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Antibody Dependent Cell-Mediated Cytotoxicity Selection Pressure Induces Diverse Mechanisms of Resistance

ABSTRACT: Antibody Dependent Cell-Mediated Cytotoxicity Selection Pressure Induces Diverse Mechanisms of Resistance

PROVIDER: PRJNA852957 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19854516_1.fastq.gz	Fastqsanger.gz
	SRR19854516_2.fastq.gz	Fastqsanger.gz
	SRR19854517_1.fastq.gz	Fastqsanger.gz
	SRR19854517_2.fastq.gz	Fastqsanger.gz
	SRR19854518_1.fastq.gz	Fastqsanger.gz

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Antibody Dependent Cell-Mediated Cytotoxicity Selection Pressure Induces Diverse Mechanisms of Resistance (CITE-Seq)

Project description:Antibody Dependent Cell-Mediated Cytotoxicity Selection Pressure Induces Diverse Mechanisms of Resistance (CITE-Seq)

| PRJNA852959 | ENA

Antibody Dependent Cell-Mediated Cytotoxicity Selection Pressure Induces Diverse Mechanisms of Resistance (scATAC-Seq)

Project description:Antibody Dependent Cell-Mediated Cytotoxicity Selection Pressure Induces Diverse Mechanisms of Resistance (scATAC-Seq)

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Antibody Dependent Cell-Mediated Cytotoxicity Selection Pressure Induces Diverse Mechanisms of Resistance (scATAC-Seq)

Project description:Targeted monoclonal antibody therapy has emerged as a powerful therapeutic strategy for cancer. Unfortunately, only a minority of patients haves durable responses and the development of resistance remains a major clinical obstacle. Antibody-dependent cell-mediated cytotoxicity (ADCC) represents a crucial therapeutic mechanism of action; however few studies have explored ADCC resistance. Using multiple in vitro models of ADCC selection pressure, we have uncovered both shared and distinct resistance mechanisms. We employed CITE sequencing and single-cell ATAC-seqeuncing to interrogate molecular mechanisms of resistance.

2023-11-13 | GSE206954 | GEO

Antibody Dependent Cell-Mediated Cytotoxicity Selection Pressure Induces Diverse Mechanisms of Resistance (CITE-Seq)

2023-11-13 | GSE206953 | GEO

Antibody Dependent Cell-Mediated Cytotoxicity Selection Pressure Induces Diverse Mechanisms of Resistance

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-11-13 | GSE206955 | GEO

Antibody dependent cell-mediated cytotoxicity selection pressure induces diverse mechanisms of resistance.

Project description:Targeted monoclonal antibody therapy has emerged as a powerful therapeutic strategy for cancer. However, only a minority of patients have durable responses and the development of resistance remains a major clinical obstacle. Antibody-dependent cell-mediated cytotoxicity (ADCC) represents a crucial therapeutic mechanism of action; however, few studies have explored ADCC resistance. Using multiple in vitro models of ADCC selection pressure, we have uncovered both shared and distinct resistance mechanisms. Persistent ADCC selection pressure yielded ADCC-resistant cells that are characterized by a loss of NK cell conjugation and this shared resistance phenotype is associated with cell-line dependent modulation of cell surface proteins that contribute to immune synapse formation and NK cell function. We employed single-cell RNA sequencing and proteomic screens to interrogate molecular mechanisms of resistance. We demonstrate that ADCC resistance involves upregulation of interferon/STAT1 and DNA damage response signaling as well as activation of the immunoproteasome. Here, we identify pathways that modulate ADCC sensitivity and report strategies to enhance ADCC-mediated elimination of cancer cells. ADCC resistance could not be reversed with combinatorial treatment approaches. Hence, our findings indicate that tumor cells utilize multiple strategies to inhibit NK cell mediated-ADCC. Future research and development of NK cell-based immunotherapies must incorporate plans to address or potentially prevent the induction of resistance.

| S-EPMC10601508 | biostudies-literature

Genetic adaptability of cancer cells under treatment selection pressure in multiple myeloma patients.

Project description:Purpose Despite advances and significant improvement in survival, multiple myeloma (MM) remains incurable and nearly all patients relapse after treatment. Previous studies have shown a complex spectrum of diverse genetic alterations in almost all patients, but evolution of genomic rearrangements throughout myeloma life cycle has not been investigated. Patients and Methods We performed genomic analysis integrating copy number, allele specific copy number, allele ratio calculations, breakpoint sequencing and rearrangement PCR genotyping on matched diagnosis and relapse samples from 24 MM patients either treated with proteasome inhibitor (bortezomib)-based induction regimen or conventional chemotherapeutic agents. Results All relapse samples have a clear relationship to the diagnosis clone with significant increase of copy number abnormalities (CNAs). Despite a wide diversity of CNAs acquired at relapse, regulators of NF-kB activity were targeted in 25% of the patients. Relapse-associated lesions either appeared as new acquisition or were selected from minor subpopulations at diagnosis. In one third of the patients, we found loss of abnormities containing loss of heterozygosity (LOH) providing evidence that the relapse clone derived from an ancestral clone shared with the dominant diagnosis clone. Remarkably, re-emergence of ancestral clones was almost exclusively found in patients treated with bortezomib, attested to a remarkable adaptability of myeloma cells under targeted drug selection pressure. Conclusion These data suggest that genomic instability and clonal selection are the main forces that drive adaptive changes in MM under drug selection pressure, and they support the proposal to combine several anti-myeloma drugs upfront in order to obtain long-term remissions. [SNP genotyping] 24 myeloma patients at diagnosis and relapse examined with high resolution genome-wide chip

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Genetic adaptability of cancer cells under treatment selection pressure in multiple myeloma patients.

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Pseudogene repair driven by selection pressure applied in experimental evolution

Project description:Pseudogene repair driven by selection pressure applied in experimental evolution

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Genetic variation and signatures of natural selection in diverse Africans

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