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  Table of Contents    
ORIGINAL ARTICLE  
Year : 2012  |  Volume : 55  |  Issue : 3  |  Page : 308-313
Correlation of p53 and KI-67 expression with grade and subtype of ependymoma


Department of Pathology, Nizam's Institute of Medical Sciences, Hyderabad, Andhra Pradesh, India

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Date of Web Publication29-Sep-2012
 

   Abstract 

Introduction: The morphological criteria for grading ependymomas were always felt subjective. Recently some studies have showed that Ki-67 and p53 immunolabeling are important prognostic markers in ependymomas. Materials and Methods: All the cases of ependymomas diagnosed from 2005 to 2010 were graded according to WHO classification for central nervous system (CNS) tumors 2007. Two tissue microarray (TMA) blocks were prepared. Immunohistochemical analysis with glial fibrillary acidic protein (GFAP), epithelial membrane antigen (EMA), Ki-67 and p53 was performed. The difference in expression of p53 and Ki-67 in various tumor grades and subtypes was evaluated using Student's t test. Results: There were 54 cases with a M: F ratio of 1.34 : 1, age ranging from 7 years to 65 years (mean 29.35 years). There were 33 intracranial and 21 spinal cases. There were 9 grade I ependymomas, 32 grade II ependymomas and 13 grade III ependymomas. GFAP immunopositivity was seen in all the cases and EMA was positive in 49% cases. The mean p53 indices were higher in grade III and grade II tumors (26.26% and 26.08%) as compared to subependymomas (7.25%). But these values did not show statistical significance (P = 0.2). The Ki-67 labeling index increased from grade I to grade III tumors. The difference was highly significant between grade II and grade III (0.5% vs. 2.75, P = 0.016). Conclusion: Ki-67 labeling index correlates with grade of ependymoma (P = 0.016). There is no correlation between p53 expression and grade of ependymomas.

Keywords: Ependymoma, grade, Ki-67, p53, subtypes, tissue microarray

How to cite this article:
Manasa LP, Uppin M S, Sundaram C. Correlation of p53 and KI-67 expression with grade and subtype of ependymoma. Indian J Pathol Microbiol 2012;55:308-13

How to cite this URL:
Manasa LP, Uppin M S, Sundaram C. Correlation of p53 and KI-67 expression with grade and subtype of ependymoma. Indian J Pathol Microbiol [serial online] 2012 [cited 2019 Jun 18];55:308-13. Available from: http://www.ijpmonline.org/text.asp?2012/55/3/308/101735



   Introduction Top


Ependymomas are uncommon glial neoplasms of central nervous system (CNS). They constitute up to 8-10% and 1-3% of CNS tumors in children and adults\ respectively. [1] World Health Organization (WHO) classification of CNS tumors grade ependymomas into three grades . [ 2] Grade I includes subependymoma and myxopapillary ependymoma. Grade II includes subtypes like cellular, clear cell, tanycytic and papillary ependymomas. Grade III includes anaplastic ependymoma. Immunohistochemistry in ependymomas reveals their glial and epithelial nature. [3],[4] Various forms of differentiation can occur which include lipomatous, cartilaginous, osseous, melanotic and neuronal differentiation. [2]

The morphological criteria for grading ependymomas were always felt subjective. Several studies have shown conflicting results about an association between grade and patient outcome. [5],[6],[7],[8],[9] The pathobiological parameters to reliably predict the post operative survival time and tumor progression were lacking. Hence, a need for additional prognostic factors that help in assessing tumor progression was always felt.

Recently some authors have advocated that Ki-67 and p53 immunolabeling are important prognostic markers in ependymomas. [10],[11],[12]

There are very few studies from India which have tested the Ki-67 labeling index and p53 immunohistochemistry in ependymomas. [13],[14] So in this study we aim to study these parameters in different grades and subtypes of ependymomas.


   Materials and Methods Top


This was a retrospective study. All the cases of ependymomas diagnosed from 2005 to 2010 were included in the study.

All the hematoxylin and eosin (H and E) stained slides were retrieved, reviewed and were graded according to WHO classification for CNS tumors 2007. The morphological criteria observed were perivascular pseudorosettes, true rosettes, pleomorphism, mitosis, giant cells, necrosis either geographical or palisading, microvascular proliferation, myxoid change and calcification.

The best sections which are free from necrosis or hemorrhage were selected for tissue micro array (TMA). Areas of cystic change, myxoid areas and calcification were also avoided. Three cores are selected for each case. Two TMA blocks were prepared from the paraffin blocks by manual method. Immunohistochemical analysis with GFAP, EMA, Ki-67, and p53 was performed by HRP Polymer technique on the TMA slides.

Immunohistochemistry Technique

Sections of 4-5-μm thick were prepared from TMA blocks and mounted on poly-L-lysine-coated slides. After deparaffinization and hydration through graded alcohol series, endogenous peroxidase was quenched by incubation with 3% peroxide in methanol for 10 minutes. Antigen retrieval was carried out by autoclaving sections at 121°C for 10 minutes in 0.01 mol/L citrate buffer, pH 6.0. The horse radish peroxidase polymer technique was used. Sections were incubated for 1 hour at room temperature with primary antibodies.

The antibodies included were GFAP antibody (ready to use), EMA (ready to use), p53 antibody (ready to use), Ki-67 antibody (ready to use) (Biogenex: San Ramon, CA, USA).

Only 100 nuclei were counted in the cores to calculate Ki-67 labeling index and p53 percentage positivity as the cores contained only few cells compared to a routine histological section. The difference in expression of p53 and Ki-67 various tumor grades and subtypes was evaluated using Student's t test.


   Results Top


A total of 128 cases of ependymomas were diagnosed in our department during the study period. Only 54 cases were included in the present study where sufficient material was available in the blocks.

There were 31 male and 23 female patients with a M: F ratio of 1.34 : 1. The age group ranged from 7 years to 65 years with a mean of 29.35 years. There were 33 intracranial and 21 spinal cases. There were 9 grade I ependymomas which included 4 subependymomas and 5 myxopapillary ependymomas. There were 32 grade II ependymomas and 13 grade III ependymomas.

[Table 1] gives the grade wise, gender wise, age wise and location wise distribution of ependymomas.
Table 1: Ependymomas - grade wise, gender wise, age wise and location wise distribution

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Morphological Features

Grade I ependymomas (n = 9)

Subependymomas (n = 4)
All the cases showed clusters of isomorphic nuclei embedded in fibrillary matrix with microcystic spaces [[Figure 1]a and b].
Figure 1: Subependymoma (a) Isomorphic nuclei in fi brillary matrix. (Hematoxylin and Eosin 40) (b) Microcys.. c change (Hematoxylin and eosin ×40). (c) Tumor cell nuclei stained nega.. ve with Ki67 (Ki67 HRPPolymer ×100) (d) Nuclear staining with p53 (p53 HRP-Polymer ×100)

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Myxopapillary ependymomas (n = 5)

All the cases showed cuboidal to elongated cells arranged in a papillary manner around vascularized stromal cores. Alcian blue positive myxoid matrix was seen around blood vessels and in microcystic areas [Figure 2]a.
Figure 2: Myxopapillary ependymoma (a) Papillae lined by tumor cells on a myxoid background (Hematoxylin and eosin ×40) (b) Alcian positive myxoid matrix around blood vessels (APASX40) (c) Negative staining with Ki67 (Ki67 HRp-Polymer ×100) (d) p53 nuclear staining (p53 HRP-Polymer ×100)

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Grade II ependymomas (n = 32)

All the cases revealed perivascular pseudorosettes. True rosettes were seen in eight cases (25%). Mild to moderate cellular pleomorphism was seen in nine cases (28%). Occasional mitosis was seen in only one case. Calcification was seen in four cases (12.5%), giant cells and myxoid change in two cases each (6.25%). Small foci of geographic necrosis were noted in three cases (9%), palisading necrosis was not seen in any case [Figure 3]a and b.
Figure 3: Grade II ependymomas (a) True rosettes (Hematoxylin and Eosin ×40). (b) Perivascular pseudorosettes (Hematoxylin and eosin, ×40) (c) Nuclear positivity of Ki67 (Ki67 ×100) (d) Tumor cells showing nuclear positivity for p53. (p53 ×100)

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Grade III ependymomas (n = 13)

All the 13 cases revealed perivascular pseudorosettes. True rosettes were seen in 4 cases (30.7%). Moderate to marked pleomorphism and necrosis were seen in eight cases (61.5%) and seven cases (53.8%), respectively. All the cases showed mitosis and microvascular proliferation was seen in nine cases (69.2%). Giant cells and myxoid change was seen in one case each. Calcification was seen in three cases (23%).One case showed brain invasion [Figure 4].
Figure 4: Grade III ependymomas (a) Perivascular pseudorosette with marked pleomorphism of cells. (Hematoxylin and eosin, ×40). (b) Microvascular proliferation (Hematoxylin and Eosin ×40). (c) High Ki67 index (Ki67 HRP-Polymer 100) (d) Most of the tumor cell nuclei showing positivity for p53. (p53 HRP-Polymer ×100)

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Two cases of clear cell ependymomas were seen in the study, one was grade II and other was grade III. Both were located intracranially. Microscopically the cells had a oligodendroglioma like appearance with clear perinuclear halos. Papillary ependymoma was a grade II tumor located in fourth ventricle. Morphology showed papillae lined by cudoidal cells with smooth contiguous surface and GFAP positive cell processes. One case showed lipomatous differentiation [Figure 5].
Figure 5: (a)-Clear cell ependymoma: cells with perinuclear clearing arranged in the form of perivascular pseudorosettes. (b). Ependymoma with lipomatous differentiation: cells arranged in sheets and perivascular pseudorosettes in a fi brillary background with lipomatous change in some of the cells (Hematoxylin and eosin, ×20). (c)- Papillary ependymoma: papillary structures lined by cells with fibrillary cytoplasm (Hematoxylin and eosin, ×4)

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Immunohistochemical Analysis

Some of the cores were lifted during the IHC procedures. Therefore the final analysis for IHC was done on GFAP (49 cases), EMA (51 cases), p53 (50 cases) and Ki-67 (53 cases).

GFAP immunopositivity was seen in all the cases in the tumor cells and the cell processes forming the perivascular pseudorosettes. The tumor cells showed EMA immunoreactivity in 25/51 ependymomas (49%). Distinct punctate intracytoplasmic staining was observed in 23/51 cases (45%) whereas ring-like EMA staining was observed in 2/51 ependymomas (3.9%). Expression of EMA was higher in subependymomas (75%) and slightly lower in grade II ependymomas (45%) compared to myxopapillary and grade III ependymomas (50%).

The p53 indices grade wise were given in [Table 2]. The mean p53 indices were higher in grade II [Figure 3]d and grade III [Figure 4]d tumors (26.27 %) and 26.08%) as compared to subependymomas (7.25%) [Figure 1]d. However, p53 index of myxopapillary ependymoma (26%) was similar to grade II and grade III tumors [Figure 2]d. But these values did not show statistical significance (P = 0.2). Papillary ependymoma (grade II) showed p53 expression in 24% cells and Ki-67 labeling index was 0.5%. Ependymoma with lipomatous differentiation was also a grade II tumor and was negative for p53 and Ki-67. Papillary ependymoma (grade II) showed p53 expression in 24% cells and Ki-67 labeling index was 0.5%. Ependymoma with lipomatous differentiation was also a grade II tumor and was negative for p53 and Ki-67.
Table 2: Immunohistochemical analysis in ependymomas grade wise

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The Ki67 labeling index increased from grade I (negative in subependymomas and 0.9% in myxopapillary ependymomas) to grade III tumors [Figure 1],[Figure 2],[Figure 3],[Figure 4]c. The difference was highly significant between grade II and grade III (0.5% vs. 2.75, P = 0.016). Grade III clear cell ependymoma showed higher Ki-67 labeling index (2%) as compared to clear cell ependymoma of grade II (negative).

[Table 2] gives the summary of immunohistochemical analysis in ependymomas grade wise.


   Discussion Top


Ependymomas are relatively rare tumors of the CNS, accounting for 3-5% of all intracranial tumors1 and 9-10% of all gliomas. [13] [Table 3] shows comparison of clinical features of different grades of ependymomas in our study with previous studies. [14],[15],[16],[17]

Morphologically, subependymomas showed clusters of isomorphic nuclei in a fibrillary matrix with microcystic spaces. Calcification, pleomorphism, occasional mitosis and necrosis were reported by Prayson et al.[15] and Rushing et al.[16] However, none of these features were seen in our study.
Table 3: Ependymomas– Comparison of clinical features of subependymoma, myxopapillary, grade II and grade III ependymomas

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Myxopapillary ependymomas were characterized by cuboidal to elongated tumor cells around vascularized stromal cores in a mucoid matrix. Prayson et al.[17] studied clinicopathological features in 14 myxopapillary ependymomas. In that study, four cases had focal, prominent, nuclear pleomorphism. From 1 to 5 mitotic figures per 10/hpf were identified in four tumors. There was no vascular proliferation or necrosis. In our study none of the cases showed mitosis, pleomorphism, microvascular proliferation or necrosis.

Grade II ependymomas showed perivascular pseudorosettes, ependymal canals with rare or no mitosis were seen on morphology. None of the cases showed palisading necrosis or microvascular proliferation. Grade III (anaplastic) ependymomas were morphologically characterized by increased cellularity, brisk mitotic activity, vascular proliferation, endothelial hyperplasia, pseudopalisading necrosis in addition to perivascular rosettes and ependymal canals.

The p53 gene is a tumor suppressor gene located on the 17p13.1 and is the single most common target for genetic alterations in human cancer. Mutated p53 lacks DNA repair regulation of cell cycle and results in metabolically stable abnormal protein that accumulates in the nucleus which can be detected by immunohistochemistry. A number of studies have documented a correlation between p53 expression and tumor grade in ependymomas. [10],[11],[14],[18] p53 over expression is reported to be significantly higher in anaplastic tumors and one of the strong predictors of worse survival and poor prognosis. [12],[19] In our study p53 expression ranged from 0 to 60% (mean 26%) in myxopapillary ependymoma, 0-92% (mean 26.27%) in grade II ependymoma and 0-86% (mean 26.08%) in Grade III ependymoma. There was no statistical significance between the grade and p53 index in our study. Two cases of subependymoma showed p53 expression and indices ranged from 0 to 20% (mean 7.25%). Similar observation was made by Rushing et al who reported p53 expression in two subependymomas. [10] TP 53 mutations were rarely reported in ependymal tumors by molecular analysis. [18],[20],[21] However, p53 protein is identified in about 60% ependymal tumors. [18] Sharma et al. reported 37.5% and we reported 66% p53 positivity in our study. The discrepancy between p53 immunolabeling and p53 mutations is not clearly understood. Shuangshoti et al.[22] opined that the discrepancy may be due to expression of wild type p53 gene in tumor cells, alternative mechanisms of p53 gene inactivation or simply a cross-reaction of the antigen-antibody complex.

Ki-67 antigen is a nonhistone protein expressed in the proliferative phase of cell cycle. [23] Many previous studies have analyzed Ki-67 antigen expression and its prognostic impact in ependymomas.[3],[10],[11],[12],[13],[14] Except for a few studies, a significant association between Ki-67/MIB-1 LI and a high tumor grade has been reported. However, the Ki67 labeling indices shows variable results in different studies. [3] Our study shows significantly high Ki-67 LI in grade III tumors compared to grade I and Grade II tumors

(P = 0.016). Suri et al.[13] and Sharma et al.[14] have also shown a similar correlation however the mean values in our study were less when compared to the other studies.

In our study, two cases of clear cell ependymomas were included. Suzuki et al. in 2001 [11] in their study on 29 patients of ependymoma advocated that the clinical course was worst in clear cell ependymoma which had significantly higher expression of Ki67 and p53 than the other subtypes. In study by Suri et al. difference was not statistically significant. [13] In our study Ki67 LI of the grade II and grade III clear cell ependymomas were 0 and 2, respectively, and did not show a higher expression than other ependymomas of same grade. Papillary ependymoma was a grade II tumor. P53 expression was seen in 24% of cells and Ki-67 labeling index as 0.5%. Ependymoma with lipomatous differentiation was also a grade II tumor and was negative for p53 and Ki-67.

In our study tissue microarray (TMA) technology was used for the analysis of immunohistochemical markers unlike the previous other studies. This technology has inherent advantages and disadvantages. [24] The staining of a few TMA sections in comparison to many more whole sections saves laboratory reagents and technician time. In addition, there is also the benefit of decreased technical variability during the staining and interpretation process. The close proximity of cores also permits more rapid and consistent biomarker scoring by a surgical pathologist. The most frequent criticism of TMA technology relates to the small size of each tissue core. Due to tumor heterogeneity, biomarker scores obtained from small TMA cores may not accurately reflect scores obtained from whole sections.[25],[26] In the present study, we could not count 1000 nuclei to calculate Ki-67 labeling index and p53 expression especially in low grade ependymomas where the cellularity was low. This may be the cause for low mean values in our study when compared to other studies.


   Conclusions Top


Ki-67 labeling index correlates with grade of ependymoma (P = 0.016). There is no correlation between p53 expression and grade of ependymomas.


   Acknowledgments Top


The authors acknowledge department of neurosurgery for providing valuable material for the study and Dr. Sanjay Navani for helping in preparation of tissue micro array blocks.

 
   References Top

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Correspondence Address:
C Sundaram
Department of Pathology, Nizam's Institute Of Medical Sciences, Punjagutta, Hyderabad - 500 082, Andhra Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0377-4929.101735

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