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Epigenome analysis of normal and lung adenocarcinoma (LUAD) samples

ABSTRACT: Epigenome analysis of normal and lung adenocarcinoma (LUAD) samples

PROVIDER: PRJNA1150555 | ENA |

REPOSITORIES: ENA

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Epigenome analysis of normal and lung adenocarcinoma (LUAD) samples

Project description:Genome wide DNA methylation profiling of peripheral blood mononuclear cells(PBMCs) in normal and LUAD samples. The Illumina Infinium 850k Human DNA methylation Beadchip was used to obtain DNA methylation profiles across approximately 820,000 CpGs in PBMC samples. Samples included 35 LUAD patients and 50 normal controls.

2024-12-14 | GSE275371 | GEO

Transcriptome sequencing of 15 normal lung parenchyma (NL), 17 atypical adenomatous hyperplasia (AAH) and 16 lung adenocarcinoma (LUAD) samples from 17 patients

Project description:We sought to characterize expression profiles signifying the development of atypical adenomatous hyperplasia (AAH) from normal lung parenchyma (NL), and its progression to lung adenocarcinomas (LUAD).

2017-11-14 | GSE102511 | GEO

Spatial transcriptomics analysis of normal lung tissues, precursor lung lesions and invasive lung adenocarcinomas

Project description:Understanding cellular processes underlying early lung adenocarcinoma (LUAD) development is needed to devise intervention strategies. Here, we performed spatial trancriptomics analysis of human treatment-naive lungs comprising various stages in the sequence of pathogenesis of LUAD including normal lung tissues, atypical adenomatous hyperplasia (AAH), adenocarcinoma in situ (AIS), minimally invasive adenocarcinoma (MIA) and LUAD.

2025-10-11 | GSE307534 | GEO

Transcriptome profiling of 57 LUAD samples and 11 peritumoral normal lung tissues

Project description:RNA was extracted from 57 LUAD patients hospitalized from 2004 to 2010 at the Pasteur Hospital (Departments of Pulmonary Medicine, and Thoracic Surgery, CHU de Nice, France) and 11 normal lung tissue specimens taken from areas at standard distance (3 cm) from the same cohort of patients.The diagnosis of LUAD patients was based on examination of all tumor specimens using the 7th pTNM classification and on the last histological classification of NSCLC. Written informed consent was obtained from participants after explaining the nature of the study, which was approved by the research ethics board of the Nice University hospital and was performed according to the guidelines of the Declaration of Helsinki. The main clinical and pathological data are summarized. Enrollment of patients in our study was conditioned by stringent criteria such as obtained signed consent, availability of resected surgical specimens, good quality RNA and time of follow-up for surviving patients (min 40 months for surviving patients).

2019-09-04 | GSE116959 | GEO

Whole-exome sequencing of normal lung tissues, precursor lesions and invasive lung adenocarcinomas

Project description:Understanding cellular processes underlying early lung adenocarcinoma (LUAD) development is needed to devise intervention strategies. Here, we performed whole exome sequencing (WES) of human treatment-naive lungs comprising various stages in the sequence of pathogenesis of LUAD including normal lung tissues, atypical adenomatous hyperplasia (AAH), adenocarcinoma in situ (AIS), minimally invasive adenocarcinoma (MIA) and LUAD.

2025-10-11 | GSE307529 | GEO

Transcriptome profiling of 57 LUAD samples and 11 peritumoral normal lung tissues

Project description:Transcriptome profiling of 57 LUAD samples and 11 peritumoral normal lung tissues

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Single-nucleus RNA-sequencing (snRNA-seq) analysis of normal lung tissues, precursor lung lesions and invasive lung adenocarcinomas

Project description:Understanding cellular processes underlying early lung adenocarcinoma (LUAD) development is needed to devise intervention strategies. Here, we performed snRNA-seq analysis of human treatment-naive lungs comprising various stages in the sequence of pathogenesis of LUAD including normal lung tissues, atypical adenomatous hyperplasia (AAH), adenocarcinoma in situ (AIS), minimally invasive adenocarcinoma (MIA) and LUAD.

2025-10-11 | GSE308103 | GEO

Quantitative proteomics of MYDGF knockdown in lung adenocarcinoma cells

Project description:Lung adenocarcinoma (LUAD) remains the leading cause of cancer-related mortality worldwide. Unlike patients harboring epidermal growth factor receptor (EGFR) mutations, those with wild-type EGFR lack effective targeted therapeutic options. We established a super-SILAC-based proteomic dataset (PXD046807) comprising LUAD tissues stratified by EGFR mutation status and clinical stages. Notably, myeloid-derived growth factor (MYDGF) was identified as a potential key regulator in patients with wild-type EGFR LUAD. To further investigate the role of MYDGF in LUAD, we applied gene knockdown combined with tandem mass tag (TMT)-based quantitative proteomic analysis to search for the specific biological processes regulated by MYDGF in normal lung fibroblasts and LUAD cells with different EGFR status.

2025-06-22 | PXD064751 | Pride

Proteomic Identification of Lung Adenocarcinoma and Normal Lung Tissue

Project description:To identify proteomic of lung adenocarcinoma, we collected five pairs of lung adenocarcinoma and normal lung tissues from the clinic for analysis

2022-01-12 | PXD027008 | Pride

Gene expression profile at single cell level of cerebrospinal fluid (CSF) cells from lung adenocarcinoma leptomeningeal metastases patients (LUAD LM)

Project description:Lung adenocarcinoma (LUAD)-derived leptomeningeal metastases (LM) represent a predominant subtype among all LM cases. Nevertheless, the cerebrospinal fluid (CSF) profile of LUAD-LM patients remains poorly characterized and reliable CSF diagnostic biomarkers for LUAD-LM have yet to be established. Using single-cell RNA sequencing data of CSF cells from six LUAD-LM patients, we drew a systematic transcriptomic atlas of the CSF cellular landscape. Our analysis revealed that LUAD-LM reprograms CSF into an immunosuppressive state, marked by the emergence of pro-tumoral LGMN-SELENOPhigh macrophages and proliferating CSF circulating tumor cells (CSF-CTC). Cell-cell communication analysis showed that CSF-CTC reinforces immunosuppression by co-inhibitory checkpoint axis NECTIN2_TIGIT axis with the CD8+T/NK cells, and via CD47_SIRPA axis with antigen-presenting cells. Furthermore, we identified the single-cell transcriptomic difference between CSF-CTC and tumor cells of parenchymal brain metastases (PBM). Notably, Trophoblast cell surface antigen 2 (TROP2) levels in CSF were significantly elevated in LUAD-LM patients versus both normal controls (NC) and LUAD patients without LM (Non-LM). It showed strong diagnostic accuracy for distinguishing LUAD LM from Non-LM or NC, and PBM did not influence the CSF TROP2 level. Collectively, our findings advance the understanding of LUAD-LM pathogenesis and highlight the potential of CSF TROP2 as a diagnostic biomarker for LM.

2026-04-03 | GSE276139 | GEO

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