Histology and histopathology Vol.35, nº7 (2020)

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Open Access
Mechanisms of neuroinflammation and inflammatory mediators involved in brain injury following subarachnoid hemorrhage
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Okada, Takeshi; Suzuki, Hidenori
Subarachnoid hemorrhage (SAH) is a devastating cerebrovascular disorder. Neuro- inflammation is a critical cause of brain injury following SAH in both acute and chronic phases. While accumulating evidence has shown that therapies targeting neuroinflammation exerted beneficial effects in experimental SAH, there is little clinical evidence. One of the factors making neuroinflammation complicated is that inflammatory signaling pathways and mediators act as protective or detrimental responses at different phases. In addition, biomarkers to detect neuro- inflammation are little known in clinical settings. In this review, first, we discuss how the inflammatory signaling pathways contribute to brain injury and other secondary pathophysiological changes in SAH. Damage-associated molecular patterns arising from mechanical stress, transient global cerebral ischemia, red blood cell breakdown and delayed cerebral ischemia following SAH trigger to activate pattern recognition receptors (PRRs) such as Toll-like receptors, nucleotide-binding oligomerization domain-like receptors, and receptors for advanced glycation end products. Most of PRRs activate common downstream signaling transcriptional factor nuclear factor-κΒ and mitogen-activated protein kinases, releasing pro-inflammatory mediators and cytokines. Next, we focus on how pro-inflammatory substances play a role during the course of SAH. Finally, we highlight an important inducer of neuroinflammation, matricellular protein (MCP). MCPs are a component of extracellular matrix and exert beneficial and harmful effects through binding to receptors, other matrix proteins, growth factors, and cytokines. Treatment targeting MCPs is being proved efficacious in pre- clinical models for preventing brain injury including neuroinflammation in SAH. In addition, MCPs may be a candidate of biomarkers predicting brain injury following SAH in clinical settings.
Open Access
Hepatocellular carcinoma in non-alcoholic fatty liver disease (NAFLD) - pathological evidence for a predominance of steatohepatitic inflammatory non-proliferative subtype
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Campos de, Priscila B.; Oliveira, Claudia P.; Stefano, José T.; Martins-Filho, Sebastião N.; Chagas, Aline L.; Herman, Paulo; Albuquerque de, Luiz C.; Alvares-da-Silva, Mário R.; Longatto-Filho, Adhemar; Carrilho, Flair J.; Alves, Venancio A.F.
Objectives. This study evaluated clinical and pathological aspects of patients with hepatocellular carcinoma (HCC) secondary to non-alcoholic fatty liver disease (NAFLD) and related these factors to immunohistochemical markers representative of the proliferative class. Methods. We evaluated 35 HCC nodules from 21 patients diagnosed with NAFLD undergoing liver resection (n=12) or liver transplantation (n=8) or both (n=1). Demographic, clinical and biochemical data were compared to histological features and to immunohisto- chemical reactivity for K19 and Ki-67. Results. Cirrhosis was present in 58% of patients. Ages ranged from 50 to 77 years. Sixteen patients (76%) were male and had type 2 diabetes mellitus, 81% had arterial hypertension, and 90% had BMI above 25 kg/m 2. Alpha-fetoprotein levels were normal in 62% of patients. Twenty-five (70%) nodules were diagnosed as “steatohepatitic HCC”. Only 32% of the nodules presented high levels of Ki-67 (>10%) and/or K19 (>5%), although 63% were poorly differentiated (G.3/G.4) according to Edmondson & Steiner grading system. K19 positivity (>5%) was associated with higher degree of intratumoral inflammation (G.2/G.3), and with fibrosis, both at the center of the tumor and at the tumor front, whereas Ki-67 positivity (>10%) was associated with ballooning of neoplastic cells and occurred in more than 70% in non-cirrhotic patients. Conclusion. NAFLD-related HCC was found in non- cirrhotic patients in 42% of cases, alpha-fetoprotein level was normal in 63% and "steatohepatitic HCC" was the predominant histological type. Immunoexpression of K19 and/or Ki-67 occurred in 32% of the nodules and were associated with intratumoral inflammation and ballooning, suggesting that HCC in MtS may be preferentially “an inflammatory, non-proliferative subtype of HCC”
Open Access
Therapeutic effects of platelet derived growth factor overexpressed-mesenchymal stromal cells and sheets in canine skin wound healing model
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Kim, Namyul; Choi, Kyeong Uk; Lee, Eunbee; Lee, Seoyun; Oh, Jiwon; Kim, Woo keyoung; Woo, Sang-Ho; Kim, Dae-Yong; Kim, Wan-Hee; Kweon, Oh-kyeong
Adipose-derived mesenchymal stromal cells (Ad-MSCs) have excellent potential for skin wound repair. Moreover, platelet-derived growth factor (PDGF) has strong wound healing properties. The purpose of the present study was to compare the healing effects of PDGF-overexpressing canine allogeneic Ad-MSCs (PDGF-MSCs) and their cell sheets (PDGF-CSs) as compared to unexpressed Ad-MSCs (U-MSCs) and their cell sheets (UCSs) in a cutaneous wound healing model induced upon dogs. In in vitro study, the expression of immunomodulatory and growth factors was assessed by qRT-PCR. In in vivo study, cells and sheets were transplanted into a square-shaped full-thickness (1.5×1.5 cm) skin defect model created in 12 dogs. After 5 and 10 days, wounds were harvested and evaluated macroscopically and histopathologically. The qRT-PCR results showed that the PDGF-B gene was significantly upregulated (p<0.05) in PDGF-CS and PDGF-MSCs groups. Upon gross analysis of the wound, all stromal cells and their sheet groups showed accelerated (p<0.05) cutaneous wound healing compared to the negative control groups. As compared to U-MSCs and UCSs, the PDGF-MSCs showed significant epithelization on days 5 and 10 of healing, whereas PDGF-CSs showed improved epithelization only on day 10. In the granulation tissue analysis, PDGF-CSs and UCSs promoted more formation (p<0.05) of upper granulation tissue, collagen, and activated fibroblasts than PDGF- MSCs, and U-MSCs. Especially, the PDGF-CSs presented the highest formation and maturation of granulation tissue among all groups. All considered, PDGF overexpressed stromal cells or cells sheets can improve cutaneous wound healing in a canine model.
Open Access
Effect of short-term betamethasone administration on the regeneration process of tissue-engineered bone
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Chihara, Takahiro; Zhang, Yiming; Li, Xianqi; Shinohara, Atsushi; Kagami, Hideaki
Local inflammation at the transplanted site of tissue-engineered bone may cause apoptosis of the transplanted cells, thus negatively affecting bone regeneration. To maximize the efficacy of bone tissue engineering, the local effect of short-term corticosteroid administration at the transplanted site of tissue- engineered bone was studied with respect to the expression of inflammatory cytokines. Compact bone- derived cells from mouse leg bones were isolated, cultured and seeded onto β-tricalcium phosphate granules. The constructs were transplanted to the back of syngeneic mice. Betamethasone sodium phosphate was administered intraperitoneally to an experimental (betamethasone) group, whereas the same amount of saline was administered to a control group. When betamethasone was administered three times (immediately after operation and 12 hours and 24 hours after transplantation), the number of SP7/osterix-positive osteoblasts was larger in the betamethasone group. Three times of betamethasone administration (immediately after operation and 12 hours and 24 hours after transplantation) did not change the number of apoptotic cells and osteoclasts, but showed a slight upregulation of IL-4 and a downregulation of IL-6. However, 7 doses of betamethasone administration (over 7 consecutive days) increased the number of apoptotic cells and osteoclasts, which was correlated with a downregulation of IL-4 and an upregulation of IL-6. TNF-α expression levels showed no significant differences between the two groups. The results showed beneficial effects of 3 betamethasone administrations for bone regeneration therapy but contrary effects when betamethasone was administered 7 times due to the downregulation of anti- inflammatory cytokines (IL-4) and the upregulation of inflammatory cytokines (IL-6). As a conclusion, our results suggested the importance of the cautious usage of corticosteroids to control local inflammation at transplanted sites in bone tissue engineering
Open Access
Effects of estrogen on STIM1/Orai1 in the sublingual gland of ovariectomized rats
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Bai, Yun; Li, Bing; Wang, Sinan; Jiang, Hai; Li, Junlei; Wang, Wenjuan; Wang, Ke; Qin, Lihua; Jia, Jing
Background. Studies have shown that estrogen can protect the function of the sublingual gland, but the specific mechanism is still unclear. Besides, the STIM1/Orai1 pathway is important to secretion in the salivary gland. Here, we explore the possible effects of estrogen on sublingual gland function by observing changes of STIM1 and Orai1 levels in the sublingual glands of ovariectomized rats. Methods. 42 adult female Sprague-Dawley rats were randomly divided into three groups: SHAM, OVX, and OVX+E (n=14 per group). Two weeks after ovariectomy, rats were treated with estrogen (β-estradiol). The expression of STIM1 and Orai1 in the sublingual gland were observed by double label-immunohistochemistry and immunofluorescence. Calcium imaging was conducted to observe changes in cellular Ca 2+ levels. Results. IHC and IF showed that the levels of both STIM1 and Orai1 decreased following ovariectomy, but increased to SHAM levels after estrogen treatment. By IF, STIM1 and Orai1 exhibited perfect co-localization. Calcium imaging results showed that the Ca 2+ in the cells decreased after ovariectomy. Estrogen intervention returned levels of these proteins and Ca 2+ to the same as those in the control group. Conclusion. This study demonstrates that low estrogen status significantly reduced the expression of STIM1 and Orai1 in the sublingual gland of rats, along with cellular Ca 2+ levels. These data provide insight into the likely mechanisms underlying sublingual gland secretion dysfunction during menopause
Open Access
Reduced histologic neo in-stent restenosis after use of a paclitaxel-coated cutting balloon in porcine coronary arteries
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Traxler, Denise; Hemetsberger, Rayyan; Spannbauer, Andreas; Zlabinger, Katrin; Gugerell, Alfred; Lukovic, Dominika; Mandic, Ljubica; Pavo, Noemi; Winkler, Johannes; Gyöngyösi, Mariann
The incidence of in-stent restenosis (ISR) has declined dramatically, but once it develops, no current treatment option, such as drug-eluting stents, drug-coated balloons, or cutting balloons (CBs), prevents re-narrowing of the stented atherosclerotic artery. In this preclinical study, we aimed to improve the efficacy of ISR treatment by coating CBs with paclitaxel (paclitaxel-eluting cutting balloon; PECB) and to characterize the histological features of neo-ISRs that arise after ISR treatment. ISR was induced by bare metal stent (BMS) implantation in coronary arteries in pigs. After one month of follow-up, BMS-induced ISR was treated with either CB or PECB. After another month, we performed quantitative coronary angiography, explanted the treated arteries and assessed histopathological and histomorphometric parameters. In addition, we compared histological features of neo-ISRs with pre-treatment ISRs. Injury, inflammation, fibrin deposition, and endothelialization scores were similar between the CB and PECB groups at one month after ISR treatment. Neointimal area (0.87±0.61 vs. 1.95±1.14 mm 2, p=0.02), mean neointimal thickness (0.40±0.39 vs. 0.99±0.56 mm, p=0.01), and percent area stenosis (27.3±20.4 vs. 48.3±22.9%, p=0.04) were decreased in PECB-treated coronary arteries compared to CB-treated arteries, respectively. Density of cells (predominantly smooth muscle cells; SMCs) was increased in neo-ISRs (3.51±3.05×10 3 vs. 6.35±2.57×10 3 cells/mm 2 , p<0.01),but significantly more CD68 + and CD20 + cells were found in pre-treatment ISRs. In conclusion, PECB treatment of ISRs led to better results in terms of smaller neointimal area and %area stenosis of neo-ISR. SMC density was increased in neo-ISRs in contrast with higher percentage of CD68 + and CD20 + cells in pre- treatment ISRs.
Open Access
Overexpression of YES1 is associated with favorable prognosis and increased platinum-sensitivity in patients with epithelial ovarian cancer
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Zhou, Yun; Chen, Ping; Huang, Qidan; Wan, Ting; Jiang, Yinan; Jiang, Senwei; Yan, Sumei; Zheng, Min
Aims. The prognostic application of YES1 in epithelial ovarian cancer (EOC) is currently unclear. We aimed to investigate the expression of YES1 and its correlation with survival outcome in patients with EOC. Methods. A retrospective study of patients diagnosed with EOC at the Cancer Center, Sun Yat-Sen University, Guangzhou, China between 2002 and 2013 was conducted. The immunohistochemical expression of YES1 was assessed using tissue microarray. Survival rates were analyzed by the Kaplan-Meier method and were compared between groups using the log-rank test. Multivariate analyses were performed using the Cox proportional hazards model. Results. A total of 132 patients with EOC were enrolled. Patients in the YES1- high group exhibited significantly better OS and PFS, compared with those in the YES1-low group (P=0.02 and P=0.03, respectively). Further univariate and multivariate regression analyses indicated YES1 as an independent prognostic factor for the OS of patients with EOC. Notably, within the high YES1 expression group, 40 cases (74.1%) were of the platinum-sensitive group while 14 (25.9%) overlapped were of the platinum- resistant group. Conversely, in the low YES1 expression group, 11 cases (47.8%) were platinum-sensitive, and 12 (52.2%) platinum-resistant. Overall, patients within the high YES1 expression group were deemed significantly more sensitive to platinum-based chemotherapy than the low YES1 expression group (P=0.03), and YES1 levels were consistently and significantly higher in the platinum-sensitive group. Conclusions. High YES1 cytoplasmic expression in EOC patient tissue is significantly correlated with favorable prognosis. Patients with high YES1 expression tend to be sensitive to platinum-based chemotherapy.
Open Access
Therapeutic effects of an azaphenothiazine derivative in mouse experimental colitis
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Artym, Jolanta; Kocięba, Maja; Zaczyńska, Ewa; Zimecki, Michał; Kałas, Wojciech; Strządała, Leon; Pawlak, Alicja; Jeleń, Małgorzata; Morak Młodawska, Beata; Pluta, Krystian; Kaleta Kuratewicz, Katarzyna; Madej, Jan P.; Kuropka, Piotr; Kuryszko, Jan
Phenothiazines represent a class of compounds of potential therapeutic utility. In this report we evaluated therapeutic value of an azaphenothiazine derivative, 6-acetylaminobutyl-9-chloroquino[3,2- b]benzo[1,4]thiazine (QBT), given intragastrically, in the model of dextran sodium sulfate-induced colitis in C57BL/6 mice using 5-aminosalicylic acid (5-ASA) as a reference drug. Colitis symptoms such as body weight loss, diarrhea and hematochezia (blood in stool) were observed and registered and disease activity index (DAI) was calculated. In addition, weight and cell numbers in the lymphatic organs and histological parameters of the colon wall were analyzed. The effects of QBT on viability of colon epithelial cell lines were also determined. We showed that weight and cell number of draining mesenteric lymph nodes were lower in mice treated with QBT in comparison to their control counterparts. The number of thymocytes, drastically reduced in control mice, was elevated in mice treated with the compounds with a significant effect of 5-ASA. In addition, an abnormal composition of blood cell types was partially corrected in these groups. Histological analysis of the colon revealed that the pathological changes were partially normalized by QBT and even to a higher degree by 5-ASA. In conclusion we demonstrated a therapeutic efficacy of the compound in amelioration of local and systemic pathological changes associated with chemically-induced colitis in mice. A possible mechanism of action of the compound is discussed.
Open Access
Chaperone-mediated autophagy in cancer: Advances from bench to bedside
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Hou, Tao; Fan, Yizeng; Dan, Weichao; Liu, Bo; Wang, Zixi; Zeng, Jin; Li, Lei
Chaperone-mediated autophagy (CMA), a selective form of autophagy, where cellular proteins with KFERQ-like motif are targeted to the lysosome for degradation, is necessary to maintain cellular homeostasis. The role of CMA in neurodegenerative diseases has been extensively studied in the past decades, with defects in the pathway being strongly associated with disease. Recently, accumulating evidence has demonstrated a consistent increase in basal CMA activity in a wide array of cancer cell lines and human tumor biopsies, suggesting a potential link between CMA and cancer. On the other hand, an anti- oncogenic role for CMA under physiological conditions in non-transformed cells is also proposed despite the pro-tumorigenic function of CMA in cancer cells. The growing number of connections between CMA and cancers has generated interest in modulating CMA activity for therapeutic purposes. Here, we describe recent advances in the understanding of the molecular regulation of CMA, and discuss the evidence in support of the contribution of CMA dysfunction to cancers
Open Access
Downregulation of nuclear ING3 expression and translocalization to cytoplasm promotes tumorigenesis and progression in head and neck squamous cell carcinoma (HNSCC)
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Li, Xiaohan; Zhang, Qun; Zhang, Mingming; Luo, Yusong
ING3 (inhibitor of growth gene 3) is a member of the ING gene family, and is considered as a candidate tumor suppressor gene. In order to explore the roles of ING3 in tumorigenesis and cancer progression of head and neck squamous cell carcinoma (HNSCC), ING3 expression was assessed in 173 cases of HNSCC by immunohistochemistry. The expression of ING3 was also compared to clinicopathological variables, and the expression of several tumorigenic markers. Nuclear expression of ING3 in HNSCC was significantly lower than that in dysplasia and normal epithelium, and was negatively correlated with a poor-differentiated status, T staging and TNM staging. In contrast, cytoplasmic expression of ING3 was significantly increased in HNSCC, and was statistically associated with lymph node metastasis and 14-3-3η expression. In addition, nuclear expression of ING3 was positively correlated with the expression of p300, p21 and acetylated p53. In conclusion, decreases in nuclear ING3 may play important roles in tumorigenesis, progression and tumor differentiation in HNSCC. Increases in cytoplasmic ING3 may be due to 14-3-3η binding and may also be involved in malignant progression. Nuclear ING3 may modulate the transactivation of target genes, promoting apoptosis through interactions with p300 and p21. Moreover, ING3 may interact with p300 to upregulate the level of acetylation of p53, and promote p53- mediated cell cycle arrest, senescence and/or apoptosis. Therefore, ING3 may be a potential tumor suppressor and a possible therapeutic target in HNSCC
Open Access
Moderate-to-strong expression of FGFR3 and TP53 alterations in a subpopulation of choroid plexus tumors
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Granberg, Kirsi J.; Raita, Annina; Lehtinen, Birgitta; Tiihonen, Aliisa M.; Kesseli, Juha; Annala, Matti; Rodriguez-Martinez, Alejandra; Nordfors, Kristiina; Zhang, Wei; Visakorpi, Tapio; Nykter, Matti; Haapasalo, Hannu K.
Deregulation of fibroblast growth factor receptor (FGFR) signaling is tightly associated with numerous human malignancies, including cancer. Indeed, FGFR inhibitors are being tested as anti-tumor drugs in clinical trials. Among gliomas, FGFR3 fusions occur in IDH wild-type diffuse gliomas leading to high FGFR3 protein expression and both, FGFR3 and FGFR1, show elevated expression in aggressive ependymomas. The aim of this study was to uncover the expression of FGFR1 and FGFR3 proteins in choroid plexus tumors and to further characterize FGFR-related as well as other genetic alterations in FGFR3 expressing tumors. Expression levels of FGFR1 and FGFR3 were detected in 15 choroid plexus tumor tissues using immunohistochemistry of tissue microarrays and 6 samples were subjected to whole mount FGFR3 staining. Targeted sequencing was used for deeper molecular analysis of two FGFR3 positive cases. Moderate expression of FGFR1 or FGFR3 was evidenced in one third of the studied choroid plexus tumors. Targeted sequencing of a choroid plexus carcinoma and an atypical choroid plexus papilloma, both with moderate-to-strong FGFR3 expression, revealed lack of protein-altering mutations or fusions in FGFR1 or FGFR3, but TP53 was altered in both tumors. FGFR3 and FGFR1 proteins are expressed in a subpopulation of choroid plexus tumors. Further studies using larger cohorts of patients will allow identification of the clinicopathological implications of FGFR1 and FGFR3 expression in choroid plexus tumors.
Open Access
Chronic atrophic gastritis aggravate chronic periodontitis with Helicobacter pylori infection and CD4+Th cytokines infiltration
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Luo, Wei; Li, Yaqiang; Luo, Zhenhua; Xu, Baohong
Objective. To investigate the potential effect of chronic atrophic gastritis on chronic periodontitis and further explore the possible mechanism. Methods. Local periodontal lesions were collected from periodontitis tissues of 30 CAG patients and 35 control adults without CAG (non-CAG). Clinical periodontal parameters were recorded, and the expression levels of distinct CD4+ Th specific cytokines at local periodontitis lesions were evaluated by real time PCR (RT-PCR). Helicobacter pylori (H. pylori) detection was carried out in both gastric and periodontitis lesions of CAG and non CAG patients. Results. Clinical parameters analysis showed that the level of clinical attachment loss in periodontitis lesions of CAG group was significantly higher than non-CAG group. It was observed that the infection rate of H. pylori in the CAG group was higher than non-CAG group. Further cytokine analysis showed that Th17 associated cytokines IL-17, IL-21 and IL-23 were increased in periodontal lesions of CAG patients when compared with non-CAG patients. However, Th1, Th2, Th9 and Treg cells specific cytokines were not significantly increased in CAG group when compared with non-CAG group. Conclusions. Patients with CAG demonstrated that significant elevated attachment loss in periodontitis lesions, while elevated Th17 cytokines IL-17, IL-21 and IL-23 participate in immunopathogenesis of both diseases
Open Access
CSN6: a promising target for cancer prevention and therapy
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Hou, Jianbing; Cui, Hongjuan
CSN6 has recently received increased attention as a multifunctional protein involved in protein stability. CSN6 plays an important role in controlling cellular proliferation, apoptosis and metastasis, modulating signal transduction, as well as regulating DNA damage and repair. Most studies have demonstrated that CSN6 is significantly upregulated in human malignant tumors such as cervical cancer, papillary thyroid cancer, colorectal cancer, breast cancer, lung adenocarcinoma, and glioblastoma, and its expression is usually correlated with poor prognosis. In this review, we summarize recent available findings regarding the oncogenic role of CSN6 in tumors, and provide a better understanding of CSN6 function at the molecular level and its potential therapeutic implications in combating human cancers
Open Access
Next generation sequencing identifies novel potential actionable mutations for grade I meningioma treatment
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Pepe, Francesco; Pisapia, Pasquale; Del Basso de Caro, Maria Laura; Conticelli, Floriana; Malapelle, Umberto; Troncone, Giancarlo; Martinez, Juan Carlos
Meningiomas are common brain tumors that arise from the meningeal membranes that envelope the brain and spinal cord. The World Health Organization classifies these tumors into three histopathological grades. Because of tumor recurrence, treating meningiomas may be challenging even in well- differentiated grade I (GI) neoplasms. Indeed, around 5% of completely resected GI meningiomas relapse within 5 years. Therefore, identifying driver mutations in GI meningiomas through next generation sequencing (NGS) assays is paramount. The aim of this study was to validate the use of the 50-gene AmpliSeq Hotspot Cancer Panel v2 to identify the mutational status of 23 GI meningioma, namely, 12 non recurrent and 11 recurrent. In 18 out of the 23 GI meningiomas analyzed, we identified at least one gene mutation (78.2%). The most frequently mutated genes were c-kit (39.1%), ATM (26.1%), TP53 (26.1%), EGFR (26.1%), STK11 (21.7%), NRAS (17.4%), SMAD4 (13%), FGFR3 (13%), and PTPN11 (13%); less frequent mutations were SMARCB1 (8.7%), FLT3 (8.7%), KRAS (8.7%), FBWX7 (8.7%), ABL1 (8.7%), ERBB2 (8.7%), IDH1 (8.7%), BRAF (8.7%), MET (8.7%), HRAS (4.3%), RB1 (4.3%), CTNNB1 (4.3%), PIK3CA (4.3%), VHL (4.3%), KDR (4.3%), APC (4.3%), NOTCH1 (4.3%), JAK3 (4.3%), and SRC (4.3%). To our knowledge, mutations in all of these genes, except for TP53, STK11, SMARCB1, PIK3CA, VHL, and BRAF, have never been described before in meningiomas. Hence, these findings demonstrate the viability of NGS to detect new genetic alterations in GI meningiomas. Equally important, this technology enabled us to detect possible novel actionable mutations not previously associated with GI and for which selective inhibitors already exist

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