Results 241 to 250 of about 345,679 (284)
In over 50% of non‐metastatic breast cancer patients, circulating tumor cells (CTCs) along the whole epithelial‐mesenchymal transition spectrum are detected. Total CTC number and individual phenotypes relate to aggressive disease characteristics, including lymph node involvement and higher tumor proliferation. At the single‐cell level, mesenchymal CTCs
Justyna Topa +14 more
wiley +1 more source
The IFNγ‐CIITA‐MHC II axis modulates melanoma cell susceptibility to NK‐cell‐mediated cytotoxicity
Natural killer (NK) cells play a central role in anti‐melanoma immunity. However, melanoma cells adapt during co‐culture by upregulating CIITA and MHC II in response to interferon gamma (IFNγ), thereby evading NK‐cell lysis. Blocking IFNγ signaling or treatment with dimethyl fumarate/simvastatin counteracts this immune escape and maintains NK‐cell ...
Lena C. M. Krause +6 more
wiley +1 more source
Poly-β amino ester-containing microparticles enhance the activity of nonviral genetic vaccines
Steven R. Little +7 more
openalex +1 more source
Cognitive Enhancement and Network Effects: how Individual Prosperity Depends on Group Traits [PDF]
Anomaly, Jonathan, Jones, Garett
core
Aggressive prostate cancer is associated with pericyte dysfunction
Tumor‐produced TGF‐β drives pericyte dysfunction in prostate cancer. This dysfunction is characterized by downregulation of some canonical pericyte markers (i.e., DES, CSPG4, and ACTA2) while maintaining the expression of others (i.e., PDGFRB, NOTCH3, and RGS5).
Anabel Martinez‐Romero +11 more
wiley +1 more source
ERRFI1, a neural crest (NC)‐associated gene, was upregulated in melanoma and negatively correlated with the expression of melanocytic differentiation markers and the susceptibility of melanoma cells toward BRAF inhibitors (BRAFi). Knocking down ERRFI1 significantly increased the sensitivity of melanoma cells to BRAFi.
Nina Wang +8 more
wiley +1 more source
Survivin and Aurora Kinase A control cell fate decisions during mitosis
Aurora A interacts with survivin during mitosis and regulates its centromeric role. Loss of Aurora A activity mislocalises survivin, the CPC and BubR1, leading to disruption of the spindle checkpoint and triggering premature mitotic exit, which we refer to as ‘mitotic slippage’.
Hana Abdelkabir +2 more
wiley +1 more source
CDK11 inhibition stabilises the tumour suppressor p53 and triggers the production of an alternative p21WAF1 splice variant p21L, through the inactivation of the spliceosomal protein SF3B1. Unlike the canonical p21WAF1 protein, p21L is localised in the cytoplasm and has reduced cell cycle‐blocking activity.
Radovan Krejcir +12 more
wiley +1 more source

