David H. Bilder

This paper shows Drosophila tumors exploit chronic wound healing pathways to disrupt intestinal homeostasis and induce inflammation through EGFR signaling.

This study shows that Tep3 limits macrophage attachment to damaged and transformed epithelia by inhibiting MMP1 proteolytic activity, reducing BM DAMP production and promoting tumor progression.

The paper shows that ADAMTS-A, a protease with intracellular activity, regulates basement membrane patterning in Drosophila egg chambers by limiting Collagen IV deposition.

The paper shows that tumors in Drosophila cause renal dysfunction through inflammatory activation of stem cells, leading to fluid retention and obstruction.

The paper identifies a minimal Dlg fragment containing SH3 and HOOK domains that is necessary and sufficient for Scrib localization and epithelial polarity in Drosophila.

This study shows that a Drosophila tumor model induces coagulopathy phenotypes similar to human patients, with hypercoagulation followed by hypocoagulation, and demonstrates that rescuing coagulopathy improves survival.

The paper identifies distinct functional roles of Scrib, Dlg, and Lgl in the Scribble module for establishing epithelial polarity, showing they are not sufficient together to antagonize the Par complex.

The paper investigates how basement membrane stiffness influences tissue elongation in Drosophila follicles through mechanosensitive junctional remodeling.