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The growth and development of tumors are closely related to the initiation and amplification of the inflammatory response. Various inflammatory biomarkers had attained growing attention for nearly two decades and were discovered strongly associated with cancer patients' prognosis, indicating that systemic inflammatory response is possibly essential to cancer progression. However, little was known about the sensitive biomarkers associated with the detection, persistence, treatment, and prognosis of GBM. Hence, the retrospective research endeavored to evaluate the prognostic value of preoperative inflammatory biomarkers in patients with GBM who initially received standardized treatment.The 232 glioblastoma patients eligible who were admitted to Qilu Hospitals in Shandong Province from January 2014 to January 2018 were collected for this analysis. Inflammatory markers, including the systemic immune-inflammation index (SII), systemic immune response index (SIRI), neutrophil-lymphocyte ratio (NLR), platelet-lymphocyte ratio (PLR), monocyte-lymphocyte ratio (MLR), and albumin/globulin ratio (AGR), were designed. Progression-free survival (PFS) and overall survival (OS) were estimated using the Kaplan-Meier method, and we calculated the area under the ROC curve to determine the AUC value. Besides, we used the Cox proportional hazard model to estimate the relationship between variables and PFS and OS. The statistical differences between variables and PFS and OS were tested through the log-rank test. What is more, the LR method was used to perform Cox multiple regression analysis. The results were represented by hazard ratio (HR), 95% CI, any 2-tailed P 0.01 was accepted as statistically different.The multivariate Cox proportional hazard model presented that SII ≥ 659.1 was an independent risk factor affecting OS (HR = 2.238, 95% CI = 1.471-3.406, P 0.001) and postoperative PFS (HR = 2.000, 95% CI = 1.472-2.716, P 0.001) in GBM patients. The 1-, 3-, and 5-year OS of the SII 659.1 group was 70.8%, 26.9%, and 14.1%, respectively, while the 1- and 3-year OS of the SII ≥ 659.1 group was 37.5% and 11.5% (P 0.001). The 1-, 3-, and 5-year PFS of the SII 659.1 group was 36.3%, 19.6%, and 13%, respectively, while the 1-year PFS of the SII ≥ 659.1 group was 11.3% (P 0.001). Results of patients' clinical and pathological characteristics paraded that in comparison to the lower SII group, the higher SII group had significantly inferior Karnofsky Performance Scale (KPS) scores (P 0.001) and more frequent cystic changes of the tumors (P 0.001), whereas the values of SIRI, NLR, PLR, MLR, and AGR were low.SII is an independent inflammatory indicator for predicting the prognosis of GBM patients after receiving initially standardized treatments.

Low grade gliomas have better outcomes following intervention compared to high grade gliomas including glioblastomas. About 14.4% of diffuse astrocytoma (WHO II) transform and progress into high grade malignant subtypes. Early diagnosis and intervention can therefore warrant halted transformation and progression and prolong survival with improved quality of life. However, asymptomatic low-grade astrocytoma lesions are difficult to diagnose, ascertain, and differentiate from other non-enhancing lesions including brain contusion. We report a case of grade II astrocytoma that was missed for three years on incidental intra-cranial imaging following two incidences of trauma. A 30-year-old female was involved in motor traffic crash and lost consciousness for less than 20 minutes, with no other neurological complaints or deficits. CT and follow up MR imaging revealed a low density, non-enhancing left frontal lesion that was thought to be non- hemorrhagic cerebral contusion sequela. Brain imaging done three years later following another accident showed the initial lesion had significantly increased in size. Astrocytoma was then suspected, and the patient underwent tumor resection with histological diagnosis of diffuse astrocytoma. There was tumor recurrence after two years with features of malignancy. Secondary resection was done with immunohistochemical and genetic analysis revealing an Isocitrate Dehydrogenase 1 (IDH1) Mutant Glioblastoma (WHO IV). Along the course of the surgical and medical interventions, the patient again underwent an additional third surgical intervention with autografting dura repair following cerebrospinal fluid effusion through the previously repaired dura. High index of suspicion is paramount for early diagnosis and intervention of asymptomatic low-grade gliomas. Along with the known hypothesis that traumatic brain injury can induce malignant transformation in the astrocytic cells, incidental findings that are synchronous with events such as trauma can also mask-off already occurring malignant changes that would otherwise require advanced diagnostic skills, experience, and techniques including structural and functional imaging.

2,5-Dimethyl-celecoxib (DMC) is a close structural analog of the selective COX-2 inhibitor celecoxib that lacks COX-2-inhibitory function. Thus, DMC is a promising drug for anti-tumor. In this study, we evaluated the efficacy and the molecular basis of DMC in the treatment of human glioblastoma multiforme (GBM). DMC inhibited the growth and proliferation of GBM cell lines (LN229, A172, U251, and U87MG) in a dose-dependent manner (P

2,5-Dimethyl-celecoxib (DMC) is a close structural analog of the selective COX-2 inhibitor celecoxib that lacks COX-2-inhibitory function. Thus, DMC is a promising drug for anti-tumor. In this study, we evaluated the efficacy and the molecular basis of DMC in the treatment of human glioblastoma multiforme (GBM). DMC inhibited the growth and proliferation of GBM cell lines (LN229, A172, U251, and U87MG) in a dose-dependent manner (P 0.001). In GBM cells treated with DMC, detection by flow cytometry showed cell cycle arrest, and proteins involved in cell cycle such as P21 were increased. Compared with control group, Annexin-V/PI-staining in DMC-treatment group was increased, indicating that DMC could induce apoptosis in GBM cells. Also, associated proteins including cleaved caspase 3 and cleaved PARP-1 were increased. It was further explored whether DMC blocked cell cycle and induced apoptosis in GBM cells through CIP2A/PP2A/AKT signaling pathway. After treatment of DMC, the phosphorylation of Akt was reduced while the total Akt level was not affected. DMC suppressed the expression of CIP2A in a time-dependent manner, while the CIP2A overexpression group reversed cell cycle and apoptotic protein expression led by DMC. Finally, in a xenograft model in nude mice using LN229 cells, DMC suppressed tumor growth. These findings proved that DMC could block cell cycle and induce apoptosis in GBM cells by suppressing CIP2A/PP2A/Akt signaling axis, which indicated that DMC could be an effective option for GBM treatment.