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The Ontogeny and Vulnerabilities of Lapatinib Drug Tolerant Persisters [NPY1R]

ABSTRACT: The Ontogeny and Vulnerabilities of Lapatinib Drug Tolerant Persisters [NPY1R]

PROVIDER: PRJNA648987 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12332939_1.fastq.gz	Fastqsanger.gz
	SRR12332939_2.fastq.gz	Fastqsanger.gz
	SRR12332940_1.fastq.gz	Fastqsanger.gz
	SRR12332940_2.fastq.gz	Fastqsanger.gz
	SRR12332941_1.fastq.gz	Fastqsanger.gz

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The Ontogeny and Vulnerabilities of Lapatinib Drug Tolerant Persisters

Project description:The Ontogeny and Vulnerabilities of Lapatinib Drug Tolerant Persisters

| PRJNA649424 | ENA

The Ontogeny and Vulnerabilities of Lapatinib Drug Tolerant Persisters [NPY1R]

Project description:Despite significant advances in HER2-targeted therapies, therapeutic resistance in HER2-positive (HER2+) breast cancer remains a significant clinical problem, especially in the metastatic setting. “Drug tolerant persisters” (DTPs), a sub-population of cancer cells that survive via reversible, non-genetic mechanisms, are implicated in resistance to tyrosine kinase inhibitors (TKIs) in several cancer models, but DTPs for HER2-targeted TKIs (e.g., lapatinib, neratinib, tucatinib) have not been characterized extensively. Here, we report that HER2+ER+ and HER2+ER- breast cancer lines give rise to distinct types of “lapatinib-DTPs,” characterized by different transcriptional programs and sensitivity to lapatinib/anti-estradiol combination. Lapatinib-DTPs from HER2+/ER+ cells rewire the PI3K/AKT/mTORC1 pathway via transcriptional induction of SGK3 to enable AKT-independent mTORC1 activation and survival. Lentiviral barcoding experiments, combined with single cell RNA-sequencing, suggest that HER2+ cells stochastically cycle through a cell state (“pre-DTP”) capable of transition to DTPs. Collectively, our results provide insight into DTP ontogeny and therapeutic vulnerabilities.

2021-12-31 | GSE155227 | GEO

The Ontogeny and Vulnerabilities of Lapatinib Drug Tolerant Persisters [Parental (P) vs. Drug-Tolerant Persister (DTP)]

2021-12-31 | GSE155341 | GEO

The Ontogeny and Vulnerabilities of Lapatinib Drug Tolerant Persisters [Parental (P) vs. Drug-Tolerant Persister (DTP)]

Project description:The Ontogeny and Vulnerabilities of Lapatinib Drug Tolerant Persisters [Parental (P) vs. Drug-Tolerant Persister (DTP)]

| PRJNA649434 | ENA

Ontogeny and Vulnerability of Lapatinib Drug-Tolerant Persisters in HER2-positive Breast Cancer

Project description:Despite advances in HER2-targeted therapeutics, resistance remains a significant clinical problem in HER2-positive (HER2+) breast cancer, especially in the metastatic setting. Drug-tolerant persisters (DTPs), a sub-population of cancer cells that survive via reversible, non-genetic mechanisms, are implicated in resistance to tyrosine kinase inhibitors (TKIs) in several cancer models, but DTPs for HER2-targeted TKIs have not been characterized extensively. We found that upon treatment with the TKI lapatinib, HER2+ breast cancer lines yielded DTPs with luminal-like or mesenchymal-like transcriptional programs and differential sensitivity to lapatinib/anti-estradiol combinations. Lentiviral barcoding and single cell RNA-sequencing indicate that HER2+/ER+ cells cycle stochastically through a pre-DTP state, characterized by a G0-like signature, which uniquely gives rise to DTPs upon lapatinib exposure.

2021-12-13 | GSE156246 | GEO

Ontogeny and Vulnerability of Lapatinib Drug-Tolerant Persisters in HER2-positive Breast Cancer

Project description:Ontogeny and Vulnerability of Lapatinib Drug-Tolerant Persisters in HER2-positive Breast Cancer

| PRJNA657182 | ENA

The Ontogeny and Vulnerabilities of Lapatinib Drug Tolerant Persisters

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

2021-12-31 | GSE155342 | GEO

Mutation independent activation of the Notch pathway is associated with Lapatinib resistance in Her2+ breast cancer cell lines

Project description:We compared untreated HCC1419 cells with Lapatinib resistant HCC1419 cells that were either treated with Lapatinib for only 9 days before harvesting (drug tolerant persisters, DTPs) or were growing in the presence of Lapatinib (>70 days) (drug tolerant expanded persisters, DTEPs). We show that the Notch pathway is significantly over-expressed in DTEPs when compared to untreated cells.

2015-01-15 | GSE62074 | GEO

Mutation independent activation of the Notch pathway is associated with Lapatinib resistance in Her2+ breast cancer cell lines

2015-01-15 | E-GEOD-62074 | biostudies-arrayexpress

Characterization of Metronidazole-tolerant Porphyromonas gingivalis Persisters

Project description:This project investigated the phenotypic characteristics of Metronidazole-tolerant Porphyromonas gingivalis persisters, the relevant modulatory effects of hemin and their underlying survival mechanisms. Proteomic analysis was performed to delineate the protein expression profiles of Metronidazole-tolerant P. gingivalis persister fractions and the controls incubated with different levels of hemin supplementation.

2018-08-29 | PXD008976 | Pride

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