PMC4965258_01
A. Image of pre surgical MRI of September 09 2013 showing within the posterior medial right temporal and occipital lobes a 3.8 x 5.8 x 4.7 cm. mass. The mass had peripheral enhancement and effacement of the atrium of the right lateral ventricle, displaced laterally. B. Post- surgery image of September 21 2013, showing interval right parietal craniotomy with significant debulking of right temporal occipital tumor. There was a large area of restricted diffusion along the margins of the resection cavity in the right occipital lobe. There was expected postoperative enhancement of the margins of the resection cavity and along the operative tract. C. At one year post- surgical intervention and completion of temozolomide adjuvant treatment, there were evolving intrinsic T1 hyper-intensities along the margins of the resection cavity in the right parietal lobe. There was improvement in the enhancement along the margins of the operative tract and section cavity. No new areas of enhancement, hydrocephalus or midline shift. D. At thirty months follow up there were post-operative changes with no new enhancing lesions, no hydrocephalus or midline shift. The patient is neurologically functional and with a ECOG PS* of 0. *Eastern Cooperative Group Performance Status.
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T1 signal. There was increased T2 signal throughout the white matter, with effacement of the atrium and right lateral ventricle and with lateral displacement (Figure 1A). September 19, 2013, he underwent a right parieto-occipital craniotomy with maximal tumor removal (Figure 1B). Surgical pathology revealed a Since completion of his concurrent chemo-radiotherapy and initiation of his adjuvant treatment there has been progressive stabilization of his clinical condition and of his brain MRI images (Figure 1 C and D) with no evidence of recurrence of his tumor.
The patient's glioblastoma multiforme (GBM) with: H&E stained section showing tumor cells with adjacent angiogenic focus (Frame A); high expression of epidermal growth factor receptor, total and vIII on the plasmalemmal aspect of the tumor cells(Frame B); nuclear compartmentalization of phosphorylated (p ) mTOR (Ser 2448) (Frame C); variable expression of Sirt1 Frame D) and EZH2 (Frame E) in the nuclei of the tumor cells; and CXCR4 on the endothelial cells including areas of tumoral angiogenesis along with occasional scattered mononuclear cells in the adjacent tissues (Frame F, see arrows) There is also an associated expression of vascular endothelial growth factor (VEGF)-A in the tumor cells in the angiogenic region. PKC-alpha, p-Akt (Ser 473) and VEGF-A are not depicted. (DAB[3,3'-diaminobenzidine] brown chromogenic signal; original magnifications x400 for Frames A-F).
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These are illustrated in Figure 2 A-F.
Key interactions modulated by potential pharmacogenomic agents in glioblastoma. Dashed lines: indirect interactions; Red coloration/t-bar: downregulation; Green coloration/arrow: upregulation; Blue coloration/arrow: dual- directional regulation or binding.
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