Purpose: To explore the potential pathogenesis and clinical features of second primary glioblastoma (spGBM) following first primary renal cell carcinoma (fpRCC).
Methods: Patients with spGBM after fpRCC were enrolled from our institution and the SEER dataset. Sanger sequencing, whole genome sequencing, and immunehistochemistry were used to detect molecular biomarkers.
Objective: Surgical treatment of advanced intracranial and extracranial communicating skull base tumors is challenging, especially for the reconstruction of the large composite defect left by tumor resection. The aim of the study is to evaluate the utility of the free flap reconstruction of the defects resulting from radical resection of these tumors in a single institution.
Methods: The clinical data of 17 consecutive patients who underwent free flap reconstruction for defect left by salvage resection of advanced intracranial and extracranial communicating tumors from 2013 to 2019 were retrospectively collected and analyzed.
Temozolomide (TMZ) is considered a standard chemotherapeutic agent for glioblastoma (GBM). Characterizing the biological molecules and signaling pathways involved in TMZ sensitivity would be helpful for selecting therapeutic schemes and evaluating prognosis for GBM. Thus, in the present study, we selected 34 glioma cell lines paired with specific IC values of TMZ obtained from CancerRxGene and RNA-seq data downloaded from the Cancer Cell Line Encyclopedia to identify genes related to TMZ sensitivity.
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