Intravenous Lidocaine Administered as Twice Daily Bolus and Continuous Infusion for Intractable Cancer Pain and Wound Care Pain.

Introduction: Intravenous lidocaine is an option for intractable pain caused by advancing cancer and wound care. We report a case of intractable cancer pain and wound care pain managed with concurrent use of lidocaine administered as a twice daily intravenous bolus in addition to continuous intravenous infusion.

Case Description: A 31-year-old male with rapidly progressing locally advanced squamous cell cancer affecting the gluteal area developed extensive painful and purulent ulcerating wounds affecting the coccyx, superior gluteal cleft, and buttocks.

Enabling a genetically informed approach to cancer medicine: a retrospective evaluation of the impact of comprehensive tumor profiling using a targeted next-generation sequencing panel.

Background: Oncogenic genetic alterations "drive" neoplastic cell proliferation. Small molecule inhibitors and antibodies are being developed that target an increasing number of these altered gene products. Next-generation sequencing (NGS) is a powerful tool to identify tumor-specific genetic changes.

Activation of the PI3K/AKT pathway induces urothelial carcinoma of the renal pelvis: identification in human tumors and confirmation in animal models.

Urothelial carcinoma of the renal pelvis is a deadly disease with an unclear tumorigenic mechanism. We conducted gene expression profiling on a set of human tumors of this type and identified a phosphatidylinositol 3-kinase (PI3K)/AKT activation expression signature in 76.9% (n = 13) of our samples.

Deficiency of FLCN in mouse kidney led to development of polycystic kidneys and renal neoplasia.

The Birt-Hogg-Dubé (BHD) disease is a genetic cancer syndrome. The responsible gene, BHD, has been identified by positional cloning and thought to be a novel tumor suppressor gene. BHD mutations cause many types of diseases including renal cell carcinomas, fibrofolliculomas, spontaneous pneumothorax, lung cysts, and colonic polyps/cancers.

Cystic renal neoplasia following conditional inactivation of apc in mouse renal tubular epithelium.

Alterations in Wnt/beta-catenin signaling have been linked to abnormal kidney development and tumorigenesis. To gain more insights into the effects of these alterations, we created mice carrying a conditional deletion of the Apc tumor suppressor gene specifically in the renal epithelium. As expected, the loss of Apc leads to increased levels of beta-catenin protein in renal epithelium.