BRAF-mutated suprasellar glioblastoma mimicking craniopharyngioma: illustrative case

Bryan Zheng Department of Neurosurgery, Rhode Island Hospital, Providence, Rhode Island; and

Search for other papers by Bryan Zheng in
Current site
jns
Google Scholar
PubMed
Close
 BS
,
Belinda Shao Department of Neurosurgery, Rhode Island Hospital, Providence, Rhode Island; and

Search for other papers by Belinda Shao in
Current site
jns
Google Scholar
PubMed
Close
 MD, PH
,
Jennifer Mingrino Department of Pathology, Rhode Island Hospital, Providence, Rhode Island

Search for other papers by Jennifer Mingrino in
Current site
jns
Google Scholar
PubMed
Close
 MD
,
Jonathan Poggi Department of Neurosurgery, Rhode Island Hospital, Providence, Rhode Island; and

Search for other papers by Jonathan Poggi in
Current site
jns
Google Scholar
PubMed
Close
 MD
,
Richard S Dowd Department of Neurosurgery, Rhode Island Hospital, Providence, Rhode Island; and

Search for other papers by Richard S Dowd in
Current site
jns
Google Scholar
PubMed
Close
 MD
,
Douglas C Anthony Department of Pathology, Rhode Island Hospital, Providence, Rhode Island

Search for other papers by Douglas C Anthony in
Current site
jns
Google Scholar
PubMed
Close
 MD, PhD
,
John E Donahue Department of Pathology, Rhode Island Hospital, Providence, Rhode Island

Search for other papers by John E Donahue in
Current site
jns
Google Scholar
PubMed
Close
 MD
, and
Curtis E Doberstein Department of Neurosurgery, Rhode Island Hospital, Providence, Rhode Island; and

Search for other papers by Curtis E Doberstein in
Current site
jns
Google Scholar
PubMed
Close
 MD
Open access

BACKGROUND

Suprasellar masses commonly include craniopharyngiomas and pituitary adenomas. Suprasellar glioblastoma is exceedingly rare with only a few prior case reports in the literature. Suprasellar glioblastoma can mimic craniopharyngioma or other more common suprasellar etiologies preoperatively.

OBSERVATIONS

A 65-year-old male with no significant history presented to the emergency department with a subacute decline in mental status. Work-up revealed a large suprasellar mass with extension to the right inferior medial frontal lobe and right lateral ventricle, associated with significant vasogenic edema. The patient underwent an interhemispheric transcallosal approach subtotal resection of the interventricular portion of the mass. Pathological analysis revealed glioblastoma, MGMT partially methylated, with a BRAF V600E mutation.

LESSONS

Malignant glioblastomas can mimic benign suprasellar masses and should remain on the differential for a diverse set of brain masses with a broad range of radiological and clinical features. For complex cases accessible from the ventricle where the pituitary complex cannot be confidently preserved via a transsphenoidal approach, an interhemispheric approach is also a practical initial surgical option. In addition to providing diagnostic value, molecular profiling may also reveal therapeutically significant gene alterations such as BRAF mutations.

ABBREVIATIONS

CT = computed tomography; GFAP = glial fibrillary acidic protein; MRI = magnetic resonance imaging

BACKGROUND

Suprasellar masses commonly include craniopharyngiomas and pituitary adenomas. Suprasellar glioblastoma is exceedingly rare with only a few prior case reports in the literature. Suprasellar glioblastoma can mimic craniopharyngioma or other more common suprasellar etiologies preoperatively.

OBSERVATIONS

A 65-year-old male with no significant history presented to the emergency department with a subacute decline in mental status. Work-up revealed a large suprasellar mass with extension to the right inferior medial frontal lobe and right lateral ventricle, associated with significant vasogenic edema. The patient underwent an interhemispheric transcallosal approach subtotal resection of the interventricular portion of the mass. Pathological analysis revealed glioblastoma, MGMT partially methylated, with a BRAF V600E mutation.

LESSONS

Malignant glioblastomas can mimic benign suprasellar masses and should remain on the differential for a diverse set of brain masses with a broad range of radiological and clinical features. For complex cases accessible from the ventricle where the pituitary complex cannot be confidently preserved via a transsphenoidal approach, an interhemispheric approach is also a practical initial surgical option. In addition to providing diagnostic value, molecular profiling may also reveal therapeutically significant gene alterations such as BRAF mutations.

ABBREVIATIONS

CT = computed tomography; GFAP = glial fibrillary acidic protein; MRI = magnetic resonance imaging

Sellar and suprasellar tumors are some of the most common indications for neurosurgical resection, often via a transsphenoidal approach. Pituitary adenomas are known to compose the vast majority of adult cases, followed by craniopharyngioma. Together, these two pathologies compose 90% of suprasellar masses.1 Less common neoplastic etiologies include atypical meningiomas and low-grade gliomas or metastases of the hypothalamus, optic nerve, or adjacent structures.2,3 Nonneoplastic suprasellar masses can include aneurysms and arachnoid cysts.

Malignant glioblastoma in this region is exceedingly rare. Additionally, the only reports of such cases have involved transsphenoidal approaches.4 A recently published report of a malignant sellar glioma involved endocrinological dysfunction similar to that of a pituitary macroprolactinoma.5 We report a case of a glioblastoma resembling a benign craniopharyngioma managed with a bifrontal craniotomy for interhemispheric, transcallosal intraventricular access to the tumor. To our knowledge, it is the only report of a suprasellar glioblastoma resected through an interhemispheric approach as well as the only case of a suprasellar BRAF-positive, MGMT partially methylated glioblastoma.

Illustrative Case

A 65-year-old male with a history of well-managed bipolar disorder presented to the emergency department with 2 weeks of worsening confusion. His condition had declined significantly in the prior days, with him making bizarre statements to his partner with nonsensical phrases. On examination, he was alert and oriented to self and year with mild confusion most noticeably to location, because he was only able to report that he was in a hospital but not which one. He had no motor, sensory, or visual field deficits on confrontational testing. An endocrine review of systems was unremarkable. He had no history of malignancy.

Computed tomography (CT) of the head demonstrated a rounded mass in the right midline frontal region with solid and cystic components, extensive perilesional vasogenic edema, and a moderate degree of hydrocephalus. Further neuroimaging evaluation with magnetic resonance imaging (MRI; Fig. 1) revealed a 3.0 × 3.4 × 3.3–cm suprasellar mass with compression of the pituitary stalk and contralateral displacement of the septum pellucidum. The lesion was mildly T2 hyperintense with postcontrast enhancement, and significant vasogenic edema extended to the right frontal lobe on fluid-attenuated inversion recovery sequences. Given the solid-cystic appearance of the lesion, craniopharyngioma was presumed; however, the associated lobar vasogenic edema was suspicious, and CT did not reveal any calcifications. Atypical meningioma and hypothalamic low-grade glioma were also considered.

FIG. 1
FIG. 1

Initial preoperative postcontrast T1-weighted MRI evaluation of the enhancing suprasellar mass. A: Midsagittal view of suspected tumor with significant suprasellar extension and vasogenic edema extending to the inferior frontal lobe. B: Coronal slice showing ventriculomegaly secondary to effacement of the right lateral ventricle by the lesion. C: The tumor had solid and cystic components, with axial slices further elucidating the extent of edema into the right frontal lobe. The mass was T2- and fluid-attenuated inversion recovery–hyperintense and measured approximately 3.0 × 3.4 × 3.3 cm.

The patient was admitted to the neurosurgical service and prepared for surgery. Endocrinologic laboratory work-up was not supportive of a functional pituitary adenoma: Prolactin was decreased (<1 ng/mL), as was thyroid-stimulating hormone (0.159 mIU/mL). However, T3 and free T4 were normal. Preoperative electrolytes, including sodium and potassium, were within normal limits, except for mild hyperglycemia. Follicle-stimulating hormone was borderline elevated to 18.4 mIU/mL, and luteinizing hormone was normal. A routine preoperative complete blood count, a basic metabolic panel, coagulopathic studies, and an electrocardiogram were unremarkable.

Procedure Description

The patient was brought to the operating room within a few days of admission for an interhemispheric transcallosal approach to the suprasellar region. This approach was chosen because of the size of the lesion, its extension up to the third ventricle, and the significant extension past the pituitary stalk and carotid arteries, which would make a transsphenoidal approach difficult and high risk. The patient was intubated under general endotracheal anesthesia. His head was pinned in a Mayfield clamp, and image navigation registration was employed using preoperative MRI (BrainLab, Brainlab AG). His cranium was prepped and draped in the usual sterile fashion. A bifrontal craniotomy was performed, and the dura was retracted after a small durotomy was created. The medial right cortical surface was retracted inferiorly from the right falx using gentle blunt dissection, initially down to the cingulate gyrus. The exposure was then continued by carefully retracting the right cingulate along with the callosomarginal artery laterally, exposing the corpus callosum. At this time, the A4 branches of the anterior cerebral artery were visualized, and the position of the intraventricular tumor was confirmed to be just deep to the anterior corpus callosum.

An anterior callosotomy was performed, revealing white matter tracts perpendicular to the sagittal plane. After a minimal amount of cerebrospinal fluid drained from deep to the callosotomy, the superior tumor was visualized in the right lateral ventricle (Fig. 2, Video 1) and confirmed to correlate with the suprasellar mass via navigation. The mass then began to be gradually debulked and was sent for intraoperative pathology. The neoplastic tissue was noted to be highly vascularized, which did not support the preoperative diagnosis of craniopharyngioma. Because the intraoperative pathology report (see below) also favored a malignant source and normal intraventricular landmarks were difficult to visualize, given the obscuration by hemorrhagic tumor, a partial resection was undertaken instead of a more aggressive resection. A ventricular drain was left in the intraventricular tumor cavity, and the layers were closed sequentially. The patient tolerated the procedure well, and there were no immediate complications. Estimated blood loss was 200 mL. His immediate postoperative examination was notable for mild confusion to location very similar to his mental status on initial presentation, and no new neurological deficits were appreciated. Multiple postoperative brain CT scans were obtained routinely and were stable, and the ventriculostomy drain could be weaned and removed on postoperative day 8. Brain MRI on postoperative day 7 showed the expected subtotal resection (Fig. 3).

VIDEO 1. Clip showing the annotated intraoperative footage of an interhemispheric transcallosal approach for the resection of a suprasellar tumor. The right hemisphere above the callosomarginal branch of the anterior cerebral artery (ACA) has been retracted laterally prior to the start of the video, leaving the falx medially and cingulate gyrus deep. L = left; R = right. Click here to view.

FIG. 2
FIG. 2

Intraoperative visualization of tumor capsule prior to resection. This sample demonstrates an interhemispheric view from above into the right lateral ventricle after transection of the anterior corpus callosum. Tumor can be seen beneath the Penfield 4. Some cerebrospinal fluid had been drained, and the anterior cerebral arteries have been retracted to the left (left).

FIG. 3
FIG. 3

Postoperative postcontrast T1-weighted MRI after tumor resection. A: Subtotal resection of the suprasellar enhancing neoplasm with debulking of the superior component on a sagittal sequence. Persistent edema with mass effect appears in the right frontal region. B: Coronal sequence showing the debulked mass with subdural hygroma. Postoperative evidence of a right frontal craniotomy defect and an interhemispheric ventriculostomy catheter placed in the right lateral ventricle.

Surgical Pathology

Two intraoperative frozen-section samples, with gliosis and focal clusters of atypical cells, were indeterminate but suggested a malignant etiology and did not resemble craniopharyngioma. A final pathological diagnosis demonstrated glioblastoma IDH1 (R132H)-wild type, World Health Organization grade 4, with a TERT promoter alteration (124C > T). A second, clinically significant molecular mutation was found in the BRAF gene region (V600E). The MGMT promoter was partially methylated with 1–2 of 4 replications tested. Immunohistochemistry revealed positive staining for glial fibrillary acidic protein (GFAP) and Olig2 within tumor cells, with focal fragments of endothelial proliferation where they were negative. Mitoses were notably rare, and the Ki-67 (MIB-1) was 5%. Last, SSTR2 staining was positive in several foci. Representative microscopic slides showing the morphology and immunohistochemistry from the intraoperative consultation and permanent sections are provided in Fig. 4.

FIG. 4
FIG. 4

Suprasellar tumor specimen. Intraoperative squash preparation (A). Cytological preparation shows clusters of atypical cells. Frozen-section diagnosis was malignant neoplasm favoring a glial source. Permanent sections (BI). Histological sections of a hypercellular neoplasm (B) with a rare mitotic figure (black arrow, C), endothelial proliferation (D), perivascular lymphocytes (E), and pseudopalisading necrosis (F). Immunohistochemical studies showed tumor positivity for GFAP (G), confirming glial cell origin with focal positivity for SSTR2 (H). Endothelial cells were negative for both GFAP and SSTR2. Ki-67 proliferative index (I) was unusually low, with very sparse immunohistochemical positivity. Hematoxylin and eosin stain (AF).

Follow-Up

At the 6-month follow-up with his neuro-oncologist, the patient was overall doing well on combination chemoradiation with temozolomide and fractionated radiotherapy. MRI at 6 months postoperatively also showed a stable appearance of his subtotal resection without evidence of progression. Notably, although an external ventricular drain was placed and weaned perioperatively on his initial admission, he later presented with hydrocephalus and underwent ventriculoperitoneal shunt implantation. He also experienced a seizure event and was subsequently started on levetiracetam. Although he is not currently on a BRAF inhibitor, the option has been discussed by the neuro-oncology team and offered to the patient as an alternative therapy, including potential inclusion in ongoing clinical trials if the current treatment regimen fails.

Patient Informed Consent

The necessary patient informed consent was obtained in this study.

Discussion

Observations

Malignant gliomas can mimic benign suprasellar masses and should remain on the differential for a diverse set of brain masses. This is the first report of a suprasellar mass mimicking craniopharyngioma, later found to be glioblastoma, resected through an interhemispheric approach. For complex cases accessible from the ventricle where the pituitary complex cannot be confidently preserved via a transsphenoidal approach, an interhemispheric approach is a practical initial surgical option. Subtotal resection was achieved in this case because of intraoperative findings of a hemorrhagic lesion, possibly a high-grade glioma requiring chemoradiation, regardless of resection extent. A decreased probability of complete resection via this approach versus the more common transsphenoidal one may be a theoretical limitation, although the choice is case dependent, based on optimizing surgical corridors. Additionally, although conventional chemoradiation with temozolomide has thus far prevented progression in this case with MGMT partial methylation, the BRAF mutation offers another potential treatment option via a BRAF inhibitor.

Lessons

This report is the first to describe the clinical course of a BRAF V600E–positive suprasellar glioblastoma with partial MGMT methylation. Preoperative imaging in this patient was mostly suggestive of craniopharyngioma, given the suprasellar location and lack of endocrinopathies. Radiographically, a solid-cystic appearance is common in craniopharyngioma.6 Although frontal lobe vasogenic edema was atypical, it is not an unprecedented radiological finding; yet, it did raise preoperative suspicion for something atypical or higher grade about this tumor.7 Conversely, glioblastoma often shows an infiltrative pattern of edema radiologically, not revealed by any preoperative imaging.8,9 Compared with the only prior report of 2 glioblastoma cases presumed to be craniopharyngioma, the mixed solid appearance with cystic components does not rule out or diminish the possibility of glioblastoma, because both cases had this radiological finding preoperatively.4 Additionally, although the BRAF mutation status has been studied as a predictive marker in glioblastoma and craniopharyngiomas, there has not yet been a published report of a BRAF-mutated suprasellar glioblastoma.10,11 Although the patient is not yet on a BRAF inhibitor, this targetable mutation status confers significant clinical value and could potentially offer an opportunity for salvage therapy if there is evidence of progression on the standard treatment protocol.12 Although patients with glioblastomas have an invariably poor prognosis, the implications of BRAF mutations on these tumors is an extremely active area of study.12–14

Microscopic examination of the tumor specimens sampled intraoperatively was nondefinitive but did significantly favor malignant neoplasm over craniopharyngioma. Even permanent sections demonstrated unusual features, including lack of mitoses, which may have been a sampling issue, and marked perivascular lymphocytic inflammation. In such cases, immunohistological testing, specifically for tumor markers such as GFAP, as well as molecular mutations, including TERT promoter mutations and EGFR amplifications, are critical in confirming the diagnosis and predicting prognosis.15 A lack of H3K27M alteration in this case ruled out diffuse midline glioma, which must be considered, given the apparent midline origin. The Ki-67 of 5% was notably low for this tumor, a factor that could be related to prolonged survival.16 Adding another layer of complexity, SSTR2, which is not typically expressed at high levels in glioblastoma, was diffusely positive in this case.17 Furthermore, with regard to the molecular pathology, MGMT methylation is well established to correlate with improved survival outcomes, although only relative to the general morbidity of glioblastoma.18,19 The partial methylation seen in this case is known to correlate with a poor prognosis, with more prognostic similarity to the unmethylated cohort.20

Author Contributions

Conception and design: Zheng, Shao, Dowd, Donahue. Acquisition of data: Zheng, Mingrino, Anthony, Donahue. Analysis and interpretation of data: Zheng, Shao, Mingrino, Dowd, Anthony, Donahue. Drafting the article: Zheng, Shao. Critically revising the article: all authors. Reviewed submitted version of manuscript: all authors. Approved the final version of the manuscript on behalf of all authors: Zheng. Administrative/technical/material support: Shao. Study supervision: Shao, Dowd, Doberstein. Pathological analysis: Mingrino.

Supplemental Information

Videos

Video 1. https://vimeo.com/892271984.

References

  • 1

    Abushamat LA, Kerr JM, Lopes MBS, Kleinschmidt-DeMasters BK Very unusual sellar/suprasellar region masses: a review. J Neuropathol Exp Neurol. 2019;78(8):673684.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 2

    Chambers AA, Lukin RR, Tomsick TA Suprasellar masses. Semin Roentgenol. 1984;19(2):8490.

  • 3

    Lubomirsky B, Jenner ZB, Jude MB, Shahlaie K, Assadsangabi R, Ivanovic V Sellar, suprasellar, and parasellar masses: imaging features and neurosurgical approaches. Neuroradiol J. 2022;35(3):269283.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 4

    Lemm D, de Oliveira FH, Bernays RL, et al. Rare suprasellar glioblastoma: report of two cases and review of the literature. Brain Tumor Pathol. 2012;29(4):216220.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 5

    Berkovskaya M, Grigoriev AY, Zhuravlev KN, Fadeev VV Malignant endo-suprasellar glioma: a case report and a brief review of the literature. Int J Endocrinol Metab. 2022;20(1):e121803.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 6

    Choi SH, Kwon BJ, Na DG, Kim JH, Han MH, Chang KH Pituitary adenoma, craniopharyngioma, and Rathke cleft cyst involving both intrasellar and suprasellar regions: differentiation using MRI. Clin Radiol. 2007;62(5):453462.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 7

    Liu JM, Garonzik IM, Eberhart CG, Sampath P, Brem H Ectopic recurrence of craniopharyngioma after an interhemispheric transcallosal approach: case report. Neurosurgery. 2002;50(3):639645.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 8

    Giese A, Westphal M Glioma invasion in the central nervous system. Neurosurgery. 1996;39(2):235252.

  • 9

    Claes A, Idema AJ, Wesseling P Diffuse glioma growth: a guerilla war. Acta Neuropathol. 2007;114(5):443458.

  • 10

    Cai X, Chen Z, Chang B, et al. Prediction of BRAF mutation status in glioblastoma multiforme by preoperative ring enhancement appearances on MRI. Front Oncol. 2022;12:937345.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 11

    Yue Q, Yu Y, Shi Z, et al. Prediction of BRAF mutation status of craniopharyngioma using magnetic resonance imaging features. J Neurosurg. 2018;129(1):2734.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 12

    Di Nunno V, Gatto L, Tosoni A, Bartolini S, Franceschi E Implications of BRAF V600E mutation in gliomas: molecular considerations, prognostic value and treatment evolution. Front Oncol. 2023;12:1067252.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 13

    McNulty SN, Schwetye KE, Ferguson C, et al. BRAF mutations may identify a clinically distinct subset of glioblastoma. Sci Rep. 2021;11(1):19999.

  • 14

    Munjapara V, Heumann T, Schreck KC, et al. BRAF V600E-mutant glioblastoma with extracranial metastases responsive to combined BRAF and MEK targeted inhibition: a case report. Case Rep Oncol. 2022;15(3):909917.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 15

    Maimaiti B, Mijiti S, Jiang T, et al. Case report: H3K27M-mutant glioblastoma simultaneously present in the brain and long-segment spinal cord accompanied by acute pulmonary embolism. Front Oncol. 2022;11:763854.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 16

    Tini P, Yavoroska M, Mazzei MA, et al. Low expression of Ki-67/MIB-1 labeling index in IDH wild type glioblastoma predicts prolonged survival independently by MGMT methylation status. J Neurooncol. 2023;163(2):339344.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 17

    He JH, Wang J, Yang YZ, et al. SSTR2 is a prognostic factor and a promising therapeutic target in glioma. Am J Transl Res. 2021;13(10):1122311234.

  • 18

    Esteller M, Hamilton SR, Burger PC, Baylin SB, Herman JG Inactivation of the DNA repair gene O6-methylguanine-DNA methyltransferase by promoter hypermethylation is a common event in primary human neoplasia. Cancer Res. 1999;59(4):793797.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 19

    Hegi ME, Diserens AC, Gorlia T, et al. MGMT gene silencing and benefit from temozolomide in glioblastoma. N Engl J Med. 2005;352(10):9971003.

  • 20

    Xia D, Reardon DA, Bruce JL, Lindeman NI The clinical implications of inconsistently methylated results from glioblastoma MGMT testing by replicate methylation-specific PCR. J Mol Diagn. 2016;18(6):864871.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • Collapse
  • Expand
  • FIG. 1

    Initial preoperative postcontrast T1-weighted MRI evaluation of the enhancing suprasellar mass. A: Midsagittal view of suspected tumor with significant suprasellar extension and vasogenic edema extending to the inferior frontal lobe. B: Coronal slice showing ventriculomegaly secondary to effacement of the right lateral ventricle by the lesion. C: The tumor had solid and cystic components, with axial slices further elucidating the extent of edema into the right frontal lobe. The mass was T2- and fluid-attenuated inversion recovery–hyperintense and measured approximately 3.0 × 3.4 × 3.3 cm.

  • FIG. 2

    Intraoperative visualization of tumor capsule prior to resection. This sample demonstrates an interhemispheric view from above into the right lateral ventricle after transection of the anterior corpus callosum. Tumor can be seen beneath the Penfield 4. Some cerebrospinal fluid had been drained, and the anterior cerebral arteries have been retracted to the left (left).

  • FIG. 3

    Postoperative postcontrast T1-weighted MRI after tumor resection. A: Subtotal resection of the suprasellar enhancing neoplasm with debulking of the superior component on a sagittal sequence. Persistent edema with mass effect appears in the right frontal region. B: Coronal sequence showing the debulked mass with subdural hygroma. Postoperative evidence of a right frontal craniotomy defect and an interhemispheric ventriculostomy catheter placed in the right lateral ventricle.

  • FIG. 4

    Suprasellar tumor specimen. Intraoperative squash preparation (A). Cytological preparation shows clusters of atypical cells. Frozen-section diagnosis was malignant neoplasm favoring a glial source. Permanent sections (BI). Histological sections of a hypercellular neoplasm (B) with a rare mitotic figure (black arrow, C), endothelial proliferation (D), perivascular lymphocytes (E), and pseudopalisading necrosis (F). Immunohistochemical studies showed tumor positivity for GFAP (G), confirming glial cell origin with focal positivity for SSTR2 (H). Endothelial cells were negative for both GFAP and SSTR2. Ki-67 proliferative index (I) was unusually low, with very sparse immunohistochemical positivity. Hematoxylin and eosin stain (AF).

  • 1

    Abushamat LA, Kerr JM, Lopes MBS, Kleinschmidt-DeMasters BK Very unusual sellar/suprasellar region masses: a review. J Neuropathol Exp Neurol. 2019;78(8):673684.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 2

    Chambers AA, Lukin RR, Tomsick TA Suprasellar masses. Semin Roentgenol. 1984;19(2):8490.

  • 3

    Lubomirsky B, Jenner ZB, Jude MB, Shahlaie K, Assadsangabi R, Ivanovic V Sellar, suprasellar, and parasellar masses: imaging features and neurosurgical approaches. Neuroradiol J. 2022;35(3):269283.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 4

    Lemm D, de Oliveira FH, Bernays RL, et al. Rare suprasellar glioblastoma: report of two cases and review of the literature. Brain Tumor Pathol. 2012;29(4):216220.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 5

    Berkovskaya M, Grigoriev AY, Zhuravlev KN, Fadeev VV Malignant endo-suprasellar glioma: a case report and a brief review of the literature. Int J Endocrinol Metab. 2022;20(1):e121803.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 6

    Choi SH, Kwon BJ, Na DG, Kim JH, Han MH, Chang KH Pituitary adenoma, craniopharyngioma, and Rathke cleft cyst involving both intrasellar and suprasellar regions: differentiation using MRI. Clin Radiol. 2007;62(5):453462.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 7

    Liu JM, Garonzik IM, Eberhart CG, Sampath P, Brem H Ectopic recurrence of craniopharyngioma after an interhemispheric transcallosal approach: case report. Neurosurgery. 2002;50(3):639645.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 8

    Giese A, Westphal M Glioma invasion in the central nervous system. Neurosurgery. 1996;39(2):235252.

  • 9

    Claes A, Idema AJ, Wesseling P Diffuse glioma growth: a guerilla war. Acta Neuropathol. 2007;114(5):443458.

  • 10

    Cai X, Chen Z, Chang B, et al. Prediction of BRAF mutation status in glioblastoma multiforme by preoperative ring enhancement appearances on MRI. Front Oncol. 2022;12:937345.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 11

    Yue Q, Yu Y, Shi Z, et al. Prediction of BRAF mutation status of craniopharyngioma using magnetic resonance imaging features. J Neurosurg. 2018;129(1):2734.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 12

    Di Nunno V, Gatto L, Tosoni A, Bartolini S, Franceschi E Implications of BRAF V600E mutation in gliomas: molecular considerations, prognostic value and treatment evolution. Front Oncol. 2023;12:1067252.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 13

    McNulty SN, Schwetye KE, Ferguson C, et al. BRAF mutations may identify a clinically distinct subset of glioblastoma. Sci Rep. 2021;11(1):19999.

  • 14

    Munjapara V, Heumann T, Schreck KC, et al. BRAF V600E-mutant glioblastoma with extracranial metastases responsive to combined BRAF and MEK targeted inhibition: a case report. Case Rep Oncol. 2022;15(3):909917.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 15

    Maimaiti B, Mijiti S, Jiang T, et al. Case report: H3K27M-mutant glioblastoma simultaneously present in the brain and long-segment spinal cord accompanied by acute pulmonary embolism. Front Oncol. 2022;11:763854.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 16

    Tini P, Yavoroska M, Mazzei MA, et al. Low expression of Ki-67/MIB-1 labeling index in IDH wild type glioblastoma predicts prolonged survival independently by MGMT methylation status. J Neurooncol. 2023;163(2):339344.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 17

    He JH, Wang J, Yang YZ, et al. SSTR2 is a prognostic factor and a promising therapeutic target in glioma. Am J Transl Res. 2021;13(10):1122311234.

  • 18

    Esteller M, Hamilton SR, Burger PC, Baylin SB, Herman JG Inactivation of the DNA repair gene O6-methylguanine-DNA methyltransferase by promoter hypermethylation is a common event in primary human neoplasia. Cancer Res. 1999;59(4):793797.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 19

    Hegi ME, Diserens AC, Gorlia T, et al. MGMT gene silencing and benefit from temozolomide in glioblastoma. N Engl J Med. 2005;352(10):9971003.

  • 20

    Xia D, Reardon DA, Bruce JL, Lindeman NI The clinical implications of inconsistently methylated results from glioblastoma MGMT testing by replicate methylation-specific PCR. J Mol Diagn. 2016;18(6):864871.

    • PubMed
    • Search Google Scholar
    • Export Citation

Metrics

All Time Past Year Past 30 Days
Abstract Views 0 0 0
Full Text Views 476 476 68
PDF Downloads 208 208 21
EPUB Downloads 0 0 0