Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Deciphering Precursor Cell Dynamics in Esophageal Preneoplasia via Genetic Barcoding and Single-Cell Transcriptomics

ABSTRACT: Esophageal preneoplastic cells, despite appearing histologically normal, exhibit early genetic alterations and lineage plasticity, yet their origins and trajectories remain unclear. This study employs genetic barcoding combined with single-cell RNA sequencing to trace the lineage of esophageal preneoplastic cells and identify a distinct progenitor-like population with high plasticity. Through a newly developed scoring system, high-plasticity cells are mapped, revealing their contributions to proliferative and basal cell populations. The study identifies key molecular markers, including Nfib and Qk, that define these precursor cells. These findings provide critical insights into early tumorigenesis, highlighting the potential of precursor cells as biomarkers for early cancer detection and therapeutic targeting. By elucidating the cellular dynamics underlying esophageal cancer initiation, this research lays the foundation for strategies to prevent malignant progression, offering broader implications for improving cancer diagnostics and treatment approaches.

ORGANISM(S): Mus musculus

PROVIDER: GSE304762 | GEO | 2025/11/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Deciphering Precursor Cell Dynamics in Esophageal Preneoplasia via Genetic Barcoding and Single-Cell Transcriptomics

Project description:Cancer cell lineage plasticity complicates tumor initiation and progression. Using genetic barcoding and single-cell RNA sequencing (scRNA-seq), we mapped esophageal preneoplastic cell lineages and developed the eXamined Ridge (XR) score to identify high-plasticity cells. We discovered preneoplastic precursor cells (PNPCs) as key progenitors and identified Nfib and Qk as conserved markers, highlighting potential biomarkers for early cancer detection and intervention.

2025-11-20 | GSE289049 | GEO

Deciphering Precursor Cell Dynamics in Esophageal Preneoplasia via Genetic Barcoding and Single-Cell Transcriptomics

Project description:Deciphering Precursor Cell Dynamics in Esophageal Preneoplasia via Genetic Barcoding and Single-Cell Transcriptomics

| PRJNA1220706 | ENA

Deciphering Precursor Cell Dynamics in Esophageal Preneoplasia via Genetic Barcoding and Single-Cell Transcriptomics

Project description:Deciphering Precursor Cell Dynamics in Esophageal Preneoplasia via Genetic Barcoding and Single-Cell Transcriptomics

| PRJNA1302466 | ENA

Computational identification of preneoplastic cells displaying high stemness and risk of cancer progression

Project description:Evidence points towards the differentiate state of cells being a marker of cancer risk and progression, in line with the cancer-stem-cell hypothesis. Measuring the differentiation state of single cells in a preneoplastic population could thus enable novel strategies for early detection and risk prediction. Here we present a novel computational method called CancerStemID that estimates a stemness index of cells from single-cell RNA-Seq data. We validate CancerStemID in two human esophageal squamous cell carcinoma (ESCC) cohorts, demonstrating how it can identify undifferentiated preneoplastic cells whose transcriptomic state is overrepresented in invasive cancer. We demonstrate decreased differentiation activity of tissue-specific TFs in cancer cells compared to the basal cell-of-origin layer, and that the differentiation state correlates with differential DNA methylation at the promoters of such TFs independently of underlying NOTCH1 and TP53 mutations. In summary, these data support an epigenetic stem-cell model of oncogenesis and highlight a novel computational strategy in which to identify stem-like preneoplastic cells that undergo positive selection.

2022-04-01 | GSE199654 | GEO

Confocal Endomicroscopy Detection of Gastric Preneoplasia and Neoplasia

Project description:This is a prospective randomised study investigating the use of chromoendoscopy and confocal laser endomicroscopy for the detection of preneoplastic neoplasm in patients at high-risk of gastric cancer.

| 2108995 | ecrin-mdr-crc

Deciphering Precursor Cell Dynamics in Esophageal Preneoplasia via Genetic Barcoding and Single-Cell Transcriptomics.

Project description:Cancer cells exhibit high heterogeneity and lineage plasticity, complicating studies of tumorigenesis and development of therapies. Recently, preneoplastic cells, although histologically normal, have been shown to possess high plasticity and early genetic alterations, yet their origins and lineage trajectories remain unclear. Herein, we introduce a lineage-tracing tool integrating genetic barcoding with single-cell RNA sequencing to map preneoplastic esophageal cell lineages. We identified preneoplastic precursor cells (PNPCs) as a distinct progenitor-like population with unique transcriptional profiles and high plasticity, contributing to proliferative and basal cell populations. To enhance lineage mapping, we developed the eXamined Ridge (XR) score, accurately identifying high-plasticity cells. Nfib and Qk emerged as conserved PNPC markers, peaking in early preneoplasia and declining after malignant transformation. These findings reveal PNPCs as key players in early tumorigenesis and highlight their potential as biomarkers for early cancer detection and therapeutic intervention, offering new strategies for preventing esophageal cancer progression.

| S-EPMC11888434 | biostudies-literature

Expression profile of oesophageal epithelium basal cells comparing DNMaml expressing cells versus controls

Project description:Multiple cancers may arise from within a clonal region of preneoplastic epithelium, a phenomenon termed M-^Qfield changeM-^R. However, it is not known how field change develops. We investigate this question and analyse the behavior of scattered single esophageal epithelial progenitor cells expressing a mutation that inhibits the Notch signaling pathway (Dominant negative Maml).

2014-04-08 | E-MTAB-2334 | biostudies-arrayexpress

Silica-mediated airway chronic inflammation promotes lung carcinogenesis through the activation of preneoplastic lesions in the context of an immunosuppressive microenvirontment

Project description:Basic studies on preneoplastic lesions are important to determine the molecular alterations that take place in early steps of lung carcinogenesis. Little is known about the molecular events preceding the development of lung cancer in the context of an inflammatory environment. In this study we report the generation of a chemical-induced lung carcinogenesis mouse model in the presence of silicotic chronic inflammation. Silica-induced lung inflammation, strongly promoted incidence of lung cancer in mice treated with NDMA, a carcinogen found in tobacco smoke. Histological and molecular analysis revealed that permanent inflammation contributed to lung tumorigenesis through the adquisition of preneoplastic changes in lung epithelial cells. Inflammatory milieu increased the expression of PDCD1, TGFÎ²-1, MCP-1, LAG3, and Foxp3 and the presence of regulatory T cells within preneoplastic lesions. In addition concomitant chronic inflammation changed the K-ras mutational profile of the generated tumors from Q61R to G12D transition. In summary, these data identify early molecular mechanisms underlying lung carcinogenesis in an inflammatory context at different steps, providing a novel approach for the identification of drivers from preneoplastic to neoplastic lesions Gene expression profile was analyzed in 11 individual lesions (8 adenomas and 3 adenocarcinomas) from the NDMA-silica treated mice and 5 lesions (2 adenomas, and 3 adenocarcinomas) from NDMA-only treated mice

2016-07-05 | E-GEOD-43453 | biostudies-arrayexpress

Silica-mediated airway chronic inflammation promotes lung carcinogenesis through the activation of preneoplastic lesions in the context of an immunosuppressive microenvirontment

Project description:Basic studies on preneoplastic lesions are important to determine the molecular alterations that take place in early steps of lung carcinogenesis. Little is known about the molecular events preceding the development of lung cancer in the context of an inflammatory environment. In this study we report the generation of a chemical-induced lung carcinogenesis mouse model in the presence of silicotic chronic inflammation. Silica-induced lung inflammation, strongly promoted incidence of lung cancer in mice treated with NDMA, a carcinogen found in tobacco smoke. Histological and molecular analysis revealed that permanent inflammation contributed to lung tumorigenesis through the adquisition of preneoplastic changes in lung epithelial cells. Inflammatory milieu increased the expression of PDCD1, TGFβ-1, MCP-1, LAG3, and Foxp3 and the presence of regulatory T cells within preneoplastic lesions. In addition concomitant chronic inflammation changed the K-ras mutational profile of the generated tumors from Q61R to G12D transition. In summary, these data identify early molecular mechanisms underlying lung carcinogenesis in an inflammatory context at different steps, providing a novel approach for the identification of drivers from preneoplastic to neoplastic lesions

2016-01-03 | GSE43453 | GEO

Integrated Multi-Omic Analysis of Epithelial and Stromal Changes during Progression of Barrett s Esophagus to Adenocarcinoma

Project description:Esophageal adenocarcinoma arises from Barrett s esophagus, the precancerous metaplastic replacement of squamous by columnar epithelium in response to chronic inflammation. Development of adenocarcinoma is accompanied by non-genetic plasticity of epithelial and stromal cells. Multiomics profiling, integrating single-cell transcriptomics, extracellular matrix proteomics, tissue mechanics and spatial multiplexed proteomics of 64 samples from 12 patient trajectories of progression from normal epithelium, to metaplasia, dysplasia and adenocarcinoma, revealed shared and patient-specific progression paths. We detected profound consistent alterations of type and composition of tumor microenvironment cells, matrix composition and cell neighborhoods. Stromal cells with characteristics of cancer-associated fibroblasts appear early at the premalignant metaplastic stage. Thus, Barrett s esophagus progresses as a coordinated multi-component system, supporting a treatment paradigm that incorporates tissue reprogramming beyond targeting cancerous cells.

2023-02-25 | MSV000091366 | MassIVE

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