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Association of frequent hypermethylation with high grade histological subtype in lung adenocarcinoma. (Infinium Methylation450K)

ABSTRACT: Comprehensive DNA methylation analysis of each histological LUAD subtype. Infinium HumanMethylation450 BeadChip was used to obtain DNA methylation profiles across 485,577 CpG sites. Samples included 6 Micropapillary subtype, 5 Papillary subtype, 5 Lepidic subype and 3 normal lung tissues.

ORGANISM(S): Homo sapiens

PROVIDER: GSE217732 | GEO | 2023/09/11

REPOSITORIES: GEO

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Association of frequent hypermethylation with high grade histological subtype in lung adenocarcinoma. (Infinium MethylationEPIC)

Project description:Comprehensive DNA methylation analysis of each histological LUAD subtype. Infinium MethylationEPIC BeadChip was used to obtain DNA methylation profiles across 850,000 CpG sites. Samples included 4 Micropapillary subtype, 5 Acinar subtype, 5 Solid subype.

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Gramd2+ alveolar type I cells can give rise to Kras-induced lung adenocarcinoma

Project description:Lung adenocarcinoma (LUAD) is the most common subtype of lung cancer and arises in the distal lung. LUAD encompasses several pathologic subtypes, including solid, lepidic, papillary, micropapillary, acinar and mixed subtypes, each with differing clinical outcomes or biological behavior. Specifically, lepidic histology is associated with improved survival relative to other LUAD histologies. Yet, the molecular and cellular underpinnings of these subtypes are largely unknown. Understanding which cell populations in the distal lung contribute to LUAD could provide insights for the marked heterogeneity in LUAD pathologic features, clinical presentation and responses to therapy.Recent studies have seen tumor-derived epithelial cells with an AT1 transcriptomic cell signature, suggesting AT1 cells may contribute to a subset of LUAD cases. We tested the ability of AT1 cells to give rise to LUAD by inducing KrasG12D, a known oncogenic driver in human LUAD. Activation of KrasG12D in Gram-domain containing 2 (Gramd2)+ AT1 cells gave rise to multiple LUAD lesions, primarily of papillary histology. In contrast, activation of KrasG12D in Sftpc+ AT2 cells resulted in LUAD lesions of lepidic histology. Immunohistochemistry established Gramd2:KrasG12D lesions were of primary lung origin and not metastatic events. Spatial transcriptomic profiling revealed distinct pathway alterations occurring within Gramd2- and Sftpc-derived LUAD. Immunofluorescence confirmed differences observed in the Spatial transcriptomic analysis in expression patterns and distribution of cell-specific markers between cell of origin, while universal upregulation of the Krt8 intermediate cell state marker was observed. Our results are consistent with Gramd2+ AT1 cells serving as a putative cell of origin for LUAD and suggest that LUAD may be a collection of adenocarcinomas that share a common location within the distal lung, but which arise from different cells of origin.

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Association of frequent hypermethylation with high grade histological subtype in lung adenocarcinoma. (Infinium Methylation450K)

Project description:Association of frequent hypermethylation with high grade histological subtype in lung adenocarcinoma. (Infinium Methylation450K)

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Association of frequent hypermethylation with high grade histological subtype in lung adenocarcinoma. (Infinium MethylationEPIC)

Project description:Association of frequent hypermethylation with high grade histological subtype in lung adenocarcinoma. (Infinium MethylationEPIC)

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TGF-β signaling activated by cancer-associated fibroblasts determines the histological signature of lung adenocarcinoma

Project description:Invasive lung adenocarcinoma (LADC) is classified histologically as lepidic, acinar, papillary, micropapillary, or solid. We found that A549 human LADC cells formed tumors with distinct histological features—solid-type or acinar-type tumors—depending on the site of development in immunodeficient mice and that a solid-to-acinar transition (SAT) could be induced by cancer-associated fibroblasts (CAFs) in 3D cocultures with A549. To clarify the molecular mechanisms contributing to SAT induction, we performed RNA-seq analysis of four A549 tumor cell samples derived from solid- or acinar-type tumor tissue formed in vivo or from 3D tumor colonies formed in the presence or absence of CAFs in vitro.

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Association of frequent hypermethylation with high grade histological subtype in lung adenocarcinoma

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Association of frequent hypermethylation with high grade histological subtype in lung adenocarcinoma.

Project description:Lung adenocarcinoma is classified morphologically into five histological subtypes according to the WHO classification. While each histological subtype correlates with a distinct prognosis, the molecular basis has not been fully elucidated. Here we conducted DNA methylation analysis of 30 lung adenocarcinoma cases annotated with the predominant histological subtypes and three normal lung cases using the Infinium BeadChip. Unsupervised hierarchical clustering analysis revealed three subgroups with different methylation levels: high-, intermediate-, and low-methylation epigenotypes (HME, IME, and LME). Micropapillary pattern (MPP)-predominant cases and those with MPP components were significantly enriched in HME (p = 0.02 and p = 0.03, respectively). HME cases showed a significantly poor prognosis for recurrence-free survival (p < 0.001) and overall survival (p = 0.006). We identified 365 HME marker genes specifically hypermethylated in HME cases with enrichment of "cell morphogenesis" related genes; 305 IME marker genes hypermethylated in HME and IME, but not in LME, with enrichment "embryonic organ morphogenesis"-related genes; 257 Common marker genes hypermethylated commonly in all cancer cases, with enrichment of "regionalization"-related genes. We extracted surrogate markers for each epigenotype and designed pyrosequencing primers for five HME markers (TCERG1L, CXCL12, FAM181B, HOXA11, GAD2), three IME markers (TBX18, ZNF154, NWD2) and three Common markers (SCT, GJD2, BARHL2). DNA methylation profiling using Infinium data was validated by pyrosequencing, and HME cases defined by pyrosequencing results also showed the worse recurrence-free survival. In conclusion, lung adenocarcinomas are stratified into subtypes with distinct DNA methylation levels, and the high-methylation subtype correlated with MPP-predominant cases and those with MPP components and showed a poor prognosis.

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Project description:Genome-wide methylation profilling on 54 paired of CRCs and their adjacent normal tissues using the Infinium Human Methylation 450K beadchip, which covers 485,577 CpG di-nucleotide sites distributed over the whole genome

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Association of frequent hypermethylation with high grade histological subtype in lung adenocarcinoma

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