This is a high-magnification histopathology image of a gastrointestinal stromal tumor (GIST) showing a spindle cell-dominant morphology. Tissue is examined by light microscopy after Hematoxylin and Eosin staining, at ×400 magnification, highlighting elongated, fusiform cells arranged in intersecting fascicles with ovoid to elongated nuclei and eosinophilic cytoplasm. The stroma appears fibrous to lightly myxoid, with preserved cellular detail and minimal necrosis in this field. The spindle cell population is characteristic of many GISTs and supports a mesenchymal neoplasm of the gastrointestinal tract. In clinical practice, GISTs commonly harbor activating mutations in the c-KIT (CD117) gene in about 80% of cases or in PDGFRA (~8%), leading to constitutive tyrosine kinase signaling. Immunohistochemical CD117 positivity is a key diagnostic surrogate; DOG1 is frequently positive and may aid in challenging cases. Accurate molecular testing for c-KIT and PDGFRA mutations informs prognosis and eligibility for targeted therapy with tyrosine kinase inhibitors such as imatinib. This image serves as a reference for recognizing spindle cell GIST histology, differentiating it from smooth muscle or neural tumors, and illustrating how morphology guides ancillary testing, mutation profiling, and therapeutic decision-making in gastroenterology oncology and surgical pathology. This education-oriented caption emphasizes diagnostic workflow and targeted therapy implications for practice.

Gross pathology photograph of a resected gastric tumor illustrating the classic appearance of a gastrointestinal stromal tumor (GIST). The specimen demonstrates a solitary, well‑circumscribed, fleshy mass arising within the gastric wall, typically submucosal with a tan-yellow cut surface and occasional surface hemorrhage or focal necrosis. Gastric GISTs represent the most common mesenchymal neoplasms of the abdomen, with a predominance in the stomach (>50%), and most patients presenting in the sixth decade; pediatric cases are rare and may occur in the context of Carney triad. On gross examination, lesions are often exophytic or intraluminal and may appear as encapsulated nodules or plaque‑like thickenings. Definitive diagnosis requires microscopic evaluation and immunohistochemistry, including positivity for KIT (CD117) and DOG1, with variable spindle or epithelioid cell morphology and mitotic activity guiding risk stratification. The illustrated tumor’s solitary, well‑defined margins are consistent with a resectable, localized GIST, but differentiation from other submucosal spindle cell tumors (leiomyoma, leiomyosarcoma, schwannoma) relies on histology and immunophenotyping. Clinically, GISTs demand surgical excision and targeted therapy in select cases, and prognosis depends on size, mitotic rate, location, and rupture risk. This image is valuable for surgical pathology education, gross pathology training, and radiology–pathology correlation discussions.

Immunohistochemical slide of a gastrointestinal stromal tumor (GIST) showing robust cytoplasmic/membranous brown staining on a hematoxylin counterstain background. The image likely represents a tissue section stained for CD117 (c-KIT) and/or DOG1, markers that confer high sensitivity and specificity for GIST. In this field, CD34 may be variably positive and SMA positivity can be focal, complicating differential diagnosis with leiomyosarcoma. The tissue is FFPE, sectioned at 4 μm, and stained with DAB chromogen to yield brown immunoreactivity. The tumor cells display spindle-cell morphology in fascicles embedded in a collagenous stroma; nuclei are ovoid to elongated with variable mitotic activity. The immunophenotype—predominant CD117 (c-KIT) and DOG1 positivity—supports the diagnosis of GIST, with DOG1 often providing superior specificity. The combined histology and IHC pattern differentiates GIST from smooth muscle and neural neoplasms. Clinically, this immunoprofile directs targeted therapy options (tyrosine kinase inhibitors such as imatinib or sunitinib) and informs mutational testing for KIT or PDGFRA to predict treatment response. This image is valuable for education in oncologic pathology, GI pathology, and diagnostic immunohistochemistry, illustrating how a mesenchymal GI tumor is identified by characteristic immunostains. It is suitable as a reference for immunophenotype, differential diagnosis, and molecular correlation in GIST research and teaching.

This is a light-m microscopy histopathology image of a gastrointestinal stromal tumor (GIST) in spindle cell form. The tissue shows spindle-shaped cells arranged in broad fascicles within a loose to moderate stroma. Nuclei are elongated with minimal pleomorphism and cytoplasm is eosinophilic to lightly basophilic; mitotic figures may be scarce in the depicted field. The overall pattern is classic for spindle cell GIST, which arises from interstitial cells of Cajal and can differentiate along smooth muscle or neural lines, though the image itself does not display immunohistochemical markers. Clinically, GISTs are most commonly located in the stomach or small intestine and require confirmation with immunostains such as KIT (CD117) and DOG1; CD34 is variably positive. The diagnostic significance lies in distinguishing GIST from other spindle cell GI tumors (e.g., leiomyosarcoma, schwannoma). Differential diagnoses include leiomyosarcoma, schwannoma, desmoid-type fibromatosis, and fibrosarcoma. Once confirmed, treatment typically involves surgical resection with adjuvant/targeted therapy guided by mutation status (e.g., imatinib for KIT/PDGFRA mutations). This image is relevant for educational discussions of GIST histology, spindle cell morphology, and differential diagnosis in GI pathology.

A composite clinical and diagnostic image set illustrating a case of metastatic paraganglioma with succinate dehydrogenase (SDH) deficiency. (A) Axial CT scan of the thorax shows an expansile, lytic-appearing metastatic deposit in the left 8th rib (indicated by a white arrow). (B) Axial 18F-FDG PET/CT fusion image demonstrates intense radiotracer uptake (avidity) at the site of the left rib lesion, indicating high glucose metabolism within the tumor. (C) Coronal I131-MIBG whole-body planar scans (anterior and posterior views) show a complete lack of tracer uptake at the rib metastasis site, highlighting the diagnostic limitation of MIBG for certain SDH-deficient neuroendocrine tumors. (D) Photomicrograph of tumor histology with SDHB immunohistochemistry (IHC) staining. The tumor cells show a diffuse loss of granular cytoplasmic staining (immunonegativity), while background stromal elements or internal controls show normal expression. This IHC pattern is a surrogate marker for deficiency in the SDH complex, specifically associated here with a germline SDHA mutation. The images demonstrate the multi-modal diagnostic approach and pathological correlation for evaluating malignant paragangliomas.

This pathophysiology diagram illustrates the post-transcriptional regulation of succinate dehydrogenase (SDH) subunits by specific microRNAs (miRNAs) in the context of cellular metabolism and cancer. The schematic identifies three primary regulatory axes: 1) miRNA-31 targets SDHA-mRNA, influencing reactive oxygen species (ROS) production, mitochondrial membrane potential, and mitochondrial mass. 2) miRNA-378 targets SDHB-mRNA, promoting cell proliferation and a metabolic shift toward glycolysis. 3) miRNA-210 inhibits SDHD-mRNA, leading to alterations in HIF1̧ activity and overall energy metabolism. Each mRNA is depicted with characteristic structural features including a 5' cap and a poly-A (AAA) tail. Upward-pointing arrows within the miRNA circles indicate overexpression, a common clinical finding in certain malignancies or post-radiation states. The diagram highlights how miRNA-mediated silencing of the SDH complex components disrupts the tricarboxylic acid (TCA) cycle and electron transport chain, contributing to metabolic reprogramming and tumor progression.

This composite educational image illustrates the molecular and developmental consequences of Sdhb (Succinate Dehydrogenase Complex Iron-Sulfur Subunit B) deletion in a rat model. Panel A: A scatter plot showing an approximately 50% reduction in Sdhb mRNA relative fold expression in heterozygous (Sdhb+/-) liver tissue compared to wild-type (Sdhb+/+), normalized to a baseline of 1. Panel B: An immunoblot (Western blot) and corresponding densitometric bar graph demonstrating reduced Sdhb protein expression in Sdhb+/- rats compared to Sdhb+/+ controls, using Actin as a loading control. Panel C: A scatter plot quantifying decreased SDH enzyme activity (mOD/min) in Sdhb+/- tissue. Panel D: A clinical macroscopic photograph of opened uteri from 12-day-old gravid rats. The top uterus (Sdhb+/- x Sdhb+/- cross) displays multiple developmentally stalled, smaller, and darker embryos (indicated by black arrows), illustrating the lethal effect of homozygous deletion. The bottom uterus (Sdhb+/+ x Sdhb+/+ cross) shows uniform, healthy embryonic development. This figure highlights the role of Sdhb in mitochondrial function and embryonic viability.