Abstract
Background
To explore the altered malignant behavior, prognosis and survival of glioblastoma in contact with Subventricular Zone (SVZ) and independent predictors on patients’ overall survival.
Method
The records of 131 patients with supratentorial primary glioblastoma who underwent surgery at our hospital between 2012 and 2018 were reviewed retrospectively. The authors reviewed preoperative MRI images and divided patients into two groups: Glioblastoma not in contact with SVZ (G-SVZ) and glioblastoma in contact with SVZ (G + SVZ). They computed and compared the overall survival (OS) of these two groups using the Kaplan–Meier method. The correlation between G + SVZ and OS was investigated using the Cox Proportional Hazard Ratio Model.
Results
The median progression-free survival (PFS) of the patient was 10 months (Interquartile Range), and the median OS was 13 months. At six months and one year, the OS was 81 percent and 51.1 percent, respectively. Patients with G + SVZ and G-SVZ had a median OS of 12 months and 15 months, respectively (p = 0.0093). According to Cox Multivariate model, repeat surgery (p = 0.001), among other independent predictors, including age ≥60, Karnofsky Performance Score (KPS) < 70, and extent of resection (Subtotal/biopsy vs total resection), had the strongest associated decreased OS. G + SVZ independently correlated significantly with reduced patient survival (p = 0.014).
Conclusion
Repeat surgery had the strongest association with decreased OS among the independent predictors of survival in patients with G + SVZ lesions. Prospective studies about molecular mechanisms are needed to explain why G + SVZ lesions are thought to be aggressive and associated with a poor prognosis.
Keywords: Glioblastoma, Subventricular zone, Survival rate, Prognosis, MRI imaging
Introduction
Glioblastoma is the most common primary malignant central nervous system (CNS) tumor in adult patients.1 Their estimated median survival time is 15 months,2 and despite recent advances in surgery and chemoradiation therapy, their prognosis is bleak.3 According to recent investigations, the poor prognosis linked with glioblastoma may be attributed to a lack of understanding of the cellular origin of these lesions.4,5 Furthermore, the heterogeneity of glioblastoma tumors has been linked to a variety of genetic alterations and intracellular processes implicated in carcinogenesis, making them resistant to treatment.5 Suggestively, a detailed understanding of the cellular origin of glioblastoma tumors could facilitate the application of molecular analyses to treatment.
Two critical neural stem cell (NSC) areas in the brain have been found in recent investigations. The subgranular section of the hippocampus (dentate gyrus) and the periventricular subependymal area are examples of these areas. Glioblastoma in contact with the subventricular zone (G + SVZ) has been identified as a form of glioblastoma caused by these NSCs.4,6,7 Although NSCs constitute a small portion of malignant glial tumors, they have been shown to have a significant role in maintaining tumor volume and ensuring adequate resistance to conventional treatments.4,6,8 Some reports have also demonstrated a direct correlation between the aggressive nature of G + SVZ lesions and their tumoral origin.5,9 For example, Gollapalli et al5 and Tchoghandjian et al9 correlated the aggressive nature of G + SVZ lesions to the prominent neuronal proliferative and migratory capacity of the NSCs of the subventricular zone.
Despite strong evidence of the aggressive nature of G + SVZ tumors,5 their effect on patient survival remains contradictory.10, 11, 12, 13, 14 Notably, patients’ characteristics such as age> 60 years, KPS <70, motor defects, and verbal defects have been associated with short-term survival.10,11,15 Various independent determinants of patient prognosis have also been discovered.10,12,18 However, only a few studies5,16,17 have provided practical molecular insight into the prognostic effect of these independent predictors on the type of G + SVZ lesions and their prognosis. A thorough understanding of the molecular mechanisms underlying these lesions could assist fill in the gaps between what we know about them and their dismal prognosis, as well as devising therapy regimens for affected patients. This study looked into the association between G + SVZ lesions and their independent effect on OS. We also looked into the molecular and genetic mechanisms that underpin the predictive impact of independent predictors on OS in the literature.
Material and methods
Study population
We conducted an Institutional Review Board-approved retrospective review of all patients with primary glioblastoma who underwent surgery in our neurosurgical center between 2012 and 2018. Patients with a previous history of lower-grade astrocytoma, evidence of secondary GBM (such as infratentorial masses), no preoperative MRI imaging, missing data, age <18 years, presence of other malignancies, and perioperative mortality (death within the first week and during the hospitalization of the first surgery) were excluded from the study. Pathological data of all patients diagnosed with glioblastoma based on the WHO classification system who underwent surgery between 2012 and 2018 were collected from our institute’s pathology department. Medical records from patients were extracted and reviewed. Except for one patient, all patients received a full session of radiotherapy and temozolomide. The KPS scale was used to calculate the performance status. Following a review of the surgical procedure, the extent of resection was classified as gross total resection (GTR), subtotal resection (STR), or biopsy. Before the study began, informed consent was obtained from all living patients and relatives of deceased patients. All guidelines as per the Declaration of Helsinki and good clinical practice guidelines were followed.
MRI imaging characteristics
MRI images and reports were obtained and reviewed. The recorded characteristics included:
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The location of the tumor (frontal, temporal, occipital, etc.)
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The tumor side (left, right, or bilateral).
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Tumor multiplicity.
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Lateral ventricular wall involvement distance between the tumor and the ventricular wall.
The tumor volume was calculated by dividing the largest diameter of the axial, sagittal, and coronal planes by two. The extent of resection was classified as GTR, STR, or biopsy based on an MRI evaluation a few hours after tumor resection.4 We were unable to determine the extent of resection based on postoperative MRI images because postoperative MRI was not possible for all patients. In patients with lateral ventricle tumors, the presence or absence of ependymal enhancement was also recorded. Patients were divided into two groups based on preoperative MRI imaging: G + SVZ and G-SVZ. Siemens, MAGNETOM Avanto, 1.5 T S MRI device was used.
Postoperative management
In this study, the standard chemoradiation therapy existing at our institute was used. After surgery, all patients (except one) underwent 6 weeks of radiotherapy with a 60 Gy irradiation dose. Following radiotherapy, patients received chemotherapy with temozolomide tablets 5 days per month for 6 months. Chemotherapy and radiotherapy were both performed on an out-patient basis at our facility.
Statistical analysis
Statistical analysis was performed using SPSS (version 22.0 for Window, IBM Corp) and NCSS software. Continuous data related were presented as mean ± standard deviation. KPS score values and survival rate were presented as Interquartile Range (IQR). The baseline characteristics of patients were performed using an independent sample t-test, Chi-square, and Mann–Whitney U test. Survival rate analyses were performed using the Kaplan–Meier product-limit method. The survival rates were compared using the Log–Rank test. Hazard Ratio and 95% CI were calculated using the Cox–Mantel Hazard Ratio method. The Cox proportional hazard model was used to investigate the SVZ involvement and predictors (age, KPS, preoperative neurologic deficit, the extent of resection, and repeat surgery) effect on survival rate. Also, univariate and multivariate analyses of these independent variables were performed. All statistical tests were considered significant when the p value was <0.05. Our institutional science ethical committee approved this study.
Results
Patient characteristics
The data of 131 patients were retrospectively studied; 77 (59%) were male, and 54 (41%) were female. The mean age of the patients was 54.9 ± 10.9. Thirty-four patients (26%) had a mild motor deficit, and four (3.1%) had a severe motor deficit. Forty-nine (37.4%) patients had G + SVZ, while 82 (62.6%) had G-SVZ. Fifteen patients (11.5%) had a verbal deficit. The mean KPS score was 62.9 ± 11.55, with a median of 70. Among 67 patients, the tumor was located in the frontal lobe (51%), in 33 patients in the temporal lobe (25.2%), in 16 patients in the parietal lobe (12.2%), in seven patients in the occipital lobe (5.3%), and in eight patients in the Insula (6.1%), respectively. Eleven patients (8.4%) had multifocal tumors. Seven patients (5.3%) had a bilateral tumor. Fifty-three patients (40.5%) underwent total resection, 70 patients (54.4%) had a subtotal resection, and eight patients (6.1%) had tumor biopsy. In 76 cases (58%), the tumor was right-sided, whereas it was left-sided in 48 patients (36.6%) (Table 1). Fig. 1 shows MRI images of glioblastoma lesions in contact with the SVZ region.
Table 1.
Clinical characteristics of all patients.
| Patient | Characteristics |
|---|---|
| No. of patients | 131 |
| Sex | |
| Male | 77 |
| Female | 54 |
| Age (years, mean ± SD) | 54 ± 10.9 |
| Year at Diagnosis | |
| 2012 | 16 |
| 2013 | 20 |
| 2014 | 20 |
| 2015 | 17 |
| 2016 | 21 |
| 2017 | 18 |
| 2018 | 19 |
| Comorbidity | |
| Hypertension | 26 |
| Diabetes | 10 |
| Motor Deficit | |
| No paresis | 93 |
| Mild paresis | 34 |
| Moderate/severe paresis | 4 |
| Verbal Deficit | |
| No deficit | 116 |
| Aphasia/Dysphasia | 15 |
| KPS (Range) | 70 (40–80) |
| Extent of resection | |
| Total/near total | 53 |
| Subtotal | 70 |
| Biopsy | 8 |
| Repeat surgery | |
| Yes | 50 |
| No | 81 |
Fig. 1.
(a, b). MRI images of a 39-year-old woman with a chief complaint of right hemiplegia. (a) T1W MRI image axial view; (b) T2W MRI image axial view; Black arrow of image 2 illustrates a butterfly tumor of the periventricular region. (c, d). MRI images of a 56-year-old man with a chief complaint of right hemiparesis. Tumor located in the left thalamus region. (c) T2 FLAIR (fluid-attenuated inversion recovery); (d) T2W MRI coronal view.
Independent predictors and overall survival between G + SVZ and G-SVZ groups
Among the patients with G + SVZ (49 patients), only 22 cases showed ependymal enhancement on MRI imaging. In terms of age (p = 0.13), sex (p = 0.3), and tumor multiplicity (p = 0.3), there was no significant difference in OS between the G + SVZ and the G-SVZ groups. However, there was a significant difference in OS between the two groups when tumor location (p = 0.02), tumor side (p = 0.02), tumor volume (p = 0.01), KPS (p = 0.013), and extent of resection (p = 0.01) were considered. (Table 2). Twenty patients (40%) in the G + SVZ group and 30 (36.6%) in the G-SVZ group had repeated surgery due to tumor recurrence. One hundred and six patients (80.9%) died during follow-up. The median time of death in deceased patients was 12 months (minimum of 2 months and maximum of 38 months). The remaining 25 patients were followed up for a minimum of 6 months and a maximum of 32 months. The median OS of all patients was 13 months (IQR = 8–18), and the median OS of patients who had repeat surgery was 8 months (IQR = 4–12). The OS at 6 months, 1 year, and 2 years were 81%, 51.1%, and 7.6%, respectively. Also, the progression-free survival (PFS) was 74.7% and 19.9% in 6 months and 1 year, respectively. The median OS of the 49 patients with G + SVZ and 82 patients with G-SVZ was 12 months and 15 months, respectively. This finding was consistent with other reports.13,21 According to the Log-rank test, this difference was statistically significant (p = 0.0093).
Table 2.
Clinical characteristics of all patients, including patients with G + SVZ and G-SVZ tumors.
| Characteristics | G + SVZ | G-SVZ | Significance (P) |
|---|---|---|---|
| No. of patients | 49 | 82 | |
| Sex | 0.3b | ||
| Male | 26 | 51 | |
| Female | 23 | 31 | |
| Age (year, mean ± SD) | 56.8 ± 11 | 53.8 ± 10 | 0.13b |
| Comorbidity | 0.26b | ||
| Hypertension | 8 | 18 | |
| Diabetes | 6 | 4 | |
| Motor Deficit | 0.8b | ||
| Mild paresis | 13 | 21 | |
| Moderate/severe paresis | 1 | 3 | |
| Verbal deficit | 0.52b | ||
| Aphasia/dysphasia | 6 | 9 | |
| KPS (IQR) | 60 (50–70) | 70 (6–70) | 0.013a |
| Extent of resection | 0.01a | ||
| Total/near total | 12 | 41 | |
| Subtotal | 34 | 36 | |
| Biopsy | 3 | 5 | |
| Repeat Surgery | 0.38b | ||
| Yes | 20 | 30 | |
| No | 29 | 52 | |
| Tumor side | 0.02a | ||
| Right | 25 | 51 | |
| Left | 18 | 30 | |
| Bilateral | 6 | 1 | |
| Tumor location | 0.02a | ||
| Frontal | 27 | 40 | |
| Temporal | 8 | 25 | |
| Parietal | 4 | 12 | |
| Insular | 4 | 4 | |
| Occipital | 6 | 1 | |
| Ependymal enhancement | 22 | N/A | N/A |
| Tumor volume cm3 (Mean ± SD) | 37.9 ± 19.8 | 26.4 ± 13.9 | 0.01a |
G + SVZ, glioblastoma contacting SVZ; G-SVZ, glioblastoma not contacting SVZ; SD, standard deviation; IQR, interquartile range; KPS, Karnofsky Performance Score.
significant.
not significant.
Univariate and multivariate analysis of clinical predictors on overall survival in the G + SVZ group
Univariate analysis revealed that age ≥60, KPS score ≤70, motor deficit, verbal deficit, tumor multiplicity, SVZ contact, the extent of resection, and repeat surgery significantly correlated with decreased OS. However, sex, tumor side, tumor volume, and ependymal enhancement had no significant reductive effect on OS (Table 3). According to Table 3, verbal deficit (p = 0.0001), repeat surgery (p < 0.0001) and KPS score ≤70 (p < 0.0001) had the most significant reductive effect on OS. In addition, we perform a multivariate analysis using the Cox proportional hazard model to investigate the independent effect of G + SVZ on OS in a stepwise forward selection. All predictors that significantly impacted the OS in univariate analysis were included in the model. Predictors with p < 0.2 were included in the model, while those with a p ≥ 0.2 were excluded. Accordingly, age≥ 60 years, verbal deficit, the extent of resection, and repeat surgery significantly correlated with decreased OS. Also, SVZ contact was independently markedly associated with decreased OS (p = 0.014). (Table 4). (Fig. 2 illustrated the Kaplan–Meier curve of OS in the two groups). Furthermore, we decided to reduce the number of predictors to improve the multivariate analysis accuracy. Therefore, we eliminated motor and verbal deficits. Also, we removed tumor multiplicity from the model because it had a p ≥ 0.2. Our findings revealed that age≥ 60 years (p = 0.04), KPS< 70 (p = 0.005), extent of resection (p = 0.035), and repeat surgery (p = 0.001) significantly correlated with decreased OS. Among the above independent predictors, repeat surgery had the most significant reductive effect on the OS (p = 0.001), followed by KPS value < 70, the extent of resection, and age≥ 60 years, respectively.
Table 3.
Univariate analysis of clinical predictors on survival rate.
| Parameter | Median survival month (IQR) | Hazard ratio | Significance (P)∗ |
|---|---|---|---|
| Sex | 1.02 (0.70–1.50) | 0.9 | |
| Male (n = 77) | 13 (8–20) | ||
| Female (n = 54) | 12 (7–20) | ||
| Age | 1.80 (1.11–2.91) | 0.0028a | |
| <60 (n = 93) | 15 (10–20) | ||
| ≥60 (n = 38) | 9 (5–13) | ||
| KPS | 2.41 (1.56–3.73) | <0.0001a | |
| ≥70 (n = 66) | 16 (12–21) | ||
| <70 (n = 65) | 10 (5–13) | ||
| Motor Deficit | 2.23 (1.26–3.94) | 0.0001a | |
| No paresis (n = 93) | 15 (10–20) | ||
| Mild to severe (n = 38) | 9 (5–13) | ||
| Verbal Deficit | 3.01 (1.28–7.10) | 0.0001a | |
| No deficit (n = 116) | 14 (9–20) | ||
| Aphasia/Dysphasia (n = 15) | 6 (3–10) | ||
| Tumor side | 1.12 (0.74–1.70) | 0.54 | |
| Right (n = 76) | 15 (10–18) | ||
| Left (n = 48) | 10 (6–20) | ||
| Multiplicity | 2.15 (0.83–5.60) | 0.018a | |
| Single (n = 120) | 13 (9–20) | ||
| Multiple (n = 11) | 8 (5–12) | ||
| Tumor volume | 1.07 (0.73–1.57) | 0.69 | |
| <30 cm3 (n = 66) | 12 (8–21) | ||
| ≥30 cm3 (n = 65) | 13 (9–18) | ||
| SVZ contact | 1.61 (1.07–2.43) | 0.0093a | |
| SVZ-Pos (n = 49) | 12 (6–15) | ||
| SVZ-Neg (n = 82) | 15 (10–21) | ||
| Ependymal enhancement | 1.11 (0.68–1.82) | 0.1 | |
| Positive (n = 22) | 12 (7–20) | ||
| Negative (n = 27) | 9 (5–13) | ||
| Extent of resection | 1.98 (1.35–2.90) | 0.0002a | |
| Total/near total (n = 53) | 18 (12–22) | ||
| Subtotal/biopsy (n = 78) | 11 (6–15) | ||
| Repeat surgery | 2.42 (1.64–3.58) | <0.0001a | |
| No (n = 81) | 10 (6–14) | ||
| Yes (n = 50) | 18 (12–23) | ||
| All patients (n = 131) | 13 (8–18) |
significant.
Table 4.
Factors affecting the prognosis based on multivariate analysis and Hazard ratio.
| Parameter | Hazard ratio | 95% Confidence interval | Significance (P) |
|---|---|---|---|
| Age ≥60 | 1.64 | 1.05–2.58 | 0.03 |
| <60 | 1 | ||
| Verbal deficit Intact Aphasia | 2.56 | 1.36–4.8 | 0.004 |
| Extent of resection | 1.13–2.97 | 0.014 | |
| Subtotal/biopsy | 1.83 | ||
| Total/near total | 1 | ||
| Repeat Surgery No | 2.47 | 1.59–3.81 | 0.001 |
| Yes | 1 | ||
| KPS <70 | 1.45 | 0.87–2.41 | 0.15 |
| ≥70 | 1 | ||
| SVZ contact SVZ positive | 1.39 | 0.89–2.1 | 0.014 |
| SVZ negative | 1 | ||
| Multiplicity Multiple Single | 1.68 | 0.8–3.52 | 0.16 |
| Motor deficit Intact Paresis | 0.93 |
Fig. 2.
Kaplan–Meier curve showing overall patient survival in the two groups.
Discussion
Summary of the results
In contrast to Tejada et al2 and consistent with previous reports,11,19,20 the median OS between the G + SVZ and G-SVZ groups in the present study was 12 months and 15 months, respectively. Multivariate analysis showed that repeat surgery, among other independent predictors, including KPS value ≥ 70, the extent of resection and age≥ 60, had the most significant reductive effect on the OS. Our findings, which were consistent with earlier studies,20,21 showed that patients with G + SVZ lesions had a shorter OS than those with G-SVZ lesions, regardless of predictors (p = 0.014). Berendsen et al also claimed that SVZ involvement was a key predictive factor in glioblastoma.16 The great difficulties experienced during extensive complete excision of tumors around the ventricles are one of the key ideas proposed to explain the difference in OS between the two groups.20 Ahmadipour et al demonstrated that G + SVZ lesions were associated with lower resection rates.22 However, gross total resection of these lesions has not shown a significant effect in prolonging a patient’s survival.19 We investigated the molecular processes of NSCs that contributed to the aggressive nature of these lesions, their simultaneous correlation with independent predictors, and their effect on OS to better understand the connection between molecular variables of NSCs, G + SVZ lesions, and independent predictors.
Molecular mechanism of neural stem cells and G + SVZ invasiveness
Quinones-Hinojosa et al investigated the cellular composition of the cytoarchitectural structure of the SVZ region. They discovered that the SVZ has a proclivity to generate neurons that migrate to other parts of the adult brain.6 Lombard et al, on the other hand, demonstrated the ability of glioma stem cells to migrate from different locations to the SVZ via the CXCL12/CXCR4 axis.7 The bi-directional locomotive nature of NSCs increases the invasiveness of glioblastoma lesions.6 Likewise, the SVZ region offers a protective environment for tumor cells by increasing resistance to chemoradiation therapy.7 Furthermore, the presence of antiapoptotic proteins, Bcl2, Mcl 1, and other molecular factors, including CXCL12 expressed by SVZ NSCs, was found to increase irradiation resistance via mesenchymal activation of G + SVZ tumor cells.7,17,23 CX3CL1 protein overexpression promoted G + SVZ tumor survival and decreased OS in adult patients.7 Gollapalli et al discovered that some tumor progression inhibitor markers (such as SERPINA3, Vitamin-D, and APOA1) were decreased in patients with G + SVZ compared to the G-SVZ group in a proteomic analysis of tissue and serum protein that distinguished G + SVZ from G-SVZ lesions. The reduced level of SERPINA3 was associated with increased aggressiveness of G + SVZ lesions.5 In addition, CD133 and Nestin markers are expressed by NSCs in glioblastoma. Previous research has found that these NSC markers are present in stem cells derived from the oncogenic transformation of more differentiated astrocytes.5,24 Exploring mesenchymal markers such as Nestin, IDH-1, and YKLl40 did not reveal an increase in the incidence of G + SVZ tumors.25,26 Mistry et al, on the other hand, discovered differences in tumor stem cells from different areas within the tumor cells, particularly in the infiltrative margins.21 The molecular environment surrounding SVZ, which is likely to be rich in growth factors, may increase the malignancy capacity of tumor cells of any origin.17
G + SVZ tumor spread and patient’s survival
Based on imaging studies, some authors classified glioblastoma tumors into four categories: Type I, G + SVZ involving the cortex; Type II, G + SVZ region only; Type III, glioblastoma in the cortex only; and Type IV, glioblastoma with neither cortical nor SVZ involvement.10,15 Lim et al 15 discovered that Type I glioblastoma tumors were more likely to be multifocal, whereas Type IV lesions were never multifocal. According to Jafri et al, 10 patients with multifocal lesions (Type I glioblastoma tumors) had faster tumor progression and a shorter OS compared to patients without multifocal lesions. In addition, Matsuda et al reported that tumor involvement with the SVZ region influences leptomeningeal tumor spread.19 The leptomeningeal spread of G + SVZ lesions, as well as tumor multifocality with SVZ involvement, reduced patients’ OS.22
Furthermore, Sonoda et al found that some patients with G + SVZ lesions experienced multifocal recurrence following tumor resection.27 We found multifocal lesions in the G + SVZ and G-SVZ groups in this study. Eight of the eleven patients with multifocal lesions were found in the G + SVZ group, while three were found in the G-SVZ group. Because of tumor recurrence, all 11 patients underwent a repeat surgery. Consistent with Sonoda et al, 27 we discovered that three patients in the G + SVZ group who had a second recurrence had their tumors recur at a noncontiguous location with the recurrent lesion. However, multivariate analysis revealed that multifocal lesions had no effect on OS (p = 0.16). The presence of lateral ventricular opening during tumor resection is another significant finding associated with G + SVZ spread. Matsuda et al discovered that ventricular opening during surgery had no effect on the leptomeningeal spread, despite the fact that SVZ involvement had a significant impact.19 Despite this, the lateral ventricular opening has been linked to tumor spread and recurrence.14 Nonetheless, the ventricular opening did not appear to be associated with decreased OS.14,19
Clinical predictors, G + SVZ, and overall survival
In patients with G + SVZ lesions, the KPS is an important independent predictor of survival. Consistent with one report,27 we found that preoperative KPS values were significantly lower in patients with G + SVZ lesions than in patients with G-SVZ lesions. We also discovered that the majority of KPS<70 patients had comorbidities, such as mild paresis and aphasia/dysphasia. Furthermore, in both the G + SVZ and G-SVZ groups, patients with KPS< 70 and other associated predictors such as old age, verbal deficit, or motor deficit had a poorer prognosis. However, patients in the G + SVZ group deteriorated rapidly as the disease progressed. There is still little known about the relationship between G + SVZ molecular nature and independent predictors. Karschnia et al 28 investigated the role of SVZ in WHO grade II gliomas based on molecular markers. They discovered that molecular markers such as IDH 12 wildtype mutation, MGMT promoter methylation, and telomerase reverse transcriptase promotor (TERT) mutation were linked to KPS values. They discovered that a lower KPS value was statistically significant for a worse prognosis in patients with G + SVZ lesions.28
Although the extent of resection is an independent predictor of OS,11 Jafri et al found no significant difference in survival between patients with and without SVZ involvement.10 In terms of resection extent, we found a statistical difference between the G + SVZ and G-SVZ groups in the current study. Furthermore, we discovered that repeat surgery was the single most important independent predictor of a patient’s OS. The G-SVZ group, on the other hand, accounted for the vast majority of cases of repeat surgery. Another important finding was that patients who had more than two repeat surgeries regressed significantly in terms of KPS values. This observation was not gender-specific. It did, however, correlate with advanced patient age. Furthermore, Chaichana et al 18 discovered that motor and verbal deficits were linked to a worse prognosis in patients with G + SVZ lesions. According to our findings, independent predictors such as ependymal enhancement, tumor size, and tumor location or side had no significant negative effects on OS. However, our findings indicated that patients with G + SVZ lesions with verbal and motor deficits had a worse prognosis. Although not all patients may have the appropriate clinical or radiological conditions for surgery during tumor recurrence, we believe that a poor overall prognosis should not preclude surgery when it is feasible.
Conclusion
In summary, the median survival of patients with G + SVZ was lower (12 months) when compared with patients with G-SVZ (15 months). The present study demonstrated that repeat surgery, among other independent predictors such as age, KPS, and the extent of resection, had the strongest association with poor prognosis in patients with G + SVZ lesions. The absence of molecular marker analysis was a significant limitation observed in the present study.
Patients/ Guardians/ Participants consent
Patients informed consent was obtained.
Ethical clearance
Institute/hospital ethical clearance certificate was obtained.
Source of support
Nil.
Disclosure of competing interest
The authors have none to declare.
Acknowledgements
We would like to acknowledge Dr. Amir Pajman Hashemi, a radiologist at Shariati hospital, Tehran, Iran who was actively involved in MRI images review process.
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