Identifying IDH-mutant and 1p/19q noncodeleted astrocytomas from nonenhancing gliomas: Manual recognition followed by artificial intelligence recognition.

Background: The T2-FLAIR mismatch sign (T2FM) has nearly 100% specificity for predicting IDH-mutant and 1p/19q noncodeleted astrocytomas (astrocytomas). However, only 18.2%-56.0% of astrocytomas demonstrate a positive T2FM. Methods must be considered for distinguishing astrocytomas from negative T2FM gliomas. In this study, positive T2FM gliomas were manually distinguished from nonenhancing gliomas, and then a support vector machine (SVM) classification model was used to distinguish astrocytomas from negative T2FM gliomas. Methods: Nonenhancing gliomas (regardless of pathological type or grade) diagnosed between January 2022 and October 2022 (N = 300) and November 2022 and March 2023 (N = 196) will comprise the training and validation sets, respectively. Our method for distinguishing astrocytomas from nonenhancing gliomas was examined and validated using the training set and validation set. Results: The specificity of T2FM for predicting astrocytomas was 100% in both the training and validation sets, while the sensitivity was 42.75% and 67.22%, respectively. Using a classification model of SVM based on radiomics features, among negative T2FM gliomas, the accuracy was above 85% when the prediction score was greater than 0.70 in identifying astrocytomas and above 95% when the prediction score was less than 0.30 in identifying nonastrocytomas. Conclusions: Manual screening of positive T2FM gliomas, followed by the SVM classification model to differentiate astrocytomas from negative T2FM gliomas, may be a more effective method for identifying astrocytomas in nonenhancing gliomas.

Distinguishing Tumor Cell Infiltration and Vasogenic Edema in the Peritumoral Region of Glioblastoma at the Voxel Level via Conventional MRI Sequences.

RATIONALE AND OBJECTIVES: The peritumoral region of glioblastoma (GBM) is composed of infiltrating tumor cells and vasogenic edema, which are difficult to distinguish manually on MRI. To distinguish tumor cell infiltration and vasogenic edema in GBM peritumoral regions, it is crucial to develop a method that is precise, effective, and widely applicable. MATERIALS AND METHODS: We retrieved the image characteristics of 379,730 voxels (marker of tumor infiltration) from 28 non-enhanced gliomas and 365,262 voxels (marker of edema) from the peritumoral edema region of 14 meningiomas on conventional MRI sequences (T1-weighted image, the contrast-enhancing T1-weighted image, the T2-weighted image, the T2-fluid attenuated inversion recovery image, and the apparent diffusion coefficient map). Using the SVM classifier, a model for predicting tumor cell infiltration and vasogenic edema at the voxel level was developed. The accuracy of the model's predictions was then evaluated using 15 GBM patients who underwent stereotactic biopsies. RESULTS: The area under the curve (AUC), accuracy, sensitivity, and specificity of the prediction model were 0.93, 0.84, 0.83, and 0.85 in the training set, and 0.90, 0.82, 0.83, and 0.83 in the test set (704,992 voxels), respectively. The pathology verification of 28 biopsy points with an accuracy of 0.79. CONCLUSION: At the voxel level, it seems possible to forecast tumor cell infiltration and vasogenic edema in the peritumoral region of GBM based on conventional MRI sequences.

Development and validation of a novel survival prediction model for newly diagnosed lower-grade gliomas.

OBJECTIVE: Diffuse gliomas are the most common primary gliomas with a poor prognosis. This study aimed to develop and validate prognostic models for predicting the survival probability in newly diagnosed lower-grade glioma (LGG) patients. METHODS: Detailed data were obtained for newly diagnosed LGG from The Cancer Genome Atlas (TCGA) and the Chinese Glioma Genome Atlas (CGGA) cohorts. Survival was assessed using Cox proportional hazards regression with adjustment for known prognostic factors. The model was established using the TCGA cohort, and independently validated using the CGGA cohort, to predict the 3-, 5-, and 10-year survival probabilities of patients. RESULTS: Data from 293 patients with newly diagnosed LGG from the TCGA cohort were used to establish a prognostic model, and from 232 patients with primary LGG in the CGGA cohort to validate the model. Age, tumor grade, molecular subtype, tumor resection, and preoperative neurological deficits were included in the prediction model. The Cox regression model had a satisfactory corrected concordance index of 0.8508, 0.8510, and 0.8516 in the internal bootstrap validation at 3, 5, and 10 years, respectively. The calibration plots demonstrated high consistency of the predicted and observed outcomes. The CGGA cohort was used for external validation and showed satisfactory discrimination of 0.7776, 0.7682, and 0.7051 at 3, 5, and 10 years, respectively. The calibration plots demonstrated an acceptable calibration capability in the external validation. CONCLUSIONS: This study established and validated a prognostic model to predict the survival probability of patients with newly diagnosed LGG. The model performed well in discrimination and calibration with ease of use, speed, accessibility, interpretability, and generalizability. An easily used nomogram based on the Cox model was established for clinical application. Moreover, a free, easy-to-use software interface based on the nomogram is provided online.

Management of central nervous system Rosai-Dorfman disease: A single center treatment experience.

Rosai-Dorfman disease (RDD) is an idiopathic histiocytic proliferation disease with various clinical manifestations. A retrospective study of patients with pathological diagnosed RDD primarily involved in the central nervous system was conducted from January 2011 to December 2020 at a tertiary center. The clinical profile, imaging, and treatment data were collected. There were 16 male and 5 female patients with RDD-CNS. The patients were aged from 6 to 68 years with a median of 37 years. Of these 21 patients, 15 presented with intracranial RDD and 6 with spinal RDD. The main symptoms of RDD-CNS included headache, epilepsy, and neurological deficits. 76.19% (16/21) of the patients showed dura-based, homogeneous enhancement lesion on magnetic resonance imaging (MRI). Twenty patients received surgery as first treatment, and one patient received biopsy after steroid therapy. Total lesion resection was achieved in 42.9% (9/21) of the patients, subtotal resection in 47.6% (10/21), and biopsy in 0.9% (2/21). The symptoms were alleviated or stayed stable. Some RDDs (80%, 4/5) in the skull base had some complications. The patients were followed up for 11-108 months with a median duration of 47 months. Lesion progression or recurrence was found in two patients. The various clinical manifestations, as well as the dura-based and homogenous enhancement imaging profiles of RDD-CNS patients pose a great diagnostic challenge for clinicians. Surgery is effective for RDD-CNS requiring treatment. Medical therapy and radiotherapy would be feasible as noninvasive treatments, varying degrees of efficacy. The overall prognosis of RDD-CNS is acceptable. Periodic long-term follow-up is necessary.

The utility of intraoperative ECoG in tumor-related epilepsy: Systematic review.

OBJECT: Epilepsy is one of the most common clinical manifestations of primary brain tumors. Intraoperative electrocorticography (ECoG) has been widely used in tumor resection. We aim to describe the indication and utility of ECoG during brain tumor surgery. METHODS: We performed a systematic review of the literature on the prognosis of tumor-related epilepsy surgery guided by intraoperative ECoG. The published studies were searched in PubMed, Embase, and Web of Science using the keyword 'seizure' or 'epilepsy' and 'electrocorticography' or 'ECoG'. Two reviewer authors screened studies and extracted data independently. RESULTS: Thirteen studies included 569 patients were finally selected, of which eight investigated medically intractable epilepsy. Three publications described temporal tumor-related epilepsy. All included studies were retrospective, and the age of all patients ranged from 1 to 71 years. The duration of epilepsy ranged from 1 month to 30 years. Patients with tumor-related epilepsy underwent surgical treatment with Engel I outcomes ranging from 56.5%-100%. CONCLUSION: Intraoperative ECoG is generally considered a useful technique in delineating epileptogenic areas and improving the prognosis of surgical treatment of tumor-related epilepsy. However, large-scale randomized control trials are still needed to verify these findings and formulate appropriate surgical strategies.

microRNA-181a promotes the proliferation of hypertrophic scar fibroblasts and inhibits their apoptosis via targeting phosphatase and tensin homolog.

BACKGROUND: This study aimed to compare the expression of microRNA (miR)-181a and phosphatase and tensin homolog (PTEN) in hypertrophic scar tissue and cells and to explore the effects of miR-181a and PTEN on the proliferation and apoptosis of the human scar fibroblast cell line HSFb. METHODS: HSFb cells were transfected with miR-negative control (miR-NC), miR-181a mimics, miR-181a inhibitor, pcDNA3.1-PTEN (pc-PTEN), or small interfence-PTEN (si-PTEN) plasmid using a Lipofectamine 2000 transfection kit. The effects of miR-181a and PTEN on the proliferation and apoptosis of HSFb were determined using a Cell Counting Kit (CCK)-8 experiment and flow cytometry, respectively. The effects of miR-181a and PTEN on the expression of apoptosis-related proteins in HSFb, including type I collagen (Col-1) and type III collagen (Col-3), were measured by western blot. Finally, the relationship between miR-181a and PTEN was explored by the dual-luciferase reporter gene experiment. RESULTS: The miR-181a in hypertrophic scar tissues and HSFb were significantly up-regulated compared to embryo skin fibroblast (ESF-1) cells and normal tissues (P<0.05), whereas the opposite results were seen for PTEN expression (P<0.05). Inhibiting miR-181a or upregulating the expression of PTEN significantly suppressed the proliferation of HSFb (P<0.05) and induced their apoptosis (P<0.05). Western blot revealed that inhibiting and upregulating miR-181a and PTEN, respectively, decreased the expression of the B-cell lymphoma-2 (Bcl-2), Col-1, and Col-3 proteins in HSFb, but significantly up-regulated the expression of Bcl-2-associated X protein (Bax), cleaved caspase-3 (c-caspase-3), and cleaved caspase-9 (c-caspase-9) (P<0.05). The dual-luciferase reporter gene experiment results confirmed PTEN to be the downstream target gene of miR-181a. Simultaneous upregulation of miR-181a and PTEN expression had no significant effect on the proliferation and apoptosis of HSFb. CONCLUSIONS: miR-181a promotes the up-regulation of Col-1 and Col-3, and regulates the proliferation and apoptosis of HSFb by targeting PTEN, thereby enhancing the formation of hypertrophic scarring (HS). Therefore, miR-181a and PTEN may be potential therapeutic targets for the treatment of HS.

Ischemic Infarction of Pituitary Apoplexy: A Retrospective Study of 46 Cases From a Single Tertiary Center.

OBJECTIVE: Ischemic infarction of pituitary apoplexy (PA) is a rare type of pituitary apoplexy. This study aims to characterize ischemic PA via clinical presentations, imaging data, histopathological manifestations, and focus on the management and prognosis of the disease. METHODS: This study retrospectively identified 46 patients with ischemic PA confirmed using histopathology at a single institution from January 2013 to December 2020. The clinical presentations, imaging data, laboratory examination, management, and outcomes were collected. We then summarized the clinical presentations, imaging features, intraoperative findings, and histopathological manifestations, and compared the outcomes based on the timing of surgical intervention. RESULTS: Headache was the most common initial symptom (95.65%, 44/46), followed by visual disturbance (89.13%, 41/46), and nausea and vomiting (58.70%, 27/46). 91.3% of the patients had at least one pituitary dysfunction, with hypogonadism being the most common endocrine dysfunction (84.78%, 39/46). Cortisol dysfunction occurred in 24 (52.17%) patients and thyroid dysfunction occurred in 17 (36.96%). Typical rim enhancement and thickening of the sphenoid sinus on MRI were seen in 35 (85.37%) and 26 (56.52%) patients, respectively. Except for one patient with asymptomatic apoplexy, the remaining patients underwent early (≤ 1 week, 12 patients) and delayed (> 1 week, 33 patients) transsphenoidal surgery. Total tumor resection was achieved in 27 patients and subtotal tumor resection in 19 patients. At surgery, cottage cheese-like necrosis was observed in 50% (23/46) of the patients. At the last follow-up of 5.5 ± 2.7 years, 92.68% (38/41) of the patients had gained a significant improvement in visual disturbance regardless of surgical timing, and 65% of the patients were still receiving long-term hormone replacement therapy. CONCLUSION: Patients with ischemic PA can be accurately diagnosed by typical imaging characteristics preoperatively. The timing of surgical intervention does not significantly affect the resolution of neurological and endocrinological dysfunctions. Preoperative endocrine dysfunctions are common and usually appear to be poor after surgical intervention.