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OBJECTIVE: Colon cancer is a primary human cancer that accounts for approximately one-tenth of all cancers and is one of the three most common cancers in incidence and mortality. This study investigated the relationship between serum preoperative carcinoembryonic antigen (CEA) and carbohydrate antigen 19-9 (CA19-9), patient characteristics and lymph node (LND) involvement in early-stage colon cancer. PATIENTS AND METHODS: A total of 154 patients who had undergone surgery for early-stage colon cancer were included in this study. Patient demographics regarding age and gender, laboratory parameters, tumor size, and tumor laterality were recorded. CEA and CA19-9 positivity was defined as patients whose tumor markers were above the cut-off values, and patients were grouped according to CEA and CA19-9 positivity. Patients were compared according to the CEA and CA19-9 status and pathological LND involvement. RESULTS: We found that patients in the CEA (+) and CA19-9 (+) groups were significantly older than the others. Our study detected LND involvement in histopathological examination in 25% of patients. LND pathological participation was significantly higher in the CEA (+) CA19-9 (+) group, and being age 65 years or older was found to be a risk factor for pathological LND involvement. CONCLUSIONS: Clinicians should pay more attention to LND involvement when both CEA and CA19-9 are elevated preoperatively in early-stage colon cancer patients. Preoperative CEA and CA19-9 status of patients is important in predicting LND involvement and, as a result, the prognosis of these patients. [ABSTRACT FROM AUTHOR]

Summary: Background: Behçet disease (BD) presents with lymphocytic and neutrophilic vasculitis of unknown aetiology. HLA‐B*51, the endoplasmic reticulum aminopeptidase 1 (ERAP1), and interleukin 23 receptor (IL23R)/IL12R are genetic risk factors. IL‐23 regulates IL‐17A, which controls the recruitment and activation of neutrophils. Objectives: To determine pathological changes in BD skin lesions related to the complex genetic predisposition. Methods: We characterized the expression of IL‐17A and IL‐23A in various cell types by immunohistological double staining of sections from papulopustular skin lesions of acute attacks of BD and psoriasis vulgaris lesions, another HLA‐class I‐associated T‐cell‐mediated autoimmune disease in which excessive T‐cell‐derived IL‐17A production promotes neutrophil activation. Results: We found that in BD lesions, as in psoriasis, actively expanding CD8+ T cells were the predominant source of IL‐17A. IL‐17A+ CD8+ T (Tc17) cells outnumbered infiltrating IL‐17A+ CD4+ T cells. Unlike the epidermal localization of CD8+ T cells in psoriasis, Tc17 cells in BD lesions mainly infiltrated the perivascular tissue and the blood vessel walls of dermis and subcutaneous tissue. They co‐localised with a marked IL‐23A expression by CD11c+ dendritic cells and CD68+ macrophages. IL‐17A expression was associated with extensive recruitment of neutrophils around blood vessels that formed neutrophil extracellular traps (NETs). Conclusions: In BD, the genetic predisposition may mediate antigen‐specific activation and differentiation of a Tc17 response, possibly targeting endothelial (auto)antigens. Neutrophils recruited by IL‐17A in this process may enhance tissue damage by extensive NET formation (NETosis). Thus, the IL‐23/IL‐17 axis presumably controls neutrophilic inflammation in BD vasculitis in the context of a predominant antigen‐specific CD8+ T‐cell response. What is already known about this topic? Behçet disease (BD) is a systemic vasculitis of unknown aetiology.HLA‐B*51 and the endoplasmic reticulum aminopeptidase 1(ERAP1), which cooperate in antigen processing and presentation to CD8+ T cells, and interleukin 23 receptor(IL23R)/IL12R are the main risk genes.IL‐17A is thought as a key cytokine in BD, which is produced under the control of IL‐23 and activates neutrophils. What does this study add? As a clinical correlate of the risk association with HLA‐B*51, ERAP1, and IL23R/IL12R, activated CD8+ T cells in the acute papulopustular skin lesions of BD massively express IL‐17A under the control of IL‐23A, which is expressed mainly by CD11c+ dendritic cells with a histiocytic morphology.Lymphocytic vasculitis by IL‐17A+ CD8+ T (Tc17) cells in BD presumably mediates neutrophil recruitment and prominent neutrophil extracellular trap (NET) release.These data reveal that, as in psoriasis, potentially autoreactive CD8+ T cells with marked IL‐17A production play an important pathogenic role in BD. What is the translational message? The results may link three major BD risk genes in a pathogenic concept, in which HLA‐B*51‐restricted endoplasmic reticulum aminopeptidase 1‐dependent antigens activate a CD8+ T‐cell response whose IL‐17A production is enhanced by an IL‐23R risk variant, leading to neutrophil recruitment and NET formation (NETosis).These findings may inspire therapeutic interventions targeting the IL‐17/IL‐23 axis or NETosis to resolve or suppress attacks of BD. An IL‐23‐driven Tc17 response dominates in skin lesions of Behcet's disease. Plain language summary available online [ABSTRACT FROM AUTHOR]

Pleuropulmonary blastoma (PPB) is a potentially aggressive, rare childhood neoplasia. We investigated histopathological features, survival, and DICER1 hotspot mutations among PPB patients. Archive records at our institution were reviewed, covering a 20-year period. Thirteen children (6 males and 7 females) with a mean age of 30.5 (range 6–83) months were included. The tumor subtypes were type I in 6 (46%), type II in 4 (31%), and type III in 3 (23%). Only tumors with type II and type III histology showed anaplasia (4/7, 57%). Median follow-up was 28 (range 9–216) months. Three-year overall survival rate was 83.3% and 3-year progression-free survival rate was 25%. Progression was seen in 60% (3/5) of type I and 66.7% (4/6) of type II and type III cases. Two patients died of disseminated disease at 9 and 44 months. Hotspot missense mutations on DICER1 gene were detected in all 11 patients with available tumor tissue. We found an additional novel germline loss-of-function mutation (c.5436dupT; p.E1813*) in 1 case. To the best of our knowledge, this is the first study to investigate hotspot missense mutations on DICER1 gene among the largest series of Turkish children with PPB. [ABSTRACT FROM AUTHOR]