Clinical profile and outcomes in brainstem glioma: An institutional experience

Lachi, Pavan Kumar; Irrakula, Monica; Ahmed, Syed Fayaz; Joseph, Deepa; Pamidighantam, Suresh; Naidu, Kotiyala V Jagannath Rao

doi:10.4103/1793-5482.162709

Cited by 10 publications

(13 citation statements)

References 27 publications

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“…It has been found that patients who had short interval of symptoms (< 3 months) had poor outcomes [7]. In contrast, in our study there was no such association.…”

Section: Discussioncontrasting

confidence: 91%

Complexity in the Management of Brainstem Gliomas: Our Experience

Nagarajan¹,

Ap²,

Banu³

2019

JCR

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Background: Brainstem gliomas (BSGs) constitutes 10% of pediatric and 2% of adult brain tumors. Overall management of BSGs is complex due to lack of biopsy, location of the tumor making it inoperable and dosimetric constraints in RT delivery. We did a retrospective analysis on clinical outcomes of BSGs in our institute. Case Series: Seven cases of BSGs (5 adults and 2 pediatric) were included. Most common presenting symptom was weakness of limbs. Magnetic Resonance Imaging was the sole imaging modality. Biopsy was feasible in two patients. Median RT dose was 50 Gy. Two patients received concurrent temozolamide and one patient received adjuvant temozolamide. Median overall survival was 7.9 months. In our cohort adults had better survival than children. Conclusion: BSGs are distinct group of brain tumors. In most of the cases biopsy is not feasible and MRI is the current standard diagnostic imaging modality. Radiotherapy is the standard treatment options for BSGs.

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“…It has been found that patients who had short interval of symptoms (< 3 months) had poor outcomes [7]. In contrast, in our study there was no such association.…”

Section: Discussioncontrasting

confidence: 91%

Complexity in the Management of Brainstem Gliomas: Our Experience

Nagarajan¹,

Ap²,

Banu³

2019

JCR

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“…Yamasaki et.al reported that a patient age <20 years was one of the poor prognostic factors in a retrospective study of 23 patients with diffuse brainstem gliomas [ 31 ]. Lachi et.al reported a similar result that pediatric age group (<15 years) was associated with worse prognosis than in adults (>=15 years) in a series of 48 patients with brainstem gliomas treated by radiation therapy [ 32 ]. Consistent with these previous studies, we showed that the children/adolescent group (0-19 years) had a shorter median overall survival than adults (20+ years) (10.0 months vs. 19.9 months, p=0.026, Figure 3 ).…”

Section: Discussionmentioning

confidence: 94%

Genetic and immune features of resectable malignant brainstem gliomas

et al. 2017

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We surveyed common genetic mutations (IDH1, H3F3A, PPM1D, and TP53) and immune features (PD-L1 expression and CD8+ T cell tumor infiltration) in a series of 62 malignant brainstem gliomas that were resected via microsurgery. IDH1 mutations were mutually exclusive with H3F3A mutations. IDH1 mutations appeared only in adults and occurred more frequently in tumors larger than 10cm3 (8/29 vs 1/32, Fisher’s exact test, p=0.010). H3F3A mutations occurred more frequently in children and adolescent patients (19/24 vs 18/38, chi-square test, p=0.013), low preoperative Karnofsky Performance Scale (KPS) patients (10/11 vs 20/43, chi-square test, p=0.021), and higher grade brainstem gliomas (8/21 in grade II vs 16/24 in grade III vs 13/17 in grade IV; chi-square test, p=0.038). PPM1D mutations clustered in H3F3A-mutated tumors (12/37), whereas were rare in H3F3A wildtype tumors (1/25). MGMT promoter methylations clustered in IDH1-mutated tumors (4/9), but were rare in H3F3A-mutated tumors (1/37). PD-L1 staining was detected in 59.7% of brainstem glioma specimens (37/62). High intra-tumoral CD8+ T cell density was less frequent in the H3F3A-mutated than H3F3A-wild-type tumors (4/37 vs. 11/25, p=0.005). Patients with H3F3A-mutated tumors (13.8 months overall survival) had much worse prognoses than those with IDH1-mutated (54.9 months, p=0.001) or H3F3A-IDH1 co-wildtype tumors (38.4 months, p=0.001). H3F3A mutations independently increased the relative risk of death as much as 4.19-fold according to a multivariate Cox regression model. Taken together, resectable malignant brainstem gliomas can be classified into three subtypes: H3F3A-mutated, IDH1 mutated and H3F3A-IDH1 co-wildtype tumors, which have distinct clinical characteristics, prognoses, genetic and immune features.

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“…[44][45][46] Malignant glioma has a poor prognosis despite the continuous progress in therapeutic technologies, including surgery, radiotherapy, photodynamic therapy, and chemotherapy. [44][45][46] Malignant glioma has a poor prognosis despite the continuous progress in therapeutic technologies, including surgery, radiotherapy, photodynamic therapy, and chemotherapy.…”

Section: Discussionmentioning

confidence: 99%

Circular RNA hsa_circ_0076248 promotes oncogenesis of glioma by sponging miR‐181a to modulate SIRT1 expression

Lei

Huang

Zhou

et al. 2018

J of Cellular Biochemistry

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Glioma is one of the most common primary malignancies of the central nervous system, which has aggressive clinical behavior and a poorer prognosis. MicroRNAs (miRs) are a class of small noncoding RNAs that function as mediators of gene expression, which can be sponged by circRNA provided with a closed circular structure. Dysregulations of circular RNAs (circRNAs) and miRs have been implicated in the development and progression of glioma. In the current study, we investigated the role of circular RNA hsa_circ_0076248 in mediating the oncogenesis of glioma by sponging miR‐181a to modulate silent information regulator 1 (SIRT1) expression in vitro and in vivo. The quantitative real‐time polymerase chain reaction results showed that the expression of miR‐181a was significantly decreased in glioma tissues and cell lines compared with normal brain tissues and normal gliocyte, respectively, and the expression of hsa_circ_0076248 and SIRT1 demonstrated the opposite. Bioinformatics analysis identified hsa_circ_0076248 could sponge miR‐181a, and miR‐181a could target the mRNA of SIRT1. Our results verified that downregulating hsa_circ_0076248 or upregulating miR‐181a could depress the proliferation and invasion of glioma in vitro and in vivo. The experiment also showed that downregulating hsa_circ_0076248 or upregulating miR‐181a could remarkably promote the temozolomide chemotherapy sensitivity. Furthermore, Western blot analysis testified that downregulating hsa_circ_0076248 or upregulating miR‐181a could promote the expression of p53 and SIRT1. In summary, our study sheds light on the regulatory mechanism of hsa_circ_0076248 in glioma growth and invasion via sponging miR‐181a, which downregulates the SIRT1 expression and also suggests that hsa_circ_0076248, miR‐181a, and SIRT1 may serve as potential therapeutic targets for glioma.

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Clinical profile and outcomes in brainstem glioma: An institutional experience

Cited by 10 publications

References 27 publications

Complexity in the Management of Brainstem Gliomas: Our Experience

Complexity in the Management of Brainstem Gliomas: Our Experience

Genetic and immune features of resectable malignant brainstem gliomas

Circular RNA hsa_circ_0076248 promotes oncogenesis of glioma by sponging miR‐181a to modulate SIRT1 expression

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