoma mouse monoclonal 139H2 which is also widely used as a research tool to study non-cancer MUC1. Here we report direct mass spectrometry-based sequencing of hybridoma-derived 139H2 IgG, which enabled reverse engineering of a recombinant 139H2.

2024-03-18 | PXD043489 | 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