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Background: Manipulation of the temporalis muscle during pterional and frontotemporal approaches poses major cosmetic and functional issues postoperatively. The temporalis muscle has usually been secured in its normal position using implants or by leaving a thin rim of muscle and fascia attached along the superior temporal line. In the present report, we have described a pure tissue-based method of anchoring the intact temporalis muscle precisely along the superior temporal line., Methods: A total of 30 consecutive cases of pterional or frontotemporal craniotomy were performed by single surgeon (SKR). A subfascial dissection technique was used to expose the transition zone of the frontal pericranium with the temporalis fascia. These were then separated by sharp dissection along the superior temporal line at which the muscle is attached. The temporalis muscle and fascia were repositioned during closure, precisely at their original anatomical location by passing multiple anchoring sutures along the free edge of the muscle and fascia lying along the superior temporal line., Results: Temporalis muscle reattachment was achieved in all 30 cases with good cosmesis and functional outcome without temporalis muscle-related complications at 6 months of follow-up., Conclusions: The approximation of sutures running through the free edge of the temporalis muscle with intact fascia along the superior temporal line from anteriorly to posteriorly restored the muscle and fascial layer to its original position. Avoidance of the formation of any potential dead space during surgical exposure will prevent periorbital edema and/or subgaleal collection postoperatively. The described inexpensive technique avoids implant-related complications, with good functional and aesthetic outcomes. A comparative study is needed to establish the superiority of this procedure over other techniques., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Glioblastoma (GBM) is one of the most aggressive and lethal types of brain tumor. Despite the advancements in conventional or targeted therapies, median survival of GBM patients is less than 12 months. Amongst various signaling pathways aberrantly activated in glioma, active Wnt/β-catenin signaling pathway is one of the crucial oncogenic players. β-catenin, an important mediator of Wnt signaling pathway, gets phosphorylated by GSK3β complex. Phosphorylated β-catenin is specifically recognized by β-Trcp1, a F-box/WD40-repeat protein and with the help of Skp1 it plays a central role in recruiting phosphorylated β-catenin for degradation. In GBM, expression of β-TrCP1 and its affinity for β catenin is reported to be very low. Hence, we investigated whether any other members of the E3 ubiquitin ligase family could be involved in degradation of nuclear β-catenin. We here report that FBXO16, a component of SCF E3 ubiquitin ligase complex, is an interacting protein partner for β-catenin and mediates its degradation. Next, we show that FBXO16 functions as a tumor suppressor in GBM. Under normal growth conditions, FBXO16 proteasomally degrades β-catenin in a GSK-3β independent manner. Specifically, the C-terminal region of FBXO16 targets the nuclear β-catenin for degradation and inhibits TCF4/LEF1 dependent Wnt signaling pathway. The nuclear fraction of β-catenin undergoes K-48 linked poly-ubiquitination in presence of FBXO16. In summary, we show that due to low expression of FBXO16, the β-catenin is not targeted in glioma cells leading to its nuclear accumulation resulting in active Wnt signaling. Activated Wnt signaling potentiates the glioma cells toward a highly proliferative and malignant state., (Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.)