Distally based sural fasciomusculocutaneous flap for treatment of wounds of the distal third of the leg and ankle with exposed internal hardware

Soft tissue reconstruction of the distal third of the lower limb with exposure of the internal hardware is a challenging problem with several potential complications, such as exposure of the fracture line, fracture instability and bacterial contamination. The treatment of these lesions usually consists of substitution of the internal hardware with external fixation devices and further flap coverage. We propose a different reconstructive approach, characterized by harvesting a sural fasciomusculocutaneous flap on the exposed internal hardware once a sterile ground has been obtained. Four patients were retrospectively analyzed. Soft tissue reconstruction was achieved in all cases. In one case hardware removal was necessary for complete healing. The sural fasciomusculocutaneous flap is a safe alternative to other pedicled and free flaps. Moreover, it allows direct coverage of internal fixators, thus completing the reconstruction in less time. This flap fits best to the morphology of the wound and internal hardware, leaving the main vascular trunk of the leg intact and at the same time providing a reliable vascular supply

The neuronal repellent SLIT2 is a target for repression by EZH2 in prostate cancer

The neuronal repellent SLIT2 is repressed in a number of cancer types primarily through promoter hypermethylation. SLIT2, however, has not been studied in prostate cancer. Through genome-wide location analysis we identified SLIT2 as a target of Polycomb group (PcG) protein EZH2. The EZH2-containing Polycomb repressive complexes bound to the SLIT2 promoter inhibiting its expression. SLIT2 was down-regulated in a majority of metastatic prostate tumors exhibiting a negative correlation with EZH2. This repressed expression could be restored by methylation inhibitors or EZH2-suppressing compounds. In addition, a low level of SLIT2 expression was associated with aggressive prostate, breast and lung cancers. Functional assays showed that SLIT2 inhibited prostate cancer cell proliferation and invasion. Thus, this study demonstrated for the first time epigenetic silencing of SLIT2 in prostate tumors, and supported SLIT2 as a potential biomarker for aggressive solid tumors. Importantly, PcG-mediated repression may serve as a precursor for the silencing of SLIT2 by DNA methylation in cancer

The mutational landscape of lethal castration-resistant prostate cancer

none27noneGrasso, Catherine S.; Wu, Yi-Mi; Robinson, Dan R.; Cao, Xuhong; Dhanasekaran, Saravana M.; Khan, Amjad P.; Quist, Michael J.; Jing, Xiaojun; Lonigro, Robert J.; Brenner, J. Chad; Asangani, Irfan A.; Ateeq, Bushra; Chun, Sang Y.; Siddiqui, Javed; Sam, Lee; Anstett, Matt; Mehra, Rohit; Prensner, John R.; Palanisamy, Nallasivam; Ryslik, Gregory A.; Vandin, Fabio; Raphael, Benjamin J.; Kunju, Lakshmi P.; Rhodes, Daniel R.; Pienta, Kenneth J.; Chinnaiyan, Arul M.; Tomlins, Scott A.Grasso, Catherine S.; Wu, Yi Mi; Robinson, Dan R.; Cao, Xuhong; Dhanasekaran, Saravana M.; Khan, Amjad P.; Quist, Michael J.; Jing, Xiaojun; Lonigro, Robert J.; Brenner, J. Chad; Asangani, Irfan A.; Ateeq, Bushra; Chun, Sang Y.; Siddiqui, Javed; Sam, Lee; Anstett, Matt; Mehra, Rohit; Prensner, John R.; Palanisamy, Nallasivam; Ryslik, Gregory A.; Vandin, Fabio; Raphael, Benjamin J.; Kunju, Lakshmi P.; Rhodes, Daniel R.; Pienta, Kenneth J.; Chinnaiyan, Arul M.; Tomlins, Scott A