Background This study investigated the cardioprotective effect of isosorbide dinitrate (ISDN) postconditioning against rat myocardial ischemia/reperfusion injury in vivo and provided a theoretical basis for clinical application. Material/Methods We randomly divided 32 Wistar rats into 4 groups: sham group, I/R (ischemia/reperfusion) group, I-PostC group (with 3 cycles of 30 s reperfusion and 30 s reocclusion applied at the onset of reperfusion), and P-PostC group (nitrate postconditioning: isosorbide dinitrate (5mg/kg) was given 1 min before reperfusion). The left anterior descending artery (LAD) was occluded for 40 min, followed by a 180-min reperfusion. Relevant indicators were tested. The LAD was occluded again, then we determined the myocardial infarct size. Paraffinized sections were prepared and TUNEL detection was performed. Results There were no significant differences in ischemic sizes between different groups. Compared with the I/R group, the levels of cTnI and myocardial infarct size in the I-PostC group and P-PostC group were significantly decreased (p<0.05). However, there were no significant difference between the I-PostC group and P-PostC group. Compared with the sham-operated group, the levels of cTnI and MDA in the I/R group, I-PostC group, and P-PostC group were significantly increased (p<0.05) and the levels of SOD were significantly decreased (p<0.05). Compared with the I/R group, I-PostC and P-PostC decreased the level of MDA and increased the level of SOD (both P <0.05). Conclusions ISDN postconditioning induces a similar cardioprotective effect as I-PostC. The potential mechanisms of cardioprotection of ISDN postconditioning might be via improvement of myocardial antioxidant capacity and reduced generation of reactive oxygen species.

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e14059 Background: Meningioma is the most common primary neoplasm of the central nervous system (CNS) in adults. Genetic variants ( NF2, AKT1, TRAF7 etc.) are strongly related to the subtypes of meningioma. TERT promoter mutation or homozygous CDKN2A and/or CDKN2B deletion are independent evidence for diagnosing WHO grade 3 meningioma according to 5th CNS WHO. Our study reclassifies meningiomas using a clinical and molecular real-world dataset. Methods: This study retrospectively analyzed the genomic alteration of 347 Chinese meningioma patients during 2019-2022. Next-generation sequencing (NGS) was performed to detect gene mutations in tumor samples. Results: TERT promoter mutation or CDKN2A/B deletion were identified in 11% (n = 39) of patients ( TERT 5.2%, CDKN2A 8.1%, CDKN2B 8.6%). Of these cases, histologic grade information was available for 26 patients, 14(53.8%) of whom were reclassified as WHO grade 3 meningiomas, including four histologic grade 1 and ten histologic grade 2. There is a male preponderance in reclassified patients (56.4% vs. 40.0%, p < 0.05), meanwhile the age showed no significant difference between them (average age: 54 vs 50, p = 0.11). The most frequently co-mutated gene was NF2. The proportion of TERT promoter mutation or CDKN2A/B deletion in NF2-mutant tumors was similar to NF2-wildtype tumors (10% vs. 11%, p > 0.05). Conclusions: In our study, 11% of Chinese adult meningioma patients found TERT promoter mutation or CDKN2A/B deletion and showed a male preponderance, among 53.8% of whom were reclassified as meningiomas WHO grade 3. Overall, these data advance the understanding of the significance of molecular profiling in the classification of meningioma patients according to the 5th WHO CNS.

e15140 Background: The dysregulation of the MYC family oncogenes ( c-MYC, MYCN and MYCL) play critical roles in tumorigenesis, prognosis and immune escape. MYC inactivation can result in sustained tumour regression and many therapeutic agents that directly target MYC are under development. MYC signaling is associated with tumor cell PD-L1, overall immune cell infiltration. Herein, we explore MYC family proto-oncogene amplification profiles and clinical characterization in chinese solid tumors. Methods: This research comprehensively characterized gene mutations by next-generation sequencing (NGS) in 23990 chinese solid tumors tissues to reveal the prevalence of MYC family proto-oncogene amplification(MYC AMP) and the association with Tumor mutational burden(TMB) and microsatellite instability(MSI). Results: The prevalence of MYC AMP (copy number, CN≥5) in the cohort was 2.1% (504/23,990), in which ovarian cancer (7.6%, 22/289) showed the highest prevalence, followed by breast cancer (6.1%, 26/429), esophagus cancer (5.9%, 17/287). Only one glioma patient(pt) carried co-amplification of MYCN and c-MYC. In 504 MYC AMP pts, c-MYC AMP accounted for 93.7%(472/504), MYCN and MYCL AMP accounted for 6.5%(33/504) in total. The CN was significantly higher in MYCN and MYCL AMP pts than c-MYC AMP pts (22.9 vs 7.6, p < 0.0001). MSI-H showed a lower detection rate in MYC AMP pts other than Non-MYC AMP pts (0% vs 1.2%, p < 0.05). The proportion of TMB-L in MYC AMP pts was similar to Non-MYC AMP pts (90.9% vs. 90.1%, p > 0.05). Conclusions: In totally, 2.1% of chinese solid tumor pts had MYC high level AMP, mainly c-MYC Amp. The CN was higer in MYCN/ MYCL AMP pts than c-MYC AMP pts. In addition, MYC AMP pts tended to have MSS and TMB-L, suggesting that MYC may be a novel target for tumor immunotherapy. MYC inhibitor combines with immunotherapy may be an important direction for the treatment of MYC AMP pts.