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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 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.
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.
Zhao et al. identified lymphatic endothelial-like cells in glioblastoma and demonstrated their role in promoting tumour growth through increased glioblastoma cholesterol metabolism.
The different compartments of the mammary stem cell hierarchy develop into distinct breast cancer subtypes as a result of specific genetic lesions. A recent study identifies aberrant ERBB3low luminal progenitors with altered proteostasis and translation as the cell of origin of BRCA2-mutant breast cancer.
In this study, Bansaccal et al. analyse why, at some skin locations, oncogene-expressing cells rarely progress to cancer and found that a dense dermal collagen network prevents skin cancer formation.
Transformation of a myeloproliferative neoplasm to a secondary acute myeloid leukemia is rare but devastating. Single-cell, multi-omic characterization of hematopoietic stem and progenitor cells now shows the role of inflammation in transformation driven by mutations in TP53, with effects on the mutant clone but also non-mutant counterparts.