Editors' Summary: This Replication Study has reproduced some parts of the original paper but other parts could not be interpreted.

A major consequence of ductal-to-squamous lineage transition in pancreatic cancer cells is to augment inflammation, which may explain the exceptionally poor clinical outcomes of squamous-subtype tumors.

Many extracellular matrix proteins that are up-regulated during breast tumor progression enhance metastasis, and some are prognostic indicators of poor survival.

Pharmacologic inhibition of DNA methylation restrains the growth of urothelial carcinoma by subtype conversion through heightened stromal Hedgehog pathway activity.

A zebrafish genetic model of Ewing sarcoma, a pediatric bone cancer, showed how molecules in the normal tissue can support tumor cells, and identified a therapeutic compound that slows tumor growth.

Stromal cell levels and localization of active α₅β₁-integrin are regulated by desmoplastic extracellular matrix control of α_vβ₅-integrin signaling, and predict clinical outcomes for pancreatic and renal cancer patients.

The earliest steps of tumor initiation in the cerebellum are regulated by critical interactions between pre-tumor cells and stromal cells, which can be manipulated by targeting the Norrin/Frizzled4 signaling axis.

Profiling spatially defined fibroblasts in the pancreatic ductal adenocarcinoma (PDAC) tumor microenvironment identifies high levels of podoplanin and hypoxia in tumor-proximal fibroblasts associated with bad prognosis, whilst inflammatory markers define more distal fibroblast regions and associate with better outcomes.

Tumor stiffness blocks T cell migration in tumors.