Meningiomas are the most common primary central nervous system tumors. Monosomy of chromosome 22 is the most frequently reported genetic abnormality in meningioma and the occurrence of IDH1 mutations in meningioma is exceedingly rare. We report an uncommon case of IDH1 R132H-mutant meningioma. A 69-year-old man presented with two intracranial masses, one of which was identified as an IDH1 R132H-mutant meningioma by next-generation sequencing and further confirmed by pyrosequencing and immunohistochemistry. The rarity of this molecular finding and the potentially favorable prognosis observed in previously reported cases highlight the need for its recognition as a distinct molecular subset. Isocitrate dehydrogenase-targeted therapy may represent a future therapeutic option, pending validation through prospective studies and larger case series.
Silicone lymphadenopathy is an uncommon but well-recognized complication of silicone implant placement resulting from migration of silicone to regional lymph nodes. In patients with prior breast implantation, silicone lymphadenopathy most commonly involves the axillary lymph nodes. Because axillary lymphadenopathy may reflect malignant disease, including metastatic carcinoma, thorough evaluation to exclude neoplasia is essential. Fine-needle aspiration cytology (FNAC) serves as a valuable initial diagnostic modality in the assessment of axillary lymphadenopathy; however, silicone-induced foreign body reactions within lymph nodes may be misinterpreted as metastatic malignancy when silicone lymphadenopathy is not included in the initial differential diagnosis. Herein, a case of axillary silicone lymphadenopathy initially misdiagnosed as metastatic carcinoma on FNAC is presented. This case highlights the importance of recognizing the distinctive cytomorphologic features of silicone lymphadenopathy, which may be sufficiently characteristic to prompt consideration of prior breast implant history during cytopathologic evaluation.
Background The behavior of gastrointestinal stromal tumors varies according to tumor size, location, mitotic rate, and rupture. Traditional mitotic counting in 50 high-power fields (HPF; 5.3 mm2) may overestimate progression risk, as 5 mm2 corresponds to 20–25 HPF under modern microscopy. However, the 50-HPF method remains widely used. This study evaluated the impact of two mitotic counting methods on risk classification and developed a prognostic model combining inflammatory biomarkers with clinicopathological factors. Methods We retrospectively analyzed 150 patients who underwent resection at Songklanagarind Hospital between 2009 and 2021. Patients who had received neoadjuvant therapy or had a second primary cancer were excluded. Mitosis was evaluated using both methods. Clinicopathological and serum biomarker data were collected. The primary outcome was 5-year disease-free or progression-free survival. The model was developed using forward stepwise variable selection based on the time-dependent area under the curve and internally validated by bootstrapping. Results The 50-HPF method overestimated the Armed Forces Institute of Pathology classification in 14.2% of cases. A model incorporating tumor size, location, rupture, mitotic count within 5 mm2, and systemic immune-inflammation index achieved the highest area under the curve of 0.939 in both training and validation sets, outperforming previous models. The 5-mm2 method demonstrated superior performance to the 50-HPF method across all models (0.939 vs. 0.919 for the proposed model). Conclusions Mitotic counting in 50 HPF overestimated risk classification in certain cases. Incorporating systemic immune-inflammation index and using a 5 mm2 mitotic count enhanced prognostic model performance.
Colorectal intramucosal carcinoma (IMC) is considered to carry negligible risk of lymph node metastasis, reflecting the presumed absence of lymphatics within the lamina propria, and current guidelines endorse endoscopic resection alone as curative. We report a 64-year-old man in whom endoscopic submucosal dissection of a lower rectal tumor revealed a well-differentiated IMC with extensive lymphatic invasion confirmed by D2-40 immunostaining. Subsequent laparoscopic ultralow anterior resection showed no residual tumor at the primary site but confirmed metastasis in one of 12 regional lymph nodes. The tumor was microsatellite-stable, epidermal growth factor receptor–positive, and harbored a KRAS codon 13 mutation (G13X). The patient received adjuvant chemoradiotherapy and remained disease-free at 2 years. This case demonstrates that regional lymph node metastasis can occur in colorectal IMC even without conventional adverse histologic features such as poor differentiation or tumor budding, challenging current risk-stratification frameworks and supporting a more cautious approach when lymphatic invasion is identified.
