Black soldier fly (Diptera: Stratiomyidae) larvae reduce cyathostomin (Nematoda: Strongylidae) eggs but develop poorly on horse manure.

Cyathostomins are common digestive tract parasites of grazing horses that spread through contact with horse feces. Horse feces are colonized by a variety of organisms, some of which could serve to reduce parasite loads in horse pastures. Black soldier fly (Hermetia illucens L.

Disseminating cells in human oral tumours possess an EMT cancer stem cell marker profile that is predictive of metastasis in image-based machine learning.

Cancer stem cells (CSCs) undergo epithelial-mesenchymal transition (EMT) to drive metastatic dissemination in experimental cancer models. However, tumour cells undergoing EMT have not been observed disseminating into the tissue surrounding human tumour specimens, leaving the relevance to human cancer uncertain. We have previously identified both EpCAM and CD24 as CSC markers that, alongside the mesenchymal marker Vimentin, identify EMT CSCs in human oral cancer cell lines.

CD73 controls Myosin II-driven invasion, metastasis, and immunosuppression in amoeboid pancreatic cancer cells.

Pancreatic ductal adenocarcinoma (PDAC) has a very poor prognosis because of its high propensity to metastasize and its immunosuppressive microenvironment. Using a panel of pancreatic cancer cell lines, three-dimensional (3D) invasion systems, microarray gene signatures, microfluidic devices, mouse models, and intravital imaging, we demonstrate that ROCK-Myosin II activity in PDAC cells supports a transcriptional program conferring amoeboid invasive and immunosuppressive traits and in vivo metastatic abilities. Moreover, we find that immune checkpoint CD73 is highly expressed in amoeboid PDAC cells and drives their invasive, metastatic, and immunomodulatory traits.

In vitro cancer models as an approach to identify targetable developmental phenotypes in cancer stem cells.

Cancer therapeutics are often highly toxic to the patient, and they often elicit rapid resistance in the tumour. Recent advances have suggested a potential new way in which we may improve on this, through two important concepts: (1) that multitudinous pathway alterations converge on a limited number of cancer cellular phenotypes, and (2) that these cancer cellular phenotypes depend on reactivation of developmental processes that are only minimally active in adult tissues. This provides a rationale for pursuing an approach of 'drugging the phenotype' focussed on targeting reactivated cellular processes from embryonic development.