Lin Tian

TL;DR: It is shown that type 1 T helper (TH1) cells play a crucial role in vessel normalization, and may be a marker and a determinant of both immune checkpoint blockade and anti-angiogenesis efficacy.

TL;DR: It is elucidated that hAJ activates the mTOR pathway in cancer cells, which drives the progression from single cells to micrometastases and provides potential therapeutic targets to block progression toward osteolytic metastases.

TL;DR: It is demonstrated that mTOR signalling in cancer cells dictates a mammary tumour’s ability to stimulate MDSC accumulation through regulating G-CSF, establishing a non-canonical oncogenic role of m TOR signalling in recruiting pro-tumorigenic MDSCs and showing how defined cancer subsets may evolve to promote and depend on a distinct immune microenvironment.

TL;DR: Interestingly, effective inhibition of these pathways can be achieved by danusertib, or a combination of everolimus and arsenic trioxide, which provide possibilities of eliminating bone micrometastases using clinically established drugs.

TL;DR: The results support a model in which signal-independent binding of SMAD3 and FOXH1 prime mesendoderm differentiation gene promoters for activation, and signal-driven SMAD2:SMAD4 binds to promoters that are preloaded withSMAD3:FOXH1 to activate transcription.