Publications by authors named "Greet Bervoets"
Article Synopsis
- Researchers studied the cellular structure of melanoma tumors and their changes when treated with immune checkpoint blockade (ICB) to understand why some patients resist this therapy.
- They found that a specific cell type with a mesenchymal-like (MES) state, which is associated with resistance to treatment, was more common in patients who did not respond to ICB.
- The study identified TCF4 as a key regulator that controls this resistance by suppressing other important immune functions, and targeting TCF4 could enhance the effectiveness of both ICB and other therapies in melanoma treatment.
Although melanoma is notorious for its high degree of heterogeneity and plasticity, the origin and magnitude of cell-state diversity remains poorly understood. Equally, it is unclear whether growth and metastatic dissemination are supported by overlapping or distinct melanoma subpopulations. Here, by combining mouse genetics, single-cell and spatial transcriptomics, lineage tracing and quantitative modelling, we provide evidence of a hierarchical model of tumour growth that mirrors the cellular and molecular logic underlying the cell-fate specification and differentiation of the embryonic neural crest.
View Article and Find Full Text PDFBackground: Precise gene dosage of the X chromosomes is critical for normal development and cellular function. In mice, XX female somatic cells show transcriptional X chromosome upregulation of their single active X chromosome, while the other X chromosome is inactive. Moreover, the inactive X chromosome is reactivated during development in the inner cell mass and in germ cells through X chromosome reactivation, which can be studied in vitro by reprogramming of somatic cells to pluripotency.
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- Scientists discovered that some cancer cells can become resistant to treatment because of special cells that don’t die off, called persister cells or minimal residual disease (MRD).
- In patients with melanoma, they found that a type of stem cell appears during treatment and helps the cancer survive in ways that aren't always genetic.
- By stopping these stem cells from growing, they were able to slow down the return of cancer in experiments, showing that the mix of cells in MRD can change how well cancer treatments work.
is one of the most studied lncRNAs, in part because its silencing in mice causes defects in mammary gland development and corpus luteum formation and protects them from skin cancer development. Moreover, depleting in established cancer cell lines reduces growth and sensitizes cells to DNA damaging agents. However, produces two isoforms and because the short isoform, , completely overlaps the 5' part of the long isoform; the respective contributions of each of the isoforms to these phenotypes has remained unclear.
View Article and Find Full Text PDFInduction and reversal of chromatin silencing is critical for successful development, tissue homeostasis, and the derivation of induced pluripotent stem cells (iPSCs). X-Chromosome inactivation (XCI) and reactivation (XCR) in female cells represent chromosome-wide transitions between active and inactive chromatin states. Although XCI has long been studied, providing important insights into gene regulation, the dynamics and mechanisms underlying the reversal of stable chromatin silencing of X-linked genes are much less understood.
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