Besides classic tobacco and alcohol risk factors, human papillomavirus (HPV) plays a role in the development of a subset of head and neck squamous cell carcinomas (HNSCCs), and notably oropharynx squamous cell carcinomas (OPSCCs). HPV-induced OPSCCs have a different biological behavior and a better prognosis compared to non-HPV-induced OPSCCs and the eighth-edition TNM classification now separates these two entities. Therefore, determining the HPV status of patients with OPSCC is now essential for treatment, prognosis, and development of clinical trials. In this review, after reminding essential steps of HPV implication in the cell cycle, we describe the existing tools that are currently feasible in routine practice according to facilities available in health structures, with their benefits and drawbacks: HPV PCR, E6/E7 mRNA RT-PCR, E6/E7 mRNA in situ hybridization, HPV DNA in situ hybridization, and P16 immunochemistry. Besides these traditional HPV detection tools, novel diagnostic approaches are being evaluated for HPV-induced OPSCC "ultrastaging." E6 humoral response and ddPCR-detecting HPVct DNA are two techniques performed on blood and are therefore non-invasive. Baseline E6 humoral levels could have a prognostic value, and HPVct DNA could be helpful for HPV OPSCC recurrence monitoring. At last, next-generation sequencing (NGS)-based "capture HPV" is a technique feasible on biopsies and circulating DNA material. It helps characterize HPV integration status and sites, and it could define prognostic subgroups in HPV-induced OPSCC. These novel precision detection tools could be further integrated in the care of patients with HPV-induced OPSCC.
Five to 10% of desmoid-type fibromatosis (DF) arise in the context of familial adenomatous polyposis (FAP). The beta-catenin gene (CTNNB1) exon 3 mutations are found in 90% of DF (except those associated with FAP) in two codonscodon 41 (p.T41A) and codon 45 (p.S45F and p.S45P) which are serine and threonine phosphorylation sites required for beta-catenin degradation. Mutations p.S45F are associated with a higher risk of recurrence. Among 64 patients with DF and documented CTNNB1 mutational status treated with oral weekly vinorelbine for 6 months, p.S45F or p.S45P mutations were associated with longer time to treatment failure compared to p.T41A or wild type tumors (HR : 2.78, 95%CI: 1.23-6.27), p = 0.04. The functional impact of codons 41 and 45 mutations is certainly different, since the phosphorylation of amino acid 45 targeted by casein kinase-1 serves as a priming phosphorylation for GSK-3β targeting the amino acid 41. Research.
Introduction
Chemotherapy, particularly oxaliplatin, has been associated with the development of focal nodular hyperplasia (FNH). Imaging diagnosis of FNH is well standardized, but it can be misdiagnosed as liver metastasis. The aim of this study was to describe the pathological features of FNH occurring after systemic chemotherapy.
Materials and methods
From our pathological files for 1990‐2021, we retrieved 15 cases of resected newly developed FNH in adults with liver metastasis treated with systemic chemotherapy. Pathological features of FNH nodules and non‐tumoral liver samples were reviewed.
Results
In 11/15 (73%) cases, FNH developed after an oxaliplatin‐based regimen. The median interval from the beginning of chemotherapy to the FNH diagnosis was 15 months. FNH was unique in 11 (73%) cases, and the median size of nodules was 1.1 cm [range 0.5‐2.5]. Histologically, 9 (60%), 11 (73%) and 11 (73%) cases exhibited fibrous central scar, dystrophic vessels and ductular proliferation, respectively, with all three criteria present in five (33%) cases. Eight (53%) cases showed intralesional steatosis and nine (60%) cases showed a glutamine synthetase immunostaining map‐like pattern. In non‐tumoral liver, eight (53%) cases exhibited sinusoidal obstruction syndrome and four (27%) nodular regenerative hyperplasia.
Conclusion
The occurrence of FNH after systemic chemotherapy is an emerging condition challenging the imaging diagnosis because typical morphological features are frequently missing. The presence of sinusoidal changes, including regenerative hyperplasia, in non‐tumoral liver supports the potential role of chemotherapy in the pathogenesis of FNH.
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