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Cancer stem cells are rare immortal cells within a tumour that can both self-renew by dividing and give rise to many cell types that constitute the tumour, and can therefore form tumours. Such cells have been found in various types of human tumours and might be attractive targets for cancer treatment.
The JAK2V617F mutation leads to epigenetic rewiring in a cell-intrinsic and cell-type-specific manner, influencing inflammation states and differentiation trajectories in patients with myeloproliferative neoplasms.
Circular RNA Circ0075305 hinders gastric cancer stem cells by indirectly increasing the expression of RPRD1A. In turn, RPRD1A disrupts TCF4-β-catenin complex formation and promotes downregulation of SOX9 transcription.
In a recent study published in Nature, Goto et al. explore mechanisms of immune evasion in early colorectal cancers and adenomas and identify SOX17 to be crucial for immune escape through suppression of interferon-γ signalling.
A CRISPR dropout screen for tRNA regulators identified YRDC as the top essential gene in glioblastoma stem cells. Threonine acts as a substrate of YRDC to facilitate the N6-threonylcarbamoyladenosine (t6A) tRNA modification and shift translation toward mitosis-related genes with a codon bias. Our findings support targeting glioblastoma growth by a well-tolerated dietary therapy.
The chemoresistant and immunoevasive characteristics of leukaemia stem cells (LSCs) impede the treatment efficacy for acute myeloid leukaemia (AML). We find that inhibiting the tyrosine phosphatase SHP-1 effectively alters the metabolic state of LSCs, making them more susceptible to chemotherapy and immune surveillance in AML.
Self-renewing cancer stem cells drive tumor initiation and progression and represent a major target for therapeutic development. A study now shows that vanoxerine, a dopamine transporter antagonist, precisely inhibits this cell population in colorectal cancer, which leads to attenuation of tumor initiation and increased infiltration by immune cells.