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A new cell type at the border of the fourth ventricle is the exclusive source of roof plate.

A novel Mendelian randomisation framework unravels one gene expression component, correlated with proliferation and genome stability-related features, associated with telomere length in lung adenocarcinoma tumours, which provides insights into how telomere length influences the genetic basis of lung cancer aetiology.

A new computational framework provides a flexible and general approach for single and collective biological motion characterisation and phenotyping ideally suited for high-throughput timelapse screens.

A resource of p63-regulated genes, genomic loci bound by p63, p63 DNA recognition motifs, and potential co-factors is generated through a meta-analysis of high-throughput datasets.

Unbiased analyses highlight context-specific crosstalk between Notch, DNA damage response genes, and PP2A, and provide a roadmap for understanding how Notch induces squamous cell differentiation.

Overexpression of TCF7L1 overrides oncogenic Ras-induced senescence, induces cell migration, and promotes growth of skin squamous cell carcinoma independently of its interaction with β-catenin.

The safety and strong antitumor effects of GPC1-specific CAR-T cells against GPC1-expressing solid tumors were demonstrated by using both syngeneic and xenogeneic mouse models.

Cancer is a consequence of the release of basal cellular functions inherited from our unicellular ancestors from the control of regulatory networks that evolved during the emergence of multicellularity.

In lung adenocarcinoma, deleting one glucose transporter, whether it is Glut1 or Glut3 is insufficient, whereas their dual deletion reduces tumor growth.

Altering the level of different oncogenic mutants of Kras induces unique tumor patterns in mice, suggesting that tissue-specific responses mold the sensitivity of normal tissues to different oncogenic RAS mutations.