Shagufta Qadri Department of Pathology, Jawaharlal Nehru Medical College, Aligarh Muslim University, Aligarh, Uttar Pradesh, India
Kausar Tasnim Junior Resident, Department of Pathology, JNMCH, Aligarh Muslim University, Aligarh, Uttar Pradesh, India
Maheshwari Veena Professor, Department of Pathology, JNMCH, Aligarh Muslim University, Aligarh, Uttar Pradesh, India
Sharma M. Raman Professor, Department of Neurosurgery, JNMCH, Aligarh Muslim University, Aligarh, Uttar Pradesh, India
Address for correspondence: Shagufta Qadri, Department of Pathology, Jawaharlal Nehru Medical College, Aligarh Muslim University, Aligarh, Uttar Pradesh, India E-mail: qadridrshagufta@gmail.com
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reusers to distribute, remix, adapt, and build upon the material in any medium
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Kausar Tasnim, Shagufta Qadri, Maheshwari Veena. Clinico-Pathological and Immunohistochemical Study of Primary CNS Tumors in a Tertiary Care Centre. Ind Jr of Path: Res and Practice 2026; 15(2) 101-110.
Timeline
Received : December 20, 2025
Accepted : January 25, 2026
Published : August 30, 2026
Abstract
Background: Primary CNS tumors show wide clinical, histomorphological, and immunohistochemical variation. Distinguishing these lesions from each other and from reactive process can be challenging due to overlapping cell morphology. So, the diagnosis and categorization of primary CNS tumors, is essential for planning the management and to determine the prognosis. Objectives: To evaluate the clinico-radiological features in diagnosing CNS tumors; to study the occurrence of CNS tumors in relation to age, sex, and anatomical sites, and the histopathological features of various CNS tumors and to evaluate the role of immunohistochemistry in diagnosing as well as classifying various CNS tumors according to CNS5. Materials and Methods: This study included a total of 242 case’ biopsy of primary CNS tumors received in the Department of Pathology over 5 years from 2020 to 2024. All specimens were examined grossly, processed routinely, stained with H&E, and evaluated using a panel of IHC markers (IDH1, ATRX, p53, Ki-67, GFAP, Synaptophysin, EMA, PR, etc.). Results: Out of 242, the most common age group was 15-39 years with male: female ratio of 1.3:1 with most common site- cerebrum. Majority of the cases were non-malignant (61%), while 39% cases were malignant. The most frequent tumors were gliomas, followed by meningiomas, schwannoma, pituitary adenomas, and medulloblastomas. IHC significantly assisted in differentiating astrocytic tumors, subtyping meningiomas, and confirming embryonal tumors. Ki‑67 index
correlated with the tumor grade. Conclusion: A combined clinico-pathological and IHC approach markedly improves diagnostic accuracy of primary CNS tumors.
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There are no additional data available. All raw data and code are available upon request.
Funding
This research received no funding.
Author Contributions
All authors contributed significantly to the work and approve its publication.
Ethics Declaration
This article does not involve any human or animal subjects, and therefore does not require ethics approval.
Acknowledgements
We would like to express our gratitude to the patients, their families, and all those who have contributed to this study.
Conflicts of Interest
No conflicts of interest in this work.
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Cite this article
Kausar Tasnim, Shagufta Qadri, Maheshwari Veena. Clinico-Pathological and Immunohistochemical Study of Primary CNS Tumors in a Tertiary Care Centre. Ind Jr of Path: Res and Practice 2026; 15(2) 101-110.
This license enables
reusers to distribute, remix, adapt, and build upon the material in any medium
or format for noncommercial purposes only, and only so long as attribution is
given to the creator.
This license enables
reusers to distribute, remix, adapt, and build upon the material in any medium
or format for noncommercial purposes only, and only so long as attribution is
given to the creator.
Description: R1 MRI showed a hypodense, non-enhancing left frontal lesion with ill-defined margins and mild mass effect. Histomorphology (Fig. 1A–1B) showed increased cellularity with mild atypia of tumor cells in a dense fibrillary
background (H&E10X & Inset 40X). IHC showed IDH mutation (Fig. 1C, 40X), ATRX loss (Fig. 1D,40X), p53 positivity
(~10%) (Fig. 1E,10X), and a low Ki-67 index. (<5%) (Fig. 1F, 10X) in tumor cells.
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Description: 2A: T2/FLAIR MRI shows a hyperintense lesion in the right frontoparietal white matter with irregular margins
and perilesional edema, causing mild compression of adjacent sulci and ventricles, Histopathology reveals increased
cellularity with nuclear atypia and mitotic activity (Fig. 2B, H&E, 40X), Tumor cells show IDH mutation (Fig. 2C, IHC,
40X) and diffuse cytoplasmic GFAP positivity (IHC, 40X) (Fig. 2D)
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Description: Fig. R3 MRI showed a heterogeneously enhancing fronto-parietal mass with central necrosis, vasogenic
edema, and midline shift. Histomorphology (Fig. 3A–3C) showed diffusely infiltrating atypical cells with geographic
necrosis, increased cellularity, microvascular proliferation, marked atypia, & mitoses. IHC showed IDH mutation
(Fig. 3D), ATRX loss (Fig. 3E), p53 positivity in 30–40% of tumor cells (Fig. 3F) and diffuse GFAP positivity (Fig. 3G).
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Description: Fig. R4 MRI showed an ill-defined right frontal intra-axial mass with T2/FLAIR hyperintensity, cystic areas, vasogenic edema, and mild midline shift; histomorphology (Fig. 4A&B, H&E,10X) showed diffuse round cells with perinuclear halos and brisk mitoses (40X). IHC showed IDH-mutation (Fig. 4C, 40X), ATRX-retained (Fig. 4D, 40X), p53-negative (Fig. 4E, 10X), Ki-67 (30–40%, 10X) (Fig. 4F, 10X), and GFAP positivity (Fig. 4G, 40X) in tumor cells
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Description: Figure R5 MRI showed an aggressive right frontoparietal mass with central necrosis, extensive edema, and marked midline shift; histology (Fig. 5A–5C) shows palisading necrosis, atypia, and microvascular proliferation. IHC shows IDH-wild type (Fig. 5D, 10X) and ATRX retained (Fig. 5E, 40X).
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Description: Figure 6A (H&E, 40X) showed moderate cellularity with piloid cells and Rosenthal fibers; Fig. 6B showed Ki-67 <2% (40X); Fig. 7A MRI showed a well-circumscribed cystic parietal lesion with an enhancing mural nodule. Fig. 7B, (H&E, 10X) showed peripheral invasion with pleomorphic cells with (Fig. 7C H&E, 40X) spindle/epithelioid cells, multinucleated astrocytes, and xanthomatous changes with BRAF V600E positivity (Fig. 7D IHC-40X) & rich reticulin network (Fig. 7E, 40X)
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Description: Fig. 8A MRI showed a large heterogeneous temporal solid-cystic mass with mass effect; Fig. 8B showed neuronal component (ganglion cells) within the tumor area (H&E, 40X). Fig. 8C showed glial component of tumor with eosinophilic granular bodies (H&E, 40X), and dystrophic calcification in ganglion cells (Fig 8D, H&E, 40X), IHC showed GFAP positivity in glial component (Fig 8E, IHC-40X) & synaptophysin positivity in neoplastic ganglion cells (Fig. 8F, IHC-40X)
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Description: Fig. 9A Section shows uniform round cells, thickened and hyalinized blood vessels and psammomatous calcification (H&E, 10X) some cells showed perinuclear clearing and intratoumoral hemorrhage. (Fig. 9B Inset H&E, 40X). Fig. 9C showed GFAP-positive reactive astrocytes (IHC, 40X) and synaptophysin-positive tumor cells (Fig. 9D, IHC 10X)
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Description: Fig. 10A MRI showed a well-defined lobulated parietal lobe lesion, heterogeneously T2-hyperintense with cystic areas, septations, mild edema, heterogeneous enhancement, and mass effect. Fig. 10B Histopathology showed pseudorosettes, true rosettes, with round-to-oval tumor nuclei (H&E, 40X) with Perinuclear dot/ ring-like EMA positivity (Fig. 10C, IHC-40X), GFAP shows perivascular accentuation (Fig. 10D, IHC-40X), and the Ki-67 index >20% (Fig. 10E, IHC-40X) in tumor cells
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Description: Figure 11A Section shows papillary pattern composed of fibrovascular fronds (H&E, 10X) with single layer of cuboidal to columnar epithelial cells & round/ oval nuclei. (Fig 11B H&E, 40X) with GFAP positivity in reactive astrocytes or entrapped glial tissue. (Fig 11C, IHC-10X).
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Description: Fig. 13A MRIshowed a hyperdense midline posterior fossa mass arising from the cerebellar vermis, compressing
the 4th ventricle and causing obstructive hydrocephalus, with surrounding edema and heterogeneoenhancement;
Fig. 13B showed small round blue cells with hyperchromatic nuclei and a high N:C ratio andHomer Wright rosettes
with focal synaptophysin positivity (Fig. 13C).
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Description: Figure 14A showed pale nodular areas with neuronal differentiation surrounded by densely packed hyperchromatic cells with reticulin-positive internodular regions (Fig. 14B, IHC-10X), NSE +ve pale nodules (Fig. 14C, IHC-10X) and synaptophysin-positive nodules and negative internodular areas (Fig. 14D, IHC-10X)
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Description: Fig. 15A showed sheets of poorly differentiated cells infiltrating adjacent CNS tissue (H&E, 4X). The tumor showed embryonal cells with a high N:C ratio and Homer Wright rosettes (Fig. 15 B&C; H&E, 10X, 40X), IHC showed synaptophysin positivity (Fig. 15D), and Ki-67 index > 50% (Fig. 15E)
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Description: Fig. 16A showed a highly cellular smallround cell tumor with a high N:C ratio and rosettes (H&E, 10X). Tumor cells were chromogranin-positive (Fig.16B, 10X), S100 positivity (Fig. 16C) and Ki-67 index of ~35% (Fig. 16D)
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Description: Figure 17A showed Antoni A areas with Verocay bodies in adjacent Antoni B area (H&E, 10X). Tumor cells- S100 positive (Fig. 17B; IHC, 40X). Figure 18 A&B showed bland spindle cells with thin, wavy nuclei in a loose myxoid stroma with collagen (H&E, 10X, 40X)
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Description: Fig. 19A showed a well-defined extra-axial CPA mass with dural attachment, compressing the cerebellum and brainstem, appearing iso- to hyperintense on T2 MRI. The tumor had syncytial meningothelial cells (Fig. 19B, 40X) with SSTR2A membranous and cytoplasmic positivity (Fig. 19C, IHC, 10X)
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Description: Fig. 20A showed Meningioma replaced by psammomatous calcifications (H&E, 10X), with EMA-positive cells seen between psammoma bodies (Fig. 20B, IHC,40X); Fig. 21A showed hyalinized small vessels with intervening meningioma cells and microcystic/metaplastic areas,and SSTR2A showed membranous and cytoplasmic positivity in tumor cells (Fig. 21B, IHC, 40X)
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Description: Fig. 22A (H& E, 40X)showed plump cells with eccentric nuclei & eosinophilic paranuclear inclusions with PR showed nuclear positivity (Fig. 22B, IHC, 40X), and SSTR2A showed membranous & cytoplasmic positivity in tumor cells (Fig. 22C, IHC, 40X)
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Description: Fig. 23A showed overtly malignant anaplasia resembling carcinoma or melanoma with mitotic activity (H&E, 40X)
with SSTR2A positivity in tumor cells (Fig. 23B, IHC-40X) and Vimentin- positivity in tumor cells (IHC-10X)