Objectives:The Sorbin and SH3 domain containing 1 (SORBS1), a protein linked to insulin signaling CBL interaction, was investigated for its role in pancreatic cancer apoptosis. This study explored polyphyllin H (PPH)'s ability to restore SORBS1-knockdown-mediated repair functions. Methods:PANC-1 cells were divided into Blank, overexpression (OE), and knockdown groups. CCK-8 assays assessed proliferation and drug toxicity. Western blot and flow cytometry analyzed SORBS1 levels and PPH effects. Comet assays quantified DNA damage. Subcutaneous xenograft tumors in nude mice (Blank vs. knockdown) were treated with PPH to evaluate in vivo efficacy. SORBS1-H2AX gene correlation was analyzed Spearman rank clustering (p < 0.05). Results:PPH suppressed pancreatic cancer growth in vitro/vivo, but its efficacy was attenuated by SORBS1 downregulation. Clinically, low SORBS1 correlated with poor prognosis. SORBS1 knockdown promoted tumor proliferation and reduced PPH-induced apoptosis. While PPH decreased tumor volume in both Blank and knockdown groups compared to controls, SORBS1 knockdown diminished PPH's inhibitory effects. Mechanistically, SORBS1 depletion mitigated PPH-triggered DNA damage, circumventing G2/M arrest by modulating WEE1, Cyclin A2, CDK1, and Cyclin B1, thereby impairing apoptosis. Conclusion:SORBS1 knockdown counteracts PPH-mediated S/G2 arrest and apoptosis by alleviating DNA damage in pancreatic cancer. These findings highlight SORBS1 as a critical modulator of PPH's therapeutic potential, linking its expression to chemoresistance mechanisms.

Abstract Background IL-13Rα2 is one of the most widely studied tumor-associated antigens in glioma research. Fused in sarcoma (FUS) is a DNA/RNA binding protein that is dysfunctional in various malignant tumors. However, the expression of IL-13Rα2 and FUS, their relationship with clinicopathological parameters and their prognostic value in glioma remain unclear. Methods In the present study, the expression of IL-13Rα2 and FUS was measured in a glioma tissue array by immunohistochemistry. Pearson’s X2 test was used to determine the correlation between immunohistochemical expressions and clinicopathological parameters. Pearson’s or Spearman's correlation test was used to determine the association between these two proteins expression. The Kaplan–Meier analysis was used to investigate the effect of these proteins on prognosis. Results The expressions of IL-13Rα2 were significantly higher in high-grade gliomas (HGG) than that in low-grade gliomas (LGG) and was associated with IDH mutation status, whereas FUS location demonstrated no significant correlation with clinicopathological parameters. Moreover, a positive relationship was found between nuclear and cytoplasmic co-localization FUS and IL-13Rα2 expression. Kaplan–Meier analysis revealed that patients with IDH wide type or IL-13Rα2 had worst overall survival (OS) compared to other biomarkers. In HGG, IL-13Rα2 combined with nuclear and cytoplasmic co-localization of FUS was associated with worse OS. Multivariate analysis showed that tumor grade, Ki-67, P53 and IL-13Rα2 could be the independent prognostic factors for OS. Conclusion IL-13Rα2 expression was significantly associated with cytoplasmic distribution of FUS in human glioma samples and could be the independent prognostic factors for OS, while the prognostic value of its co-expression with cytoplasmic FUS in glioma need to be addressed in the future studies.

Objective To investigate the effect of intraoperative epileptic seizure on postoperative mood and muscle strength during awake anesthesia (AA) for the resection of gliomas. Methods A total of 90 patients with glioma admitted to Xijing Hospital, Air Force Military Medical University of Chinese PLA from September 2020 to September 2022 were collected and divided into general anesthesia group (GA group, n = 30), awake anesthesia without intraoperative epileptic seizure group (AA group, n = 30), and awake anesthesia with intraoperative epileptic seizure group (AA + IE group, n = 30) according to the anesthesia method and the presence of intraoperative epileptic seizure. Patients' mood and muscle strength changes were assessed preoperatively and one week postoperatively by using Hamilton Anxiety Rating Scale (HAMA), Hamilton Depression Rating Scale (HAMD) and muscle strength division method. Results The differences in HAMD score (F = 9.985, P = 0.000) and muscle strength (F = 4.472, P = 0.014) at one week postoperatively were statistically significant among 3 groups. HAMD score was increased in AA group (q = 3.177, P = 0.014) and AA + IE group (q = 9.468, P = 0.000) when compared with GA group. HAMD scores was increased in AA + IE group (q = 6.290, P = 0.003) when compared with AA group. Postoperative muscle strength of AA group (q = 9.172, P = 0.006) and AA + IE group (q = 5.310, P = 0.000) was increased when compared with GA group. Muscle strength of AA + IE group was decreased compared with AA group (q = 3.862, P = 0.007). Conclusions Awake anesthesia can aggravate postoperative depression, but improve muscle strength. Intraoperative epileptic seizure can aggravate postoperative depression and decrease muscle strength. A reasonable preventive treatment plan needs to be developed in advance to reduce the incidence of intraoperative epileptic seizure.

目的 探讨加速康复外科(ERAS)理念联合清醒麻醉下开颅对脑功能区胶质瘤患者预后的影响.方法 分析2019年9月—2020年9月西京医院神经外科收治的脑功能区胶质瘤患者90例,根据不同麻醉及处理方式分为全身麻醉(GA)组、清醒麻醉(AA)组和清醒麻醉联合加速康复外科理念(AA+ERAS)组各30例,收集并比较3组患者的性别、年龄、术前症状、肿瘤位置、侧别、病理级别、失血量、手术时间、切除程度、术后恶心呕吐、住院时间、术后癫痫、术后1周功能改善、术后2个月卡诺夫斯凯计分(KPS)等资料.所有病例都有2年随访资料,根据随访对死亡情况绘制生存曲线.结果 3组患者的预后指标中,AA+ERAS组的肿瘤全切程度高、术后恶心呕吐发生率低、住院时间短、术后2个月KPS高,结果均优于GA组和AA组,差异具有统计学意义(P＜0.05),其余指标差异无统计学意义(P＞0.05).生存曲线结果显示术后2年的无进展生存率、总存活率均高于GA组和AA组,差异具有统计学意义(P＜0.05).结论 ERAS理念联合清醒麻醉可明显改善脑胶质瘤患者的预后,术后近期可减少患者术后应激反应和并发症,术后远期可延长患者生存率、提高患者生活质量,为临床治疗提供有力的理论依据和指导意义.

目的 探讨固摄补肾针刺法配合经颅直流电刺激治疗脑卒中尿失禁的效果.方法 选择2020 年12 月—2021 年12 月空军军医大学第一附属医院收治的脑卒中尿失禁患者84 例,随机分成对照组和观察组各42 例.2 组患者均予内科常规治疗和排尿反射训练,对照组联合经颅直流电刺激治疗,观察组联合经颅直流电刺激及固摄补肾针刺法治疗,2 组均连续治疗8 周.观察比较2 组患者治疗前及治疗8 周后国际尿失禁咨询委员会尿失禁问卷简表(ICIQ-UI SF)评分、尿失禁生活质量问卷量表(I-QOL)评分、72 h排尿日记、膀胱最大容量、残余尿量变化,评估 2 组临床疗效及治疗安全性.结果 与治疗前比较,治疗8 周后2 组患者ICIQ-UI SF评分明显降低,夜尿次数、白天排尿次数、总排尿次数、尿失禁次数、残余尿量均明显减少,I-QOL评分明显升高,平均每次尿量、膀胱最大容量均明显增加,且观察组上述指标较对照组改善更明显,差异均有统计学意义(P均<0.05);观察组总有效率为92.9％(39/42),明显高于对照组的69.0％(32/42),差异有统计学意义(P<0.05);2 组治疗期间均未发生与经颅直流电刺激和针刺治疗相关的不良事件.结论 固摄补肾针刺法配合经颅直流电刺激治疗脑卒中尿失禁疗效十分显著,能够减少尿失禁次数,减轻尿失禁程度,增大膀胱容量,改善患者生活质量,有助于促进患者机体功能康复.

目的 考察重楼皂苷Ⅶ对耐药胶质瘤的作用机制.方法 采用划痕和Transwell小室检测细胞迁移,CCK-8检测细胞增殖,流式细胞检测细胞周期,Western blot检测蛋白表达.结果 重楼皂苷Ⅶ呈剂量依赖性抑制替莫唑胺耐药胶质瘤细胞增殖和迁移,涉及下调迁移相关蛋白N-cadherin,β-catenin,TGF-β受体1和smad2.耐药胶质瘤细胞具有天然G1期阻滞现象,重楼皂苷Ⅶ可上调cyclin D1下调P21和P27影响其周期阻滞.结论 重楼皂苷Ⅶ具有抗替莫唑胺耐药胶质瘤的作用和进一步开发的前景.

目的 研究重楼皂苷H诱导耐替莫唑胺胶质瘤SHG44R细胞程序性死亡的途径和初步分子机制.方法 CCK-8法检测给药后细胞活力影响,透射电子显微镜(TEM)检测给药后细胞形态及细胞器变化,流式细胞术检测给药后细胞凋亡率,Western blot法检测凋亡和焦亡的相关蛋白表达,RT-qPCR检测焦亡相关mRNA表达水平.结果 CCK-8法检测结果表明重楼皂苷H呈时间剂量依赖性地抑制SHG44R增殖;TEM观察到给药后细胞膜破裂、胞质出现囊泡,提示具有细胞凋亡和焦亡的表征;流式细胞术检测结果表明重楼皂苷H剂量依赖性地介导细胞凋亡;Western blot 法检测结果表明 Bax、Cleaved-caspase-3、Cleaved-caspase-1、Cleaved-N-terminal-GSDMD、IL-1β、IL-18和NLRP3蛋白上调,Bcl-2蛋白下调;RT-qPCR结果表明,与正常组相比,给药后 caspase-1、caspase-11、GSDMD、IL-1β、IL-18 和 NLRP3 的 mRNA表达水平显著上升.结论 重楼皂苷H诱导耐替莫唑胺胶质瘤SHG44R细胞凋亡与焦亡.

Background::Awake craniotomy (AC) has become gold standard in surgical resection of gliomas located in eloquent areas. The conscious sedation techniques in AC include both monitored anesthesia care (MAC) and asleep-awake-asleep (AAA). The choice of optimal anesthetic method depends on the preferences of the surgical team (mainly anesthesiologist and neurosurgeon). The aim of this study was to compare the difference in physiological and blood gas data, dosage of different drugs, the probability of switching to endotracheal intubation, and extent of tumor resection and dysfunction after operation between AAA and MAC anesthetic management for resection of gliomas in eloquent brain areas.Methods::Two-hundred and twenty-five patients with super-tentorial tumor located in eloquent areas underwent AC from 2009 to 2021 in Xijing Hospital. Forty-one patients underwent AAA technique, and the rest one-hundred eighty-four patients underwent MAC technique. Anesthetic management, dosage of different drugs, intraoperative complications, postoperative outcomes, adverse events, extent of resection and motor, and sensory and language dysfunction after operation were compared between MAC and AAA.Result::There was no significant difference in gender, KPS score, MMSE score, glioma grade, type, and growth site between the patients in the two groups, except the older age of patients in MAC group than that in AAA group. During the whole process of operation, there were greater pulse pressure difference ( P=0.046), shorter operation time ( P=0.039), less dosage of remifentanil ( P=0.000), more dosage of dexmedetomidine ( P=0.013), more use of antiemetics (81%, P=0.0067), lower use of vasoactive agent (45.1%, P=0.010), and lower probability of conversion to general anesthesia (GA, P=0.027) in MAC group than that in AAA group. Blood gas analysis showed that PetCO2 ( P=0.000), Glu concentration ( P=0.000), and PaCO2 ( P=0.000) were higher, but SPO2 ( P=0.002) and PaO2 ( P=0.000) were lower in MAC group than that in AAA group. In the postoperative recovery stage, compared with that of AAA group, the probability of dysfunction in MAC group at 1, 3, 5, and 7 days after operation was lower, which were 27.8% vs 53.6% ( P=0.003), 31% vs 68.3% ( P=0.000), 28.8% vs 63.4% ( P=0.000), and 25.6% vs 58.5% ( P=0.000), respectively. Conclusion::Compared with AAA, it seems that MAC has more advantages in the management for resection of gliomas in eloquent brain areas, and MAC combined with multiple monitoring such as cerebral cortical mapping, neuronavigation, and ultrasonic detection is worthy of popularization for the resection of gliomas in eloquent brain areas.

Many glioma patients develop resistance to temozolomide (TMZ) treatment, resulting in reduced efficacy and survival rates. TMZ‐resistant cell lines SHG44R and U87R, which highly express O6‐methylguanine DNA methyltransferase (MGMT) and P‐gp, were established. CN‐3, a new asterosaponin, showed cytotoxic effects on TMZ‐resistant cells in a dose‐ and time‐dependent manner via reactive oxygen species (ROS)‐mediated apoptosis and autophagy. Transmission electron microscopy and monodansylcadaverine (MDC) staining showed turgidity of the mitochondria and autophagosomes in CN‐3‐treated SHG44R and U87R cells. The autophagy inhibitor 3‐methyladenine was used to confirm the important role of autophagy in CN‐3 cytotoxicity in TMZ‐resistant cells. The ROS scavenger N‐acetyl‐ l‐cysteine (NAC) attenuated the levels of ROS induced by CN‐3 and, therefore, rescued the CN‐3 cytotoxic effect on the viability of SHG44R and U87R cells by Cell Counting Kit‐8 assays and JuLI‐Stage videos. MDC staining also confirmed that NAC rescued an autophagosome increase in CN‐3‐treated SHG44R and U87R cells. Western blotting revealed that CN‐3 increased Bax, cleaved‐caspase 3, cytochrome C, PARP‐1, LC3‐Ⅱ, and Beclin1, and decreased P‐AKT, Bcl‐2, and p62. Further rescue experiments revealed that CN‐3 induced apoptosis and autophagy through ROS‐mediated cytochrome C, cleaved‐caspase 3, Bcl‐2, P‐AKT, PARP‐1, and LC3‐Ⅱ. In addition, CN‐3 promoted SHG44R and U87R cells sensitive to TMZ by reducing the expression of P‐gp, MGMT, and nuclear factor kappa B p65, and it had a synergistic cytotoxic effect with TMZ. Moreover, CN‐3 disrupted the natural cycle arrest and inhibited the migration of SHG44R and U87R cells by promoting cyclin E1 and D1, and by decreasing P21, P27, N‐cadherin, β‐catenin, transforming growth factor beta 1, and Smad2.

Background: Gliomas remain among the most difficult cancers to treat, with a 5-year overall survival no greater than 5%. Many saponins showed a wide spectrum of anti-cancer activities at low concentration. Polyphyllin II is one of the common saponins from Paris polyphylla. However, the effect of Polyphyllin II on glioma cells has not been evaluated. Objective of the present study was to investigate whether Polyphyllin II have inhibition on glioma cells, and the possible mechanisms. Methods: The viability of U87 and U251 cells was detected by cell counting kit-8, cell counting real time cellular analysis and cell clone formation methods. Transwell was used to estimate the aggression of U87 and U251. The cell apoptosis rate was tested by flow cytometry. The morphological change was determined by transmission electron microscopy. The levels of AKT, phosphorylation of AKT, Bax, Bcl-2, cytochrome c, and cleaved caspase 3 proteins were assessed by Western blot. N-acetyl-L-cysteine was used to check the role of ROS in polyphyllin II inhibition to glioma cells. Results: Polyphyllin II showed significant suppress to proliferation and aggression of U87 and U251 in a dose-and time-dependent manner. Result of flow cytometry confirmed that Polyphyllin II induced apoptosis to U87 and U251 cells. Transmission electron microscopy observation revealed majority of the glioma cells treated with Polyphyllin II had turgidity of mitochondrion, disarrangement, diminution and vacuolization, those refer to mitochondrial apoptosis. Western blot indicated that Polyphyllin II promoted cyt-c, Bax, caspase 3 and cleaved-caspase 3, and decreased Bcl-2, AKT and p-AKT. Rescue experiments using N-acetyl-L-cysteine, a reactive oxygen species scavenger, reversed the levels of Bax and cyt-c, and the inhibition in Polyphyllin II-treated U87 and U251 cells. Conclusions: The present findings revealed that polyphyllin II may be a potential drug against glioma.

To compare and characterize metabolic features of high‐ and low‐grade glioma tumors using 68Ga‐PSMA‐617 and 18F‐FDG positron emission tomography/computed tomography (PET/CT).

Recently we isolated CN-3, a new asterosaponin from starfish Culcita novaeguineae, and reported that asterosaponin arrests glioma cell cycle via SCUBE3. However, the multiple mechanisms underlying CN-3 anti-glioma action remains poorly known. Thus, the focus of this study was to evaluate the inhibitory effect of CN-3 on human glioma cells and its underlying molecular mechanisms. U87 and U251 cells were incubated with various concentrations of CN-3, and CCK-8, transmission electron microscopy, ICELLigence, TUNEL, flow cytometry, N-acetyl-L-cysteine, and western blot were conducted. As a result, it was found that CN-3 significantly inhibited U87 and U251 cell viability and proliferation in a time- and dose- dependent manner, and also induced mitochondrial apoptosis. Furthermore, we detected that CN-3 downregulated PI3K, P-Akt, AKT and BCL-2, and upregulated cytochrome C and BAX in U87 and U251 cells. Moreover, ROS triggered the inhibition and cell apoptosis for CN-3 via inactivation of P-Akt and activation of cytochrome C. In conclusion, these findings suggest that CN-3 may be a promising candidate for the development of a therapy of glioma.

Many saponins are characterized as exhibiting a wide spectrum of antitumor activities at low concentrations. Most of the previous studies that aimed to understand the mechanisms underlying anticancer saponins have focused on numerous classical signaling pathways. However, at the oncogene level, little is known about the action of saponins, especially asterosaponin. In this study, CN-3, a new asterosaponin isolated from the starfish Culcita novaeguineae, decreased the proliferation of U87 and U251 cells at low doses in a dose- and time-dependent manner. Microarray analysis revealed CN-3 significantly induced the differential expression of 661 genes that are related to its antiglioma effect in U251. Nine downregulated genes (SCUBE3, PSD4, PGM2L1, ACSL3, PRICKLE1, ABI3BP, STON1, EDIL3, and KCTD12) were selected, for further verification of their low expression. Then, shRNA transfection and high-content screening were performed and significantly decreased U251 cell proliferation rate was only observed for the SCUBE3 knockdown. qPCR confirmed SCUBE3 was highly expressed in U251 and U87 cells, and had medium expression levels in U373 cells. Real-time cellular analysis using iCELLigence demonstrated that SCUBE3 is an oncogene in U251 and U87 cells, with knockdown of SCUBE3 inhibiting U251 and U87 cell proliferation while, conversely, SCUBE3 overexpression promoted their proliferation. Afterward, SCUBE3 protein was found to have high expression in primary glioma specimens from patients examined by immunohistochemistry but low expression in normal brain. PathScan ELISA analysis in conjunction with TEM observation demonstrated that the effect of SCUBE3 knockdown in U251 does not appear to be related to the induction of apoptosis. Employing CCK-8, iCELLigence, flow cytometry, western blotting, and shRNA transfection (knockdown and overexpression) experiments, we reveal that the reduction of SCUBE3 expression, induced by CN-3, mediated both inhibition and G1/S arrest of U251 via the Akt/p-Akt/p53/p21/p27/E2F1 pathway.

RATIONABLE:Large cell neuroendocrine carcinoma of the lung is rare, especially in the area of the foramen magnum. No previous studies have reported metastatic large cell neuroendocrine lung cancer to the foramen magnum. This paper will be the first time to report this special case.PATIENT CONCERNS:A case of a 37-year-old woman presented with headache that had developed 20 days previously. Imaging examination revealed a circular abnormal signal at the posterior margin of the foramen magnum.DIAGNOSES:The patient we report was diagnosed with a metastatic intracranial tumor.INTERVENTIONS:The patient underwent occipital craniotomy. Pathological results showed metastatic neuroendocrine carcinoma of the brain. Whole body PET-CT examination showed that fusiform soft tissue shadows could be seen near the hilum of the lower lobe of the left lung.OUTCOMES:The final bronchoscopy pathological results showed the large cell neuroendocrine carcinoma of the lung. The patient underwent further chemotherapy and radiotherapy in the oncology department.LESSONS:Diagnosis and treatment of large cell neuroendocrine carcinoma of the lung are difficult. The prognosis is poorer, and effective treatment is urgently needed.

Abnormal metabolism serves a critical role in the development and progression of different types of malignancies including glioblastoma (GBM), and may therefore serve as a promising target for treatment of cancer. Preclinical studies have indicated that a ketogenic diet (KD) may exhibit beneficial effects in patients with GBM; however, the underlying mechanisms remain incompletely understood. The aim of the present study was to evaluate the effects of a KD on glioma stem‑like cells (GSCs), by culturing patient‑derived primary GSCs as well as a GSC cell line in glucose‑restricted, β‑hydroxybutyrate‑containing medium (BHB‑Glow) which was used to mimic clinical KD treatment. GSCs cultured in BHB‑Glow medium exhibited reduced proliferation and increased apoptosis compared with cells grown in the control medium. Furthermore, decreased expression of stem cell markers, diminished self‑renewal in vitro, and reduced tumorigenic capacity in vivo, providing evidence that the stemness of GSCs was compromised. Mechanistically, culturing in BHB‑Glow medium reduced glucose uptake and inhibited glycolysis in GSCs. Furthermore, culturing in the BHB‑Glow medium resulted in morphological and functional disturbances to the mitochondria of GSCs. These metabolic changes may have reduced ATP production, promoted lactic acid accumulation, and thus, increased the production of reactive oxygen species (ROS) in GSCs. The expression levels and activation of mammalian target of rapamycin, hypoxia‑inducible factor 1 and B‑cell lymphoma 2 were decreased, consistent with the reduced proliferation of GSCs in BHB‑Glow medium. ROS scavenging reversed the inhibitory effects of a KD on GSCs. Taken together, the results demonstrate that treatment with KD inhibited proliferation of GSCs, increased apoptosis and attenuated the stemness in GSCs by increasing ROS production.

异地口音综合征(FAS)是一种极为罕见的运动性语言障碍疾病.迄今为止,国内外仅有100多例FAS患者的病例报道.通过对FAS病因、发病机制、临床表现、诊断及鉴别诊断、治疗等方面相关内容的文献综述研究,发现FAS的病因至今尚未明确,但其临床症状和诊断明确.经过相关对因治疗后,异地口音症状可得到改善.同时,FAS的出现也是语言功能恢复的早期表现,它预示着患者语言功能由之前的障碍状态正在逐渐好转的理念.

INTRODUCTION:Tumour-associated angiogenesis is associated with the malignancy and poor prognosis of glioma. Isocitrate dehydrogenase (IDH) mutations are present in the majority of lower-grade (WHO grade II and III) and secondary glioblastomas, but their roles in tumour angiogenesis remain unclear.METHODS:Using magnetic resonance imaging (MRI), the cerebral blood flow (CBF) of IDH-mutated glioma was measured and compared with the IDH-wildtype glioma. The densities of microvessels in IDH-mutated and wildtype astrocytoma and glioblastoma were assessed by immunohistochemical (IHC) staining with CD34, and the pericytes were labelled with α-smooth muscle antigen (α-SMA), neural-glial antigen 2 (NG2) and PDGF receptor-β (PDGFR-β), respectively. Furthermore, glia-specific mutant IDH1 knock-in mice were generated to evaluate the roles of mutant IDH1 on brain vascular architectures. The transcriptions of the angiogenesis-related genes were assessed in TCGA datasets, including ANGPT1, PDGFB and VEGFA. The expressions of these genes were further determined by western blot in U87-MG cells expressing a mutant IDH1 or treated with 2-HG.RESULTS:The MRI results indicated that CBF was reduced in the IDH-mutated gliomas. The IHC staining showed that the pericyte coverages of microvessels were significantly decreased, but the microvessel densities (MVDs) were only slightly decreased in IDH-mutated glioma. The mutant IDH1 knock-in also impeded the pericyte coverage of brain microvessels in mice. Moreover, the TCGA database showed the mRNA levels of angiogenesis factors, including ANGPT1, PDGFB and VEGFA, were downregulated, and their promoters were also highly hyper-methylated in IDH-mutated gliomas. In addition, both mutant IDH1 and D-2-HG could downregulate the expression of these genes in U87-MG cells.CONCLUSIONS:Our results suggested that IDH mutations could reduce the pericyte coverage of microvessels in astrocytic tumours by inhibiting the expression of angiogenesis factors. As vascular pericytes play an essential role in maintaining functional blood vessels to support tumour growth, our findings imply a potential avenue of therapeutic strategy for IDH-mutated gliomas.

BACKGROUND AND PURPOSE:Conventional magnetic resonance imaging (MRI) is sometimes difficult to distinguish primary central nervous system lymphoma (PCNSL) from other malignant brain tumors effectively. The study aimed to evaluate the diagnostic performance of arterial spin labeling (ASL) and dynamic contrast-enhanced (DCE)-derived permeability parameters to differentiate PCNSL from high-grade glioma (HGG) and brain metastasis.MATERIALS AND METHODS:Eight patients with PCNSL, twenty one patients with HGG and six brain metastasis underwent preoperative 3.0-T MR imaging including conventional, ASL and DCE. Quantitative parameters including relative cerebral blood flow (rCBF), extravascular extracellular volume fraction (Ve) and the volume transfer constant (Ktrans) among PCNSL, HGG and metastasis were compared with a one-way analysis of variance. In addition, the area under the receiver-operating characteristic (ROC) curve (AUC) was constructed to evaluate the differentiation diagnostic performance of each parameter and the combination.RESULTS:The PCNSL demonstrated significantly lower rCBF, higher Ktrans and Ve compared with HGG and metastasis. For the ROC analyses, both Ktrans and rCBF had good diagnostic performance for discriminating PCNSL from HGG and metastasis, with the AUC of 0.880 and 0.889. With the combination of rCBF and Ktrans, the diagnostic ability for PCNSL was improved with AUC of 0.986.CONCLUSION:rCBF and Ktrans are useful parameters for differentiating PCNSL from HGG and brain metastasis. The combination of rCBF and Ktrans further helps to improve the diagnostic performance of PCNSL.

To noninvasively evaluate the value of three-dimensional pseudo-continuous arterial spin labeling (3D pCASL) and diffusion-weighted imaging (DWI) in diffuse gliomas grading as well as isocitrate dehydrogenase (IDH) 1 mutation status.