Dina Morein

TL;DR: Novel tumor-stroma-inflammation networks that may promote TNBC aggressiveness by increasing the pro-malignancy potential of the TME and of the tumor cells themselves are identified, and key roles for CXCL8 are revealed in mediating these metastasis-promoting activities.

TL;DR: The roles of chemokines and their receptors at atypical levels that are exerted on the cancer cell themselves are addressed: promoting tumor cell proliferation and survival; controlling tumor cell senescence; enriching tumors with cancer stem cells; inducing metastasis-related functions such as epithelial-to-mesenchymal transition (EMT) and elevated expression of matrix metalloproteinases (MMPs).

TL;DR: DAPT, inhibitor of γ-secretase that participates in activation of Notch receptors, inhibited the migration and invasion of TNBC cells that were grown in “Contact” co-cultures with MSCs or with patient-derived cancer-associated fibroblasts (CAFs), in the presence of TNFα.

TL;DR: In this article, the impact of consistent inflammatory stimulation on stromal cell plasticity was determined, showing that chronic inflammation can induce mesenchymal stem cells (MSCs) to undergo conversion at the tumor site to cancer-associated fibroblasts (CAFs), which are generally connected to enhanced tumor progression.

TL;DR: Over-expressed WT-PD-L1 in human TNBC cells and in luminal-A breast cancer cells demonstrated that cell-autonomous PD-L 1 activities lead to increased tumor cell growth, invasion and release of pro-metastatic factors, which were promoted by PD-1 and were inhibited by mutating S283 in PD- L1.