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LETTERS TO EDITOR
Year : 2018  |  Volume : 66  |  Issue : 1  |  Page : 245-248

Primary sphenoid wing meningioma in contiguity with a glioblastoma


Department of Neurosurgery, Bombay Hospital Institute of Medical Sciences, Mumbai, Maharashtra, India

Date of Web Publication11-Jan-2018

Correspondence Address:
Dr. Chandrashekhar E Deopujari
Room No 126B, MRC Building, Bombay Hospital, 12, New Marine Lines, Mumbai - 400 020, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.222854

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How to cite this article:
Shaikh ST, Chawda MD, Mohanty CB, Deopujari CE. Primary sphenoid wing meningioma in contiguity with a glioblastoma. Neurol India 2018;66:245-8

How to cite this URL:
Shaikh ST, Chawda MD, Mohanty CB, Deopujari CE. Primary sphenoid wing meningioma in contiguity with a glioblastoma. Neurol India [serial online] 2018 [cited 2019 Oct 19];66:245-8. Available from: http://www.neurologyindia.com/text.asp?2018/66/1/245/222854




Sir,

The simultaneous occurrence of primary brain tumors with differing histology is seen in 0.3% of all brain tumors.[1] Occurrence of multiple intracranial tumors of varied origin is not uncommon but is usually observed in genetic diseases such as neurofibromatosis or tuberous sclerosis, or in the case of secondary tumors occurring as a sequelae of cranial radiotherapy. The earliest reported case of two different tumors in the same patient is by Feiring and Davidoff in 1947.[2] Till date, the most frequently reported combination of lesions in such cases is that of a meningioma and a glioma.[3]

A 56-year old female patient presented with complaints of memory lapses since 2 months and vomiting with visual blurring for 4 days. On examination, she was disoriented and confused. Vision was 6/60 on the left side and normal on the right side. Fundus examination showed left-sided hyperemic disc with edema. Perimetry was attempted but was not possible due to her memory disorder. Rest of the neurological examination was normal. Computed tomography (CT) scan showed the presence of a left frontal lesion with patchy hemorrhages within it and sphenoid wing hyperostosis. Magnetic resonance imaging (MRI) was suggestive of an extra-axial left frontal lobe infiltrative lesion extending into the corpus callosum and right frontal lobe, causing mass effect and midline shift [Figure 1]. On contrast scans, a well-defined homogenously enhancing lesion in the left frontal lobe was seen, suggestive of a meningioma, along with an abutting heterogeneous lesion, which appeared to be a high-grade glioma [Figure 2]a and [Figure 2]b. Left frontotemporal craniotomy with gross total excision of the glioma and complete excision of the sphenoid wing meningioma was done. Inferiorly, the tumor was in contiguity with the meningioma. Histopathology showed two lesions: (1) Transitional meningioma of World Health Organization (WHO) grade I [Figure 3]; and, (2) glioblastoma with oligodendroglial component of WHO grade IV [Figure 4]. On immunohistochemistry analysis, meningioma had a Ki 67 score of 1–2% and glioblastoma showed P53 positive, isocitrate dehydrogenase negative, and alpha thalassemia/mental retardation syndrome X-linked (ATRX) retained status as well as a methylation-inhibited binding protein-1(MIB-1) score of 10–15%. Postoperative computed tomographic (CT) scan showed complete excision of the lesions [Figure 5]. She underwent adjuvant therapy in the form of concurrent chemotherapy (temozolamide) and cranial radiotherapy.
Figure 1: T2 weighted axial section of MRI showing an extra-axial fairly large, heterogeneous expansile infiltrative left frontal lobe lesion extending into corpus callosum and right frontal lobe with mass effect, midline shift to the right and obstructive dilatation of the right lateral ventricle

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Figure 2: (a and b) Contrast MRI (axial and sagittal sections) showing a well-defined homogenously enhancing lesion in the left basi-frontal lobe suggestive of a meningioma. In close proximity, another lesion is seen which appears to be a high-grade glioma

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Figure 3: Histopathology image (hematoxylin and eosin stain, magnification ×100) showing the presence of spindle cells (arrow) suggestive of a meningioma

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Figure 4: Histopathology image (hematoxylin and eosin stain, magnification ×40) showing the presence of pseudo-palisading necrosis (black arrow) and vascular proliferation (white arrow)

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Figure 5: Postoperative CT scan showing excision of both the lesions

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Many theories have been hypothesized for the simultaneous occurrence of different intracranial tumors in the same patient. There is no consensus yet on their exact mechanism of origin. A few studies have attributed it to be an incidental finding.[3] This is a prevalent belief as both meningioma and glioma are fairly common central nervous system tumors. Nestler et al.,[4] described three cases where a meningioma and a glioblastoma occurred together. Specimens from the two patients were cultivated in cell culture and were examined for chromosomal aberrations by the conventional karyotyping and comparative genomic hybridization. In one patient, it was possible to compare the data. In that case, a common genetic aberration in the tumor cells was not found. Another theory suggests that the astrocytoma may develop due to neoplastic transformation of the reactive glial cells surrounding a meningioma.[5] It may be a possibility that one tumor may act as the stimulus for local proliferation and growth of the other, inducing neoplastic transformation. However, these theories do not hold ground in explaining the inability of majority of intracranial meningiomas to transform reactive glial cells surrounding it, and also fails to explain the simultaneous occurrence of two tumors which are in opposite hemispheres or are far apart in the same hemisphere.

The main pathways that have been linked to meningioma proliferation and progression are [6] [Figure 6]:
Figure 6: Signal transduction pathways involved in meningiomas

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  1. The p53/pRB pathway which controls the transition from G1 to S phase through the tumor suppressor gene pRB
  2. The hedgehog/patched (PTCH) pathway which has genes that are responsible for cell growth activation and suppression regulated by the smoothened (SMO) gene
  3. The notch pathway mediated by a number of transmembranes and serves as an intracellular communication system relaying messages throughout the cell
  4. The PI3K/AKT/MAPK pathways that have been linked to malignant meningiomas with high levels of phosphorylated AKT found in Grade II/III meningiomas
  5. The Wnt/β-catenin pathway which deals more with benign meningiomas because many benign meningiomas have been shown to have deletions in the adenomatous polyposis coli (APC) gene, which is a major gene of this pathway.


The genetic alterations in glioblastoma signal transduction pathways are [7] [Figure 7]:
Figure 7: Genetic alterations in glioblastoma signal transduction. Adapted from The Cancer Genome  Atlas More Details Research Network. Comprehensive genomic characterization defines human glioblastoma genes and core pathways. Nature 2008;455(7216):1061-8

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  1. PI3K signaling altered in 88% of glioblastomas
  2. p53 signaling altered in 87% of glioblastomas
  3. Retinoblastoma protein (RB) gene signaling altered in 78% of glioblastomas.


Thus, signal transduction pathways could be considered as important determinants of tumor growth in these patients. Suzuki et al.,[8]analyzed a similar case and concluded that platelet-derived growth factor (PDGF)-mediated paracrine system may induce one tumor from another. Three subunits of PDGF—the PDGF-AA, PDGF-BB, and PDGF-AB—are secreted by astrocytomas. There are two receptor subtypes: PDGF-α-R and PDGF-β-R. Astrocytomas have the PDGF-α-R receptor and their growth is stimulated by PDGF in an autocrine fashion.[9] Meningiomas have the PDGF-β-R receptor and PDGF-BB acting on these receptors is shown to stimulate cell division.[10] Thus, glioblastoma may stimulate growth of meningiomas by production of a common growth factor. Li et al.,[11] described a case of meningioma–glioma, which possessed the morphology of a meningioma on pathology but its immunohistochemistry characteristics belonged to a glioma. Specific immunohistochemistry staining should be an important determinant for ascertaining the origin of tumors. N-myc downstream-regulated gene 2 (NDRG2) is expressed in normal brain tissue but downregulated in glioblastomas. Of late, this gene has been found to be commonly downregulated in aggressive meningiomas too.[12],[13]

To conclude, edema or hemorrhage away from the site of a primary well-defined lesion necessitates ruling out additional lesions. A primary glioma and meningioma adjacent to each other is a rare occurrence but a definite possibility. Immunohistochemistry is advised as it provides valuable knowledge about the genetic alterations, if present. Though there is a school of thought which attributes such cases to an incidental finding, a review of literature suggests a genetic or reactive cause for the simultaneous occurrence of the two tumors, which makes it imperative to study them in greater depth.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Nomura K. Analysis of therapeutic factors related to survival rate for malignant glioma patients—report from Brain Tumor Registry in Japan, Vol. 6, 1987. Gan No Rinsho 1989;35:1219-25.  Back to cited text no. 1
    
2.
Feiring EH, Davidoff LM. Two tumors, meningioma and glioblastoma multiforme, in one patient. J Neurosurg 1947;4:282-9.  Back to cited text no. 2
    
3.
Strong AJ, Symon L, MacGregor BJ, O'Neill BP. Coincidental meningioma and glioma. Report of two cases. J Neurosurg 1976;45:455-8.  Back to cited text no. 3
    
4.
Nestler U, Schmidinger A, Schulz C, Huegens-Penzel M, Gamerdinger UA, Koehler A, et al. Glioblastoma simultaneously present with meningioma—report of three cases. Zentralbl Neurochir 2007;68:145-50.  Back to cited text no. 4
    
5.
Drlicek M, Aichholzer M, Wurm G, Bodenteich A, Fischer J. Collision tumour composed of glioblastoma and meningioma—a case report. Pathologe 2004;25:402-5.  Back to cited text no. 5
    
6.
Miller R, DeCandio ML, Dixon-Mah Y, et al. Molecular targets and treatment of meningioma. J Neurol Neurosurg 2014;1 (1). pii: 1000101.  Back to cited text no. 6
    
7.
Parsons DW, Jones S, Zhang X, Lin JC, Leary RJ, Angenendt P, et al. An integrated genomic analysis of human glioblastoma multiforme. Science 2008;321:1807-12.  Back to cited text no. 7
    
8.
Suzuki K, Momota H, Tonooka A, Noguchi H, Yamamoto K, Wanibuchi M, et al. Glioblastoma simultaneously present with adjacent meningioma: Case report and review of the literature. J Neurooncol 2010;99:147-53.  Back to cited text no. 8
    
9.
Goumnerova L, Guha A. Oncogenes and growth factors in astrocytomas. In: Black PM, Schoene WC, Lampson LA, editors. Astrocytomas: Diagnosis, Management and Biology. Oxford: Blackwell; 1992. p. 211-27.  Back to cited text no. 9
    
10.
Black PM, Carroll R, Glowacka D, Riley K, Dashner K. Platelet-derived growth factor expression and stimulation in human meningiomas. J Neurosurg 1994;81:388-93.  Back to cited text no. 10
    
11.
J Li, W Hu, Z Zhang, D Wei. Clinical and pathological studies of meningioma-glioma mixed tumor. Surg Sci 2011;2:140-3.  Back to cited text no. 11
    
12.
Shinde SV, Shenoy AS, Savant HV, Balasubramaniam SB. Coexistent intracerebral metastatic melanoma and meningioma. Neurol India 2017;65:110-2.  Back to cited text no. 12
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13.
Lusis EA, Watson MA, Chicoine MR, Lyman M, Roerig P, Perry A, et al. Integrative genomic analysis identifies NDRG2 as a candidate tumor suppressor gene frequently inactivated in clinically aggressive meningioma. Cancer Res 2005;65:7121-6.  Back to cited text no. 13
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]



 

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