scholarly journals NKX6-1 mediates cancer stem-like properties and regulates sonic hedgehog signaling in leiomyosarcoma

2021 ◽  
Vol 28 (1) ◽  
Author(s):  
Po-Hsuan Su ◽  
Rui-Lan Huang ◽  
Hung-Cheng Lai ◽  
Lin-Yu Chen ◽  
Yu-Chun Weng ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Sonic Hedgehog ◽  
Poor Prognosis ◽  
Cancer Genome ◽  
The Cancer Genome Atlas ◽  
Shh Pathway ◽  
Cancer Genome Atlas ◽  
Genome Atlas

Abstract Background Leiomyosarcoma (LMS), the most common soft tissue sarcoma, exhibits heterogeneous and complex genetic karyotypes with severe chromosomal instability and rearrangement and poor prognosis. Methods Clinical variables associated with NKX6-1 were obtained from The Cancer Genome Atlas (TCGA). NKX6-1 mRNA expression was examined in 49 human uterine tissues. The in vitro effects of NXK6-1 in LMS cells were determined by reverse transcriptase PCR, western blotting, colony formation, spheroid formation, and cell viability assays. In vivo tumor growth was evaluated in nude mice. Results Using The Cancer Genome Atlas (TCGA) and human uterine tissue datasets, we observed that NKX6-1 expression was associated with poor prognosis and malignant potential in LMS. NKX6-1 enhanced in vitro tumor cell aggressiveness via upregulation of cell proliferation and anchorage-independent growth and promoted in vivo tumor growth. Moreover, overexpression and knockdown of NKX6-1 were associated with upregulation and downregulation, respectively, of stem cell transcription factors, including KLF8, MYC, and CD49F, and affected sphere formation, chemoresistance, NOTCH signaling and Sonic hedgehog (SHH) pathways in human sarcoma cells. Importantly, treatment with an SHH inhibitor (RU-SKI 43) but not a NOTCH inhibitor (DAPT) reduced cell survival in NKX6-1-expressing cancer cells, indicating that an SHH inhibitor could be useful in treating LMS. Finally, using the TCGA dataset, we demonstrated that LMS patients with high expression of NKX6-1 and HHAT, an SHH pathway acyltransferase, had poorer survival outcomes compared to those without. Conclusions Our findings indicate that NKX6-1 and HHAT play critical roles in the pathogenesis of LMS and could be promising diagnostic and therapeutic targets for LMS patients.

scholarly journals Role of INSL4 Signaling in Sustaining the Growth and Viability of LKB1-Inactivated Lung Cancer

2018 ◽  
Vol 111 (7) ◽  
pp. 664-674 ◽  
Author(s):  
Rongqiang Yang ◽  
Steven W Li ◽  
Zirong Chen ◽  
Xin Zhou ◽  
Wei Ni ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Transcriptome Profiling ◽  
Cancer Genome ◽  
The Cancer Genome Atlas ◽  
Growth And Survival ◽  
Cancer Genome Atlas ◽  
Lung Adenocarcinomas ◽  
Genome Atlas

Abstract Background The LKB1 tumor suppressor gene is commonly inactivated in non-small cell lung carcinomas (NSCLC), a major form of lung cancer. Targeted therapies for LKB1-inactivated lung cancer are currently unavailable. Identification of critical signaling components downstream of LKB1 inactivation has the potential to uncover rational therapeutic targets. Here we investigated the role of INSL4, a member of the insulin/IGF/relaxin superfamily, in LKB1-inactivated NSCLCs. Methods INSL4 expression was analyzed using global transcriptome profiling, quantitative reverse transcription PCR, western blotting, enzyme-linked immunosorbent assay, and RNA in situ hybridization in human NSCLC cell lines and tumor specimens. INSL4 gene expression and clinical data from The Cancer Genome Atlas lung adenocarcinomas (n = 515) were analyzed using log-rank and Fisher exact tests. INSL4 functions were studied using short hairpin RNA (shRNA) knockdown, overexpression, transcriptome profiling, cell growth, and survival assays in vitro and in vivo. All statistical tests were two-sided. Results INSL4 was identified as a novel downstream target of LKB1 deficiency and its expression was induced through aberrant CRTC-CREB activation. INSL4 was highly induced in LKB1-deficient NSCLC cells (up to 543-fold) and 9 of 41 primary tumors, although undetectable in all normal tissues except the placenta. Lung adenocarcinomas from The Cancer Genome Atlas with high and low INSL4 expression (with the top 10th percentile as cutoff) showed statistically significant differences for advanced tumor stage (P < .001), lymph node metastasis (P = .001), and tumor size (P = .01). The INSL4-high group showed worse survival than the INSL4-low group (P < .001). Sustained INSL4 expression was required for the growth and viability of LKB1-inactivated NSCLC cells in vitro and in a mouse xenograft model (n = 5 mice per group). Expression profiling revealed INSL4 as a critical regulator of cell cycle, growth, and survival. Conclusions LKB1 deficiency induces an autocrine INSL4 signaling that critically supports the growth and survival of lung cancer cells. Therefore, aberrant INSL4 signaling is a promising therapeutic target for LKB1-deficient lung cancers.

scholarly journals METTL3-Mediated m6A mRNA Modification of FBXW7 Suppresses Lung Adenocarcinoma

2020 ◽  
Author(s):  
Yingtong Wu ◽  
Ning Chang ◽  
Yong Zhang ◽  
Xinxin Zhang ◽  
Leidi Xu ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Cell Model ◽  
Biological Effects ◽  
Cancer Genome ◽  
The Cancer Genome Atlas ◽  
Luciferase Reporter ◽  
Rna Immunoprecipitation ◽  
Cancer Genome Atlas ◽  
Genome Atlas

Abstract BackgroundFBXW7 m6A modification plays an important role in lung adenocarcinoma (LUAD) progression; however, the underlying mechanisms remain unclear.MethodsThe correlation between FBXW7 and various genes related to m6A modification was analyzed using The Cancer Genome Atlas database. The regulatory effects of METTL3 on FBXW7 mRNA m6A modification were examined in a cell model, and the underlying mechanism was determined by methylated RNA immunoprecipitation, RNA immunoprecipitation, luciferase reporter, and mutagenesis assays. In vitro experiments were performed to further explore the biological effects of METTL3-mediated FBXW7 m6A modification on LUAD development.ResultsDecreased FBXW7 expression was accompanied by downregulated METTL3 expression in human LUAD tissues and was associated with a worse prognosis for LUAD in The Cancer Genome Atlas database. m6A was highly enriched in METTL3-mediated FBXW7 transcripts, and increased m6A modification in the coding sequence region increased its translation. Functionally, METTL3 overexpression or knockdown affected the apoptosis and proliferation phenotype of LUAD cells by regulating FBXW7 m6A modification and expression. Furthermore, FBXW7 overexpression in METTL3-depleted cells partially restored the suppression of LUAD cells in vitro and in vivo.ConclusionsOur findings reveal that METTL3 positively regulates FBXW7 expression and confirm the tumor-suppressive role of m6A-modified FBXW7, thus providing insight into its epigenetic regulatory mechanisms in LUAD initiation and development.

scholarly journals Local Delivery of Minocycline and Vorinostat Act Synergistically to Inhibit Recurrence of Gliomas

2020 ◽  
Author(s):  
Gang Zhao ◽  
Jun Jia ◽  
Lansheng Wang ◽  
Yongkang Zhang ◽  
Han Yang ◽  
...  
Keyword(s):  
High Performance ◽  
Postoperative Recurrence ◽  
The Cancer Genome Atlas ◽  
The Public ◽  
Continuous Release ◽  
Clinical Consequences ◽  
Cancer Genome Atlas ◽  
Genome Atlas

Abstract Background:Postoperative recurrence is the main reason of poor clinical consequences in glioma patients, so preventing recurrence of tumors is crucial in management of gliomas. Methods:In this study, the expression of matrix metalloproteinases (MMPs)in tissues from normal were detected by using RNA-seq analysis.Glioma cases from the public databases (The Cancer Genome Atlas (TCGA), The Chinese Glioma Genome Atlas(CGGA), Betastasis) were included in this study.The hydrogelcontains minocycline (Mino) and vorinostat (Vor)(G/Mino + Vor) was formed under 365 nm when photoinitiator was added in. High Performance Liquid Chromatography (HPLC) assay was used to assessed the release of drugs in G/Mino + Vor hydrogel. MTT assay was used to explore the biosecurity of GelMA. Immunohistochemistry assay, ELISA assay, Tunel assay were used to demonstrate the antitumor effect of G/Mino + Vor hydrogel.Results:We developed G/Mino + Vor hydrogel successfully. Thenthe experiment in vitro and in vivo confirmed MMPs-responsive delivery of minocycline and vorinostat in hydrogel and the anti-glioma effect on incomplete tumor operation model, which indicated that G/Mino + Vor hydrogel effectively inhibited the recurrence of glioma after surgery.Conclusions: In summary, G/Mino + Vor hydrogel could continuous release minocycline and vorinostat in surgical cavity for inhibiting local recurrence of glioma after operation.

scholarly journals TP53 hot spot mutations in ovarian cancer: Selective resistance to microtubule stabilizers in vitro and differential survival outcomes from The Cancer Genome Atlas

2015 ◽  
Vol 138 (1) ◽  
pp. 159-164 ◽  
Author(s):  
Brandon-Luke L. Seagle ◽  
Chia-Ping Huang Yang ◽  
Kevin H. Eng ◽  
Monica Dandapani ◽  
Oluwatosin Odunsi-Akanji ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Hot Spot ◽  
Cancer Genome ◽  
The Cancer Genome Atlas ◽  
Survival Outcomes ◽  
Differential Survival ◽  
Cancer Genome Atlas ◽  
Genome Atlas

TMOD-04. T-TYPE CALCIUM CHANNELS DRIVE GLIOBLASTOMA INITIATION AND PROGRESSION

2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi216-vi216
Author(s):  
Collin Dube ◽  
Ying Zhang ◽  
Myron Gibert Jr ◽  
Elizabeth Mulcahy ◽  
Matteo Ottolini ◽  
...  
Keyword(s):  
Calcium Channels ◽  
Tumor Growth ◽  
The Cancer Genome Atlas ◽  
Cellular Processes ◽  
Cancer Genome Atlas ◽  
The Individual ◽  
First Time ◽  
Extended Survival ◽  
Genome Atlas

Abstract Glioblastoma is the most common primary malignant brain tumor with a dismal median survival of 15 months. Calcium signaling regulates a plethora of cellular processes making it an ideal target for therapeutic intervention. Our group identified T-type calcium channels (TTCCs) as upregulated in GBM cells, stem cells and human tumors. Analysis of the Cancer Genome Atlas (TCGA) demonstrates for the first time that &gt;20% of GBM patients exhibit mutation, amplification or mRNA upregulation of TTCCs. TCGA and Chinese Glioma Genome Atlas (CGGA) data analyses demonstrate that patients with alterations in TTCC trend toward worse survival compared to normal TTCC expression. Our group utilized an FDA repurposed TTCC blocker Mibefradil to demonstrate inhibition of TTCCs decreases cancer associated signaling, transcription, malignancy parameters and in vivo tumor growth. Mibefradil treatment sensitized Gliomas stem like cells (GSC) xenografts to temozolomide (TMZ) chemotherapy and radiotherapy. To elucidate the roles of the individual TTCCs in vivo we created RCAS/Tva-shTTCC mice for silencing of Cav3.1 and Cav3.2. The silencing of the TTCCs individually decreased tumor growth as measured by MRI and H&E staining. Silencing of TTCCs extended survival of mice in vivo. Silencing of TTCC decreases proliferation (Ki67) and increases apoptosis (Caspase 3). Our findings suggest T-type calcium channels contribute to tumor initiation and progression.

scholarly journals METTL3-mediated m6A mRNA modification of FBXW7 suppresses lung adenocarcinoma

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Yingtong Wu ◽  
Ning Chang ◽  
Yong Zhang ◽  
Xinxin Zhang ◽  
Leidi Xu ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Cell Model ◽  
Biological Effects ◽  
Cancer Genome ◽  
The Cancer Genome Atlas ◽  
Luciferase Reporter ◽  
Rna Immunoprecipitation ◽  
Cancer Genome Atlas ◽  
Genome Atlas

Abstract Background FBXW7 m6A modification plays an important role in lung adenocarcinoma (LUAD) progression; however, the underlying mechanisms remain unclear. Methods The correlation between FBXW7 and various genes related to m6A modification was analyzed using The Cancer Genome Atlas database. The regulatory effects of METTL3 on FBXW7 mRNA m6A modification were examined in a cell model, and the underlying mechanism was determined by methylated RNA immunoprecipitation, RNA immunoprecipitation, luciferase reporter, and mutagenesis assays. In vitro experiments were performed to further explore the biological effects of METTL3-mediated FBXW7 m6A modification on LUAD development. Results Decreased FBXW7 expression was accompanied by downregulated METTL3 expression in human LUAD tissues and was associated with a worse prognosis for LUAD in The Cancer Genome Atlas database. m6A was highly enriched in METTL3-mediated FBXW7 transcripts, and increased m6A modification in the coding sequence region increased its translation. Functionally, METTL3 overexpression or knockdown affected the apoptosis and proliferation phenotype of LUAD cells by regulating FBXW7 m6A modification and expression. Furthermore, FBXW7 overexpression in METTL3-depleted cells partially restored LUAD cell suppression in vitro and in vivo. Conclusions Our findings reveal that METTL3 positively regulates FBXW7 expression and confirm the tumor-suppressive role of m6A-modified FBXW7, thus providing insight into its epigenetic regulatory mechanisms in LUAD initiation and development.

scholarly journals The Smyd5 protein promotes the develpoment of heppatocellular carcinoma in mice

2021 ◽  
Author(s):  
Άνα-Τερέσα Ρούμπιο-Τομάς
Keyword(s):  
Human Cancer ◽  
Cancer Genome ◽  
Rna Seq ◽  
Enhancer Of Zeste ◽  
Cancer Genome Atlas ◽  
Genome Atlas

ΙΣΤΟΡΙΚΟ: Η πρωτεΐνη SMYD5 είναι μια μεθυλοτρανσφεράση των ιστονών που περιέχει τις δομικές περιοχές Su(Var)3-9, Enhancer-of-zeste και Trithorax (SET) και Myeloid, Nervy, και DEAF-1 (MYND) και η οποία αρχικά περιγράφηκε ως συστατικό του συμπλόκου πυρηνικού υποδοχέα (NCoR) που καταλύει την τριμεθυλίωση της λυσίνης 20 της ιστόνης 4 (H4K20me3). ΛΟΓΙΚΗ: Με βάση τη δομή και τα στοιχεία που έχουν δημοσιευτεί στο παρελθόν που δείχνουν το ρόλο της πρωτεΐνης SMYD5 ως μεθυλοτρανσφεράση, επιδιώξαμε να εντοπίσουμε εν δυνάμει υποστρώματα μεθυλίωσης του μορίου SMYD5 in vitro. Επιπλέον, δεδομένου ότι άλλα μέλη της οικογένειας SMYD, όπως η SMYD2 και η SMYD3 πρωτεΐνες, έχει δειχθεί ότι παίζουν σημαντικό ρόλο στην ανάπτυξη του καρκίνου, συμπεριλαμβανομένου του καρκίνου του ήπατος και του παχέος εντέρου, διερευνήσαμε την πιθανή επίπτωση του SMYD5 στην καρκινογένεση χρησιμοποιώντας μοντέλα ποντικών και ανθρώπινα δείγματα. ΠΡΟΣΕΓΓΙΣΗ: Πραγματοποιήσαμε μια δοκιμασία in vitro μεθυλίωσης χρησιμοποιώντας την ανασυνδυασμένη ανθρώπινη πρωτεΐνη SMYD5 με υποστρώματα ιστονών και μη ιστονικά υποστρώματα. Επιπλέον, δημιουργήσαμε ανασυνδυασμένους ποντικούς με έλλειψη του Smyd5 γονιδίου, στους οποίους το γονίδιο Smyd5 απενεργοποιήθηκε είτε σε όλους τους ιστούς (Smyd5flox / MX-Cre) είτε συγκεκριμένα στο ήπαρ (Smyd5flox / Alfp-Cre and Smyd5flox / Alb-Cre). Επιπλέον, δημιουργήσαμε ποντίκια με έλλειψη Smyd5 ειδικά για το έντερο (Smyd5flox / Villin-Cre). Η ανάλυση της έκφρασης του γονιδίου SMYD5 σε ανθρώπινο ηπατοκυτταρικό καρκίνωμα (HCC) και καρκίνο του παχέος εντέρου πραγματοποιήθηκε χρησιμοποιώντας τα σύνολα δεδομένων The Human Cancer Genome Atlas (TCGA). ΑΠΟΤΕΛΕΣΜΑΤΑ: Στην παρούσα μελέτη παρουσιάζουμε ότι η υπερεκφρασμένη με βακιλοϊό και καθαρισμένη SMYD5 πρωτεΐνη μεθυλιώνει, κατά προτίμηση, τις ιστόνες 2Α και 2Β (H2A και H2B) in vitro. Και τα τέσσερα στελέχη SMYD5 knockout (KO) ποντικών που δημιουργήθηκαν αναπτύχθηκαν κανονικά και δεν εμφάνισαν ορατό φαινότυπο. Ωστόσο, όταν υποβλήθηκε σε πρωτόκολλο χημικώς επαγόμενης καρκινογένεσης diethylnitrosamine (DEN), τα ποντίκια με πλήρη έλλειψη του γονιδίου Smyd5 από όλους τους ιστούς καθώς και μεμονωμένα στο ήπαρ, παρουσίασαν καθυστερημένη ανάπτυξη όγκου του ήπατος σε σύγκριση με ποντίκια άγριου τύπου (WT) που εκτέθηκαν στην ίδια θεραπεία. Τα ποντίκια υποβλήθηκαν σε μακροσκοπική και ιστολογική ανάλυση, συμπεριλαμβανομένων των κηλίδων για την αξιολόγηση της ηπατικής βλάβης του DNA και του πολλαπλασιασμού, καθώς και σε ανάλυση του προτύπου έκφρασης του μεταγραφώματος με αλληλούχιση RNA (RNA-seq) και με ποσοτική αλυσιδωτή αντίδραση πολυμεράσης αντίστροφης μεταγραφάσης (qPCR). Ορισμένα γονίδια που σχετίζονται με τον καρκίνο και τον πολλαπλασιασμό έδειξαν μειωμένη έκφραση στο ήπαρ ποντικών με έλλειψη του Smyd5 γονιδίου σε σύγκριση με ποντίκια WT. Ανάλυση ποντικών Smyd5flox / Villin-Cre που υποβλήθηκαν σε χημική θεραπεία προκαλώντας καρκινογένεση του παχέος εντέρου δεν έδειξε εμφανείς φαινοτυπικές διαφορές σε σύγκριση με τα ποντίκια WT που έλαβαν την ίδια θεραπεία.Σύμφωνα με τα δεδομένα από την ανάλυση των ανασυνδυασμένων ποντικών, βρήκαμε μια σημαντική συσχέτιση μεταξύ της έκφρασης του SMYD5 και της επίπτωσης στον ηπατοκυτταρικό καρκίνο. Η έκφραση του SMYD5 γονιδίου σε δείγματα από όγκο ανθρώπινου ήπατος σχετίζεται αρνητικά με τη συνολική επιβίωση του ασθενούς και την πιθανότητα επιβίωσης “χωρίς όγκο” μετά από χημειοθεραπεία για ένα δεδομένο χρονικό πλαίσιο, αλλά σχετίζεται θετικά με την πιθανότητα προόδου σε όγκους υψηλού βαθμού (G3/G4). Επιπλέον, βάσει των πειραμάτων ποντικών και των δειγμάτων καρκίνου του παχέος εντέρου από την TCGA, καταλήξαμε στο συμπέρασμα ότι το γονίδιο SMYD5 δεν φαίνεται να παίζει ρόλο στον καρκίνο του παχέος εντέρου, χρησιμοποιώντας τουλάχιστον τις συγκεκριμένες παραμέτρους της ανάλυσής μας. ΣΥΜΠΕΡΑΣΜΑΤΑ: Στην παρούσα διδακτορική διατριβή διαπιστώσαμε ότι η πρωτεΐνη SMYD5 παρουσιάζει δραστικότητα μεθυλοτρανσφεράσης των ιστονών in vitro, με τα in vivo δεδομένα από μοντέλα SMYD5 KO ποντικών και δείγματα από καρκίνο στον άνθρωπο να υποστηρίζουν το ρόλο της και τη σημασία της στην καρκινογένεση του ήπατος.

scholarly journals Integrative genome analysis reveals an oncomir/oncogene cluster regulating glioblastoma survivorship

2010 ◽  
Vol 107 (5) ◽  
pp. 2183-2188 ◽  
Author(s):  
Hyunsoo Kim ◽  
Wei Huang ◽  
Xiuli Jiang ◽  
Brenton Pennicooke ◽  
Peter J. Park ◽  
...  
Keyword(s):  
Copy Number ◽  
The Cancer Genome Atlas ◽  
Glioblastoma Cell ◽  
Methylation Data ◽  
Data Set ◽  
Akt Activation ◽  
Cancer Genome Atlas ◽  
Genome Atlas

Using a multidimensional genomic data set on glioblastoma from The Cancer Genome Atlas, we identified hsa-miR-26a as a cooperating component of a frequently occurring amplicon that also contains CDK4 and CENTG1, two oncogenes that regulate the RB1 and PI3 kinase/AKT pathways, respectively. By integrating DNA copy number, mRNA, microRNA, and DNA methylation data, we identified functionally relevant targets of miR-26a in glioblastoma, including PTEN, RB1, and MAP3K2/MEKK2. We demonstrate that miR-26a alone can transform cells and it promotes glioblastoma cell growth in vitro and in the mouse brain by decreasing PTEN, RB1, and MAP3K2/MEKK2 protein expression, thereby increasing AKT activation, promoting proliferation, and decreasing c-JUN N-terminal kinase-dependent apoptosis. Overexpression of miR-26a in PTEN-competent and PTEN-deficient glioblastoma cells promoted tumor growth in vivo, and it further increased growth in cells overexpressing CDK4 or CENTG1. Importantly, glioblastoma patients harboring this amplification displayed markedly decreased survival. Thus, hsa-miR-26a, CDK4, and CENTG1 comprise a functionally integrated oncomir/oncogene DNA cluster that promotes aggressiveness in human cancers by cooperatively targeting the RB1, PI3K/AKT, and JNK pathways.

scholarly journals Jagged1 is Clinically Prognostic and Promotes Invasion of Glioma-Initiating Cells by Activating NF-κB(p65) Signaling

2018 ◽  
Vol 51 (6) ◽  
pp. 2925-2937 ◽  
Author(s):  
Long Hai ◽  
Peidong Liu ◽  
Shengping Yu ◽  
Li Yi ◽  
Zhennan Tao ◽  
...  
Keyword(s):  
Survival Data ◽  
Molecular Mechanisms ◽  
The Cancer Genome Atlas ◽  
Glioma Initiating Cells ◽  
Cancer Genome Atlas ◽  
Genome Atlas ◽  
Invasion Assays

Background/Aims: Jagged1 is the ligands of the Notch signaling and has been shown to promote glioma-initiating cells (GICs) in glioblastoma. The role of Jagged1 in GICs invasion and underlying molecular mechanisms remain unclear. Methods: Survival data from R2 genomics analysis, the Cancer Genome Atlas (TCGA), the Chinese Glioma Genome Atlas (CGGA) and visualization platform database were used to evaluate the effects of Jagged1 on overall patient survival. we investigated Jagged1 induced the GICs cells’ invasion by matrix degradation assays and Transwell cell invasion assays in vitro, then we further explored the underlying molecular mechanisms using Co-immunoprecipitation (co-IP) analysis. Results: High expression of Jagged1 in human glioma was associated with poor survival. Clinical data analysis showed that the Jagged1 was positively correlated with NF-κB(p65). Jagged1-induced invasion of GICs cells through activation of NF-κB(p65) pathway. In vivo, knockdown of Jagged1 could suppress the tumorigenicity of GICs cells through NF-κB(p65) signaling. Conclusion: Insights gained from these findings suggest that Jagged1 plays an important oncogenic role in GICs malignancy by activation of NF-κB(p65) signaling, and Jagged1 could be employed as an effective therapeutic target for GICs.

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