Son SM, et al. J Gastric Cancer. 2024 Dec;25:e2. https://doi.org/10.5230/jgc.2025.25.e2

Kim JH, et al. J Korean Med Sci. 2022 Mar;37(11):e91. https://doi.org/10.3346/jkms.2022.37.e91

PurposeHistologic change is a resistant mechanism in lung cancer. The most common histological change is the switch from adenocarcinoma (AdenoCa) to small cell carcinoma (SCC) against to tyrosine kinase inhibitors (TKI). However, it is not clear whether other treatment modalities are involved in the histologic changes.Materials and MethodsWe investigated histological changes in eight cases, after various treatments, and compared the molecular profiles between primary tumors and changed tumors using exome sequencing where tissue was available.ResultsThree cases of AdenoCa that were changed into SCC retained the initial mutations after TKI and/or surgical treatment. After treatment with TKI and immunotherapy, an EGFR (epidermal growth factor receptor)-mutant AdenoCa changed to squamous cell carcinoma (SqCa). SqCa in a patient treated with surgery was changed into combined AdenoCa and SqCa. These two cases showed the same genetic variations between the two distinct non–small cell carcinomas (NSCC). Three patients experienced two histologic changes, which the changed tumors returned to its original subtype or changed to a combined tumor after treatments. Four cases showed combined histology in the first or second change.ConclusionThe histology of NSCC can be changed to a single pattern or combined subtypes after various treatment modalities, and the phenotypic changes seem not fixed. Therefore, additional morphologic changes may occur regardless of their genetic status and types of treatments. To refine the new treatment strategy, consecutive repeated biopsies in progressive disease or recurrent tumor are necessary.

Rationale: Gangliocytic paraganglioma (GP) is a rare tumor that mostly develops in the duodenum and is composed of the following 3 cell types: epithelioid endocrine, spindle-like, and ganglion-like cells. It manifests as symptoms such as abdominal pain, gastrointestinal bleeding, and weight loss; however, occasionally, it is incidentally detected on endoscopic or radiologic examinations. Although GP is usually benign, it can metastasize to the lymph nodes, and distant metastases have been reported in some cases. Patient concerns: A 46-year-old woman presented with anemia on health surveillance examination. She had no other specific symptoms, and her physical examination did not reveal any abnormal finding. Diagnosis: Endoscopic ultrasound-guided fine-needle aspiration biopsy was performed, and the endoscopist obtained samples from the inner side of the ampullary mass. Pathological examination suggested GP or a neuroendocrine tumor. Interventions: Initially, we planned transduodenal ampullectomy with lymph node excision. However, there was severe fibrosis around the duodenum, and an examination of a frozen biopsy sample from the periduodenal lymph node showed atypical cells in the lymph node. Therefore, we performed pylorus-preserving pancreaticoduodenectomy with lymph node dissection. Outcomes: The final pathological diagnosis was GP located in the ampulla of Vater. The GP showed lymphovascular and perineural invasion and invaded the duodenal wall. Furthermore, 4 out of 18 harvested lymph nodes showed metastasis. Lessons: We described a case of GP confined to the ampulla with regional lymph node metastasis and reviewed published literature on ampullary GP with lymph node metastasis.

Introduction. Nestin, a type VI intermediate filament, is expressed in neuroepithelial cells during embryogenesis and has been expressed in various human tumors. Recent studies reported that the expression was associated with poor prognosis in brain tumors, but the results were inconclusive. In this study, we evaluated usefulness of nestin expression as a prognostic biomarker in consideration of IDH mutation and the World Health Organization (WHO) classification fifth edition. Methods. To investigate nestin expression, immunohistochemistry was performed on 92 adult brain gliomas using tissue microarrays. We analyzed the clinical characteristics and survival outcomes according to nestin expression and examined whether nestin expression alone affects the prognosis, independent of IDH mutation. Results. Sixty patients (65.2%) were nestin-positive (weak and strong). Nestin expression and intensity were significantly correlated with pathologic diagnosis and IDH mutation. The patients with high-grade gliomas showed a higher frequency and stronger intensity of nestin expression than those with low-grade gliomas ( P < .001). The majority (93.6%) of gliomas with IDH mutation showed no expression or weak positivity. Multivariate Cox proportional hazard regression analysis for overall survival demonstrated that nestin expression (weak, hazard ratio [HR] 5.39, P = .036; strong, HR 8.43, P = .007) was an independent prognostic factor. Moreover, patients with nestin-expressing glioma showed shorter survival ( P < .001). Conclusions. Nestin seems to be strongly expressed in the vast majority of glioblastomas, IDH-wildtype and rarely in IDH-mutant gliomas. Clear correlation between nestin expression and pathologic diagnosis makes an accurate patient diagnosis. Expression and intensity of nestin were significantly correlated with worse survival.