Journal of Clinical Pathology and Laboratory Medicine

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Commentary - Journal of Clinical Pathology and Laboratory Medicine (2025) Volume 7, Issue 3

Gastrointestinal stromal tumors: A histopathological and immunohistochemical study.

Wenlong Qin*

Department of Pathology, Muhimbili University of Health and Allied Sciences, Tanzania

*Corresponding Author:
Wenlong Qin
Department of Pathology
Muhimbili University of Health and Allied Sciences, Tanzania
E-mail: qinen@163.com

Received: 10-Sep-2025, Manuscript No. AACPLM- 25-166913; Editor assigned: 11-Sep-2025, Pre QC No. AACPLM- 25-166913 (PQ); Reviewed: 20-Sep- 2025, QC No. AACPLM- 25-166913; Revised: 21-Sep-2025, Manuscript No. AACPLM- 25-166913 (R); Published: 28-Sep-2025, DOI: 10.35841/ aacplm-7.3.274

Citation: Qin W. Gastrointestinal stromal tumors: A histopathological and immunohistochemical study. J Clin Path Lab Med.2025;(7)3:274

Introduction

Gastrointestinal stromal tumors (GISTs) represent the most common mesenchymal neoplasms of the gastrointestinal (GI) tract, accounting for approximately 1–3% of all GI malignancies. They originate from the interstitial cells of Cajal or their precursors and exhibit distinct histopathological and immunohistochemical characteristics that aid in diagnosis and prognostication.[1].

Gastrointestinal stromal tumors (GISTs) represent the most common mesenchymal neoplasms of the gastrointestinal (GI) tract, accounting for approximately 1–3% of all GI malignancies. They originate from the interstitial cells of Cajal or their precursors and exhibit distinct histopathological and immunohistochemical characteristics that aid in diagnosis and prognostication.[2].

Immunohistochemistry (IHC) plays a crucial role in the diagnosis of GISTs. The majority (>95%) express CD117 (c-KIT), a transmembrane tyrosine kinase receptor, which is a hallmark marker for GIST [3]. DOG1 (Discovered on GIST-1) is another sensitive and specific marker, particularly useful in CD117-negative cases . CD34 is positive in approximately 70–80% of cases, while SMA (smooth muscle actin), S100, and desmin are variably expressed [3]

The discovery of c-KIT and PDGFRA mutations has revolutionized the understanding and management of GISTs. These mutations lead to constitutive activation of tyrosine kinase signaling pathways, driving tumorigenesis. Molecular testing for these mutations is recommended, especially in cases considered for targeted therapy. Imatinib mesylate, a tyrosine kinase inhibitor, remains the first-line treatment for advanced or metastatic GISTs and has significantly improved survival rates. Histopathological assessment also helps identify tumor necrosis, cellular atypia, and mucosal ulceration, which are additional features associated with aggressive behavior. Furthermore, IHC can help distinguish GISTs from other mimickers such as leiomyomas, schwannomas, and desmoid tumors, which lack CD117 and expression [4].

Histopathological assessment also helps identify tumor necrosis, cellular atypia, and mucosal ulceration, which are additional features associated with aggressive behavior. Furthermore, IHC can help distinguish GISTs from other mimickers such as leiomyomas, schwannomas, and desmoid tumors, which lack CD117 and DOG1 expression. [5].

Conclusion

GISTs are distinct mesenchymal tumors of the GI tract with specific histologic and immunohistochemical profiles. Histopathology in combination with IHC, particularly CD117 and DOG1, is essential for accurate diagnosis. Molecular characterization further supports personalized treatment strategies, underscoring the importance of an integrated diagnostic approach.

References

  1. Bleecker ER, FitzGerald JM, Chanez P, et al. Efficacy and safety of benralizumab for patients with severe asthma uncontrolled with high-dosage inhaled corticosteroids and long-acting ß2-agonists (SIROCCO): a randomised, multicentre, placebo-controlled phase 3 trial.The Lancet. 2016; 388(10056):2115-27.

    2. Indexed at, Google Scholar, Cross Ref

  2. Corren J, Weinstein S, Janka L, et al. Phase 3 study of reslizumab in patients with poorly controlled asthma: effects across a broad range of eosinophil counts.Chest. 2016; 150(4):799-810.

    3. Indexed at, Google Scholar, Cross Ref

  3. Rosenwasser LJ, Busse WW, Lizambri RG, et al. Allergic asthma and an anti-CD23 mAb (IDEC-152): results of a phase I, single-dose, dose-escalating clinical trial.J Allergy Clin Immunol. 2003; 112(3):563-70.

    4. Indexed at, Google Scholar, Cross Ref

  4. Schwab U, Stein H, Gerdes J, et al. Production of a monoclonal antibody specific for Hodgkin and Sternberg–Reed cells of Hodgkin's disease and a subset of normal lymphoid cells.Nature.1982; 299(5878):65-7.

    5. Indexed at, Google Scholar, Cross Ref

  5. Andreesen R, Osterholz J, Lohr GW, et al. A Hodgkin cell-specific antigen is expressed on a subset of auto-and alloactivated T (helper) lymphoblasts.Blood. 1984; 63(6):1299-302.

    6. Indexed at, Google Scholar, Cross Ref

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