From This Month's Histopathology

Abstract

‘Our study showed a 4.6% incidence of FH loss of expression in uterine leiomyomas from patients aged less than 30 years. Importantly, we found 86% of FH-negative tumours detected by IHC harboured FH mutations, 50% of which contained a germline mutation. While genetic mutations confer a loss of expression, epigenetic regulation of the FH gene appears to be unrelated to protein expression.’ Immunohistochemistry for FH reveals loss-of-expression pattern with an arrow indicating an internal positive control. Liu et al. (p. 354) ‘In summary, this study confirmed the presence of POLE mutations in microsatellite-stable CRC and provides a better understanding of the link between mutation burden and intratumoural immune response in these hypermutated tumours. The characterisation of MMR-intact CRCs based on features such as histological subtype or tumour-infiltrating lymphocytes could help to triage CRC for POLE mutation testing, especially given the prognostic and therapeutic implications of POLE mutations and IMMUNOSCORE in colorectal carcinoma.’ Increased tumour-infiltrating lymphocytes in a POLE mutated tumour. Forgo et al. p. 366 ‘Nuclear pan-Trk IHC positivity is highly specific for NTRK3 fusion and for SC of the salivary gland, permitting its use as an adjunct tool in clinical diagnosis. On the other hand, any pan-Trk immunopositivity seems to be highly sensitive for NTRK3 fusion, showing a sensitivity of 100% and a positive predictive value of 87%. Therefore, pan- Trk IHC may be utilised as a screening tool to select patients who can undergo NTRK3 molecular testing to determine eligibility for clinical trials.’ A Secretory carcinoma showing pan-Trk immunopositivity, with both nuclear and cytoplasmic staining. Xu et al. (p. 375) ‘We have highlighted the clinicopathological features of a large cohort of pyloric gland adenomas arising in the duodenum. We have shown that larger lesions and those with tubulovillous architecture are more likely to harbour high-grade dysplasia and invasive carcinoma. The low rate of recurrence suggests that local endoscopic removal, when feasible, is an appropriate treatment strategy.’ Pyloric gland adenoma with high-grade dysplasia showing tubulovillous architecture. Miller et al. (p. 404) ‘In conclusion, this retrospective study shows that TB is associated with various adverse clinicopathological features and patient outcomes. The current results are similar to the data from other malignancies and confirm the value of TB assessment in GC. The authors suggest that the recommendations of ITBCC can now also be applied for the assessment of TB in GC. TB status should be included in surgical pathology reports of GC (regardless of the count of tumour buds), as it provides valuable prognostic information readily available on H&E-stained tissue sections. The assessment of TB in GCs after neoadjuvant treatment is not recommended. Larger studies regarding TB in early invasive GCs should be designed to help in stratifying patients into low- and high-risk groups and in choosing optimal treatment methods.’ Kaplan–Meier curve demonstrating association between tumour budding and tumour specific survival (B, P < 0.001). Ulase et al. (p. 433) ‘In conclusion, hepatobiliary irAEs caused by pembrolizumab and atezolizumab shared microscopic features of those caused by nivolumab and ipilimumab, including predominantly lobular injury with many CD8+ lymphocytes. In addition, sclerosing cholangitis, granulomatous hepatitis or bland cholestasis were observed in ~50% of cases, suggesting that diverse histological changes may emerge in liver tissue in response to blockage of the PD-1–PD-L1 interaction.’ Bile duct injury secondary to pembrolizumab with many CD8+ cells observed, some infiltrating into the epithelial layer. Zen et al. (p. 470)