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Gutin, J.

Publications and source records attributed to Gutin, J..

2 recordsLinked to original sources

Subtyping of Small Cell Lung Cancer using plasma cell-free nucleosomes

Emerging data on small cell lung cancer (SCLC), an aggressive malignancy with exceptionally poor prognosis, support subtypes driven by distinct transcription regulators, which engender unique therapeutic vulnerabilities. However, the translational potential of these observations is limited by access to tumor biopsies. Here, we leverage chromatin immunoprecipitation of cell-free nucleosomes carrying active chromatin modifications followed by sequencing (cfChIP-seq) on 442 plasma samples from individuals with advanced SCLC, neuroendocrine carcinomas (NEC), non-SCLC cancers, and healthy adults. Beyond providing reliable estimates of SCLC circulating free DNA tumor fraction, cfChIP-seq captures the unique epigenetic states of SCLC tissue- and cell-of-origin. Comparison of cfChIP-seq signals to matched tumor transcriptomes reveals genome-wide concordance, establishing a direct link between gene expression in the tumor and plasma cell-free nucleosomes. Exploiting this link, we develop a classifier that discriminates between SCLC lineage-defining transcription factor subtypes based on cfChIP-seq data. This work sets the stage to non-invasively profile SCLC transcriptomes using plasma cfDNA histone modifications.

cancer biology↗

Temporal profiling of redox-dependent heterogeneity in single cells

Cellular redox status affects diverse cellular functions, including proliferation, protein homeostasis, and aging. Thus, individual differences in redox status can give rise to distinct sub-populations even among cells with identical genetic backgrounds. Here, we have created a novel methodology to track redox status at single cell resolution using the redox-sensitive probe roGFP. Our method allows identification and sorting of sub-populations with different oxidation levels in either the cytosol, mitochondria or peroxisomes. Using this approach we defined redox-dependent heterogeneity of yeast cells, and characterized growth, as well as proteomic and transcriptomic profiles of subpopulations of cells that differ in their redox status, but are similar in age. We report that, starting in late logarithmic growth, cells of the same age have a bi-modal distribution of oxidation status. A comparative proteomic analysis between these populations identified three key proteins, Hsp30, Dhh1, and Pnc1, which affect basal oxidation levels and may serve as first line of defense proteins in redox homeostasis.

biochemistry↗