Percutaneous treatment of ranulas: ultrasound-guided drainage with salivary gland chemical ablation.

BACKGROUND: Ranulas are salivary pseudocysts in the floor of the mouth adjacent to damaged salivary glands. Current surgical management is drainage of the ranula with removal of the offending gland. An analogous percutaneous procedure could potentially offer similar treatment efficacy in a more minimally invasive way. OBJECTIVE: To evaluate the outcomes of a cohort of patients with ranulas treated with percutaneous ranula aspiration and chemical ablation of the source salivary gland to see whether this technique could be proposed as a minimally invasive treatment alternative. MATERIALS AND METHODS: This retrospective single-center study evaluated 24 patients treated percutaneously for ranulas between January 2004 and December 2014. All patients were treated with percutaneous ranula aspiration and chemical ablation of the offending salivary gland. Treatment success and any complications were recorded. RESULTS: Complete ranula eradication was successfully accomplished in 87.5% of the patients with no complications. CONCLUSION: Initial results suggest that our technique of percutaneous aspiration of ranulas and chemical ablation of the source salivary gland is safe and effective.

EGFL7 Antagonizes NOTCH Signaling and Represents a Novel Therapeutic Target in Acute Myeloid Leukemia.

PURPOSE: EGF-like domain 7 (EGFL7) is a secreted protein and recently has been shown to play an important role in acute myeloid leukemia (AML); however, the underlying mechanism by which EGFL7 promotes leukemogenesis is largely unknown. EXPERIMENTAL DESIGN: Using an antibody interaction array, we measured the ability of EGFL7 to bind directly approximately 400 proteins expressed by primary AML blasts. Primary patient samples were stimulated in vitro with recombinant EGFL7 (rEGFL7) or anti-EGFL7 blocking antibody to assess alterations in downstream signaling and the ability to effect blast differentiation and survival. We treated three independent AML models with anti-EGFL7 or IgG1 control to determine whether anti-EGFL7 could prolong survival in vivo. RESULTS: We found EGFL7 significantly binds several signaling proteins important for normal and malignant hematopoiesis including NOTCH. Stimulation of AML blasts with rEGFL7 reduced NOTCH intracellular domain and NOTCH target gene expression while treatment with an anti-EGFL7 blocking antibody resulted in reactivation of NOTCH signaling, increased differentiation, and apoptosis. Competitive ligand-binding assays showed rEGFL7 inhibits DELTA-like (DLL) 4-mediated NOTCH activation while anti-EGFL7 combined with DLL4 significantly increased NOTCH activation and induced apoptosis. Using three different AML mouse models, we demonstrated that in vivo treatment with anti-EGFL7 alone results in increased survival. CONCLUSIONS: Our data demonstrate that EGFL7 contributes to NOTCH silencing in AML by antagonizing canonical NOTCH ligand binding. Reactivation of NOTCH signaling in vivo using anti-EGFL7 results in prolonged survival of leukemic mice, supporting the use of EGFL7 as a novel therapeutic target in AML.