The human cytomegalovirus (HCMV) and glioma symposium was convened on April 17, 2011 in Washington, DC, and was attended by oncologists and virologists involved in studying the relationship between HCMV and gliomas. The purpose of the meeting was to reach a consensus on the role of HCMV in the pathology of gliomas and to clarify directions for future research. First, the group summarized data that describe how HCMV biology overlaps with the key pathways of cancer. Then, on the basis of published data and ongoing research, a consensus was reached that there is sufficient evidence to conclude that HCMV sequences and viral gene expression exist in most, if not all, malignant gliomas, that HCMV could modulate the malignant phenotype in glioblastomas by interacting with key signaling pathways; and that HCMV could serve as a novel target for a variety of therapeutic strategies. In summary, existing evidence supports an oncomodulatory role for HCMV in malignant gliomas, but future studies need to focus on determining the role of HCMV as a glioma-initiating event.

Purpose The molecular heterogeneity of glioblastoma has been well recognized and has resulted in the generation of molecularly defined subtypes. These subtypes (classical, neural, mesenchymal, and proneural) are associated with particular signaling pathways and differential patient survival. Less understood is the correlation between these glioblastoma subtypes with immune system effector responses, immune suppression and tumor-associated and tumor-specific antigens. The role of the immune system is becoming increasingly relevant to treatment as new agents are being developed to target mediators of tumor-induced immune suppression which is well documented in glioblastoma. Experimental Design To ascertain the association of antigen expression, immune suppression, and effector response genes within glioblastoma subtypes, we analyzed the Cancer Genome Atlas (TCGA) glioblastoma database. Results We found an enrichment of genes within the mesenchymal subtype that are reflective of anti-tumor proinflammatory responses, including both adaptive and innate immunity and immune suppression. Conclusions These results indicate that distinct glioma antigens and immune genes demonstrate differential expression between glioblastoma subtypes and this may influence responses to immune therapeutic strategies in patients depending on the subtype of glioblastoma they harbor.

Purpose CMV has been ubiquitously detected within high-grade gliomas, but its role in gliomagenesis has not been fully elicited. Experimental Design Glioblastoma multiforme (GBM) tumors were analyzed by flow cytometry to determine CMV antigen expression within various glioma-associated immune populations. The gCSC CMV IL-10 production was determined by ELISA. Human monocytes were stimulated with recombinant CMV IL-10 and levels of expression of p-STAT3, VEGF, TGF-β, viral IE1 and pp65 were determined by flow cytometry. The influence of CMV IL-10 treated monocytes on gCSC biology was ascertained by functional assays. Results CMV demonstrated a tropism for macrophages (MΦs)/microglia and CD133+ gCSCs within GBMs. The gCSCs produce CMV IL-10, which induces human monocytes (the precursor to the CNS MΦs/microglia) to assume an M2 immunosuppressive phenotype (as manifested by down modulation of the major histocompatibility complex and costimulatory molecules) while up regulating immune inhibitory B7-H1. CMV IL-10 also induces expression of viral IE1, a modulator of viral replication and transcription in the monocytes. Finally, the CMV IL-10-treated monocytes produced angiogeneic VEGF, immunosuppressive TGF-β, and enhanced migration of gCSCs. Conclusions CMV triggers a feed-forward mechanism of gliomagenesis by inducing tumor-supportive monocytes.

To address a paucity of literature and treatment guidelines regarding the management of butterfly glioblastomas, we performed a ten year retrospective analysis of data from twenty-three consecutive patients treated for this disease at a single institution. Clinical characteristics and outcomes were assessed. Median age was 59 years; 52 % were female; median preoperative Karnofsky performance score (KPS) was 80. Twelve patients underwent biopsy and eleven underwent surgical decompression. The median tumor volume for the biopsy group was 60.6 cm3 and for the surgically decompressed group 40.5 cm3. In the biopsy group, five patients received adjuvant therapy but one died prior to its completion; two died prior to the initiation of adjuvant therapy and five were lost to follow up. In the surgical decompression group, seven patients received adjuvant therapy, one died prior to the initiation of adjuvant therapy, two were treated with palliative measures only, and one was lost to follow up. Kaplan–Meier estimates of overall median post surgical-survival of the whole group was 180 days, the biopsy group 48 days, and the surgically decompressed group 265 days (p = 0.14). Our results show that there was a higher median survival in the surgically decompressed group; but a direct correlation could not be established, and that the median KPS did not improve in either group after treatment. A larger multi-center review is required to quantitatively assess the factors, including tumor biomarkers that are associated with patient outcome.

Subfrontal schwannomas, sometimes referred to as olfactory groove schwannomas, are rare tumors (34 cases reported to date). Despite the name and several theories proposed in the literature, there is no officially recognized description of the tumor's cell origin. Yasuda proposed the concept of an olfactory ensheathing cell (OEC) tumor in 2006. Olfactory ensheathing cells are glial cells that ensheath the axons of the first cranial nerve. Microscopically, both olfactory ensheathing cells and Schwann cells have similar morphological and immunohistochemical features. However, immunohistochemically olfactory ensheathing cells are negative for Leu7 and Schwann cells positive. A 30-year-old woman presented with a subfrontal, extraaxial, enhancing tumor, and underwent gross total resection. Immunohistochemical reactivity data suggested a schwannoma (positive for S-100 and negative for epithelial membrane antigen). However, the tumor was negative for Leu7. Accordingly, our final diagnosis was that of an OEC tumor. Subfrontal schwannoma immunohistochemical staining, if negative for Leu7, is indicative of an OEC tumor. It is possible that schwannoma-like extraaxial tumors at the anterior skull base are OEC tumors, which negative Leu7 staining can confirm.

Sensitivity, specificity, positive and negative predictive values of these methods improve when applied to CT scans because of better visualization of anatomic landmarks. This result suggests CT scans of the cervical spine may be warranted in all trauma patients suspected of having cervical spine injury.

No abstract

Pituitary apoplexy is an infrequent but potentially devastating complication in patients with pituitary adenomas. Previous studies have cited an association between MR visualized sphenoid sinus mucosal thickening and apoplexy. However, uncertainties still remain on the significance and temporal association of this finding with pituitary apoplexy. We provide a clinical study that better delineates this temporal association and also provides histopathologic data for sinus thickening compared to control subjects. ÖZaMaÇ: Pitüiter apopleksi pitüiter adenomları olan hastalarda sık görülmeyen ama çok tehlikeli olabilecek bir komplikasyondur. Önceki çalışmalar MR'de sfenoid sinüste mukoza kalınlaşması görülmesiyle apopleksi arasında bir ilişki belirtmiştir ancak bu bulgunun pitüiter apopleksiyle temporal ilişkisi ve önemi halen şüphelidir. Burada bu temporal ilişkiyi daha iyi gösteren bir klinik çalışma sunuyoruz ve ayrıca kontrol hastalarıyla karşılaştırıldığında sinüs kalınlaşması için histopatolojik veriler sağlıyoruz. yÖnteM ve gereÇLer: Pitüiter apopleksi tanısı koyacak şekilde seri MR taramaları yapılan iki hasta bildiriyoruz. Hasta 1'de apopleksi başlangıcıyla yeni sfenoid sinüs mukoza kalınlaşması görüldü. Hasta 2'de başlangıçtan apopleksinin görüldüğü tekrar taramaya kadar sfenoid sinüs mukozasında progresif kalınlaşma saptandı. Her iki hastada pitüiter adenom için transsfenoidal rezeksiyon yapıldı ve patoloji enflame sfenoid sinüs mukozası gösterdi. sOnuÇ: MRG'de gösterildiği şekilde sfenoid sinüs mukoza kalınlaşması muhtemelen akut ve önceki bir bulgu şeklinde temporal olarak pitüiter apopleksiyle ilişkilidir.anaHtar sÖZcÜkLer: Pitüiter apopleksi, Sfenoid sinüs, Manyetik rezonans görüntüleme