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

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

PROVIDER: PRJNA821067 | ENA |

REPOSITORIES: ENA

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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

Predictive computational obesity risk framework through integration of gene expression profiles and genetic risk score.

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Proteomic-based computational stratification of intermediate-risk prostate cancer patients.

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2023-11-30 | PXD041005 | Pride

Senescent Stromal-Derived Osteopontin Promotes Preneoplastic Cell Growth

Project description:Alterations in the tissue microenvironment collaborate with cell autonomous genetic changes to contribute to neoplastic progression. The importance of the microenvironment in neoplastic progression is underscored by studies demonstrating that fibroblasts isolated from a tumor stimulate the growth of preneoplastic and neoplastic cells in xenograft models. Similarly, senescent fibroblasts promote preneoplastic cell growth in vitro and in vivo. Because senescent cells accumulate with age, their presence is hypothesized to facilitate preneoplastic cell growth and tumor formation in older individuals. To identify senescent stromal factors directly responsible for stimulating preneoplastic cell growth, we carried out whole genome transcriptional profiling and compared senescent fibroblasts to their younger counterparts. We identified osteopontin (OPN) as one of the most highly elevated transcripts in senescent fibroblasts. Importantly, reduction of OPN protein levels by RNAi did not impact senescence induction in fibroblasts; however, it dramatically reduced the growth-promoting activities of senescent fibroblasts in vitro and in vivo, demonstrating that OPN is necessary for paracrine stimulation of preneoplastic cell growth. In addition, we found that recombinant OPN was sufficient to stimulate preneoplastic cell growth. Finally, we demonstrate that OPN is expressed in senescent stroma within preneoplastic lesions that arise following DMBA/TPA treatment of mice, suggesting that stromal-derived OPN-mediated signaling events impact neoplastic progression.

2009-03-30 | GSE13330 | GEO

Gene expression profiling of preneoplastic K8-creERT2/PIK3CAH1047R mammary subsets

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Gene expression profiling of preneoplastic Lgr5-creERT2/PIK3CAH1047R mammary subsets

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