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  1. Strona główna
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Przeglądaj wg Autor "Biesaga, Beata"

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    Membranous E-Cadherin Expression in Different Subtypes of Pituitary Neuroendocrine Tumors and Its Association with Invasiveness
    (MDPI, 2026-03-14) Krzentowska, Anna; Biesaga, Beata; Merklinger-Gruchała, Anna; Gołkowski, Filip
    Pituitary neuroendocrine tumors (PitNETs) are usually benign intracranial neoplasms that may exhibit invasion of the cavernous sinus, complicating surgery and increasing the risk of recurrence. This study aimed to investigate membranous E-cadherin (mE-cad) expression across PitNET subtypes and transcription factor (TF) lineages, including Pit-1 (pituitary-specific positive transcription factor 1), SF-1 (Steroidogenic Factor 1), and TPIT (T-box pituitary transcription factor), and its association with tumor invasiveness in sixty-nine patients. mE-cad expression was evaluated as the percentage of positive cells (0%, 1–10%, >10%) and by immunoreactive score (IRS). Staining intensity was scored as: 0, no staining; 1, weak; 2, moderate; 3, strong. The proportion of positive cells was scored as: 0, none; 1, <10%; 2, 10–50%; 3, 51–80%; 4, >80%. Mean mE-cad expression was 5.2% in gonadotroph, 3.2% in corticotroph, 0.5% in lactotroph, and 17.5% in plurihormonal PitNETs. By TF lineage, the mean expression was 5.3% for Pit-1, 3.2% for TPIT, and 5.1% for SF-1. Low mE-cad expression (IRS 1–2) was associated with higher odds of cavernous sinus invasion compared with IRS 3–6 (adjusted OR = 6.0, 95% CI 1.08–33.4, p = 0.04), independent of tumor volume (adjusted OR = 4.0, 95% CI 1.50–10.7, p = 0.01). After restricting the analysis to the gonadotroph PitNET group, tumors with an IRS of 1–2 showed significantly higher invasiveness compared with those with an IRS of 3–6 (p = 0.012). These findings suggest that mE-cad may serve as a biomarker of PitNET invasiveness, with expression varying according to TF lineage and tumor subtype.
  • Ładowanie...
    Miniatura
    Pozycja
    Peripheral complement C3 and C4 are associated with clinical features of schizophrenia
    (Frontiers, 2026-03-30) Szwajca, Marta; Śmierciak, Natalia; Biesaga, Beata; Donicz, Paulina; Szwajca, Krzysztof; Pilecki, Maciej
    Aim: Schizophrenia is a severe psychiatric disorder with heterogeneous outcomes; factors such as anxiety, childhood trauma, and duration of untreated psychosis (DUP) may influence symptom severity and disease progression. Growing evidence highlights immune dysregulation—particularly alterations in complement components C3 and C4—in the pathophysiology of schizophrenia; however, findings regarding peripheral complement levels and their clinical associations remain inconsistent. Method: Thirty-nine patients with schizophrenia underwent clinical assessment using the Childhood Trauma Questionnaire (CTQ), the Positive and Negative Syndrome Scale (PANSS), the State–Trait Anxiety Inventory (STAI), and the Montreal Cognitive Assessment (MoCA). Serum concentrations of C3 and C4 were measured at admission. Results: In exploratory analyses (nominal p-values), baseline C3 correlated with DUP (r=0.407, p=0.010) and length of hospitalization (r=0.353, p=0.028). Higher C3 was associated with greater symptom severity on PANSS-P1 (r=0.325, p=0.043) and PANSS-G1 (r=0.330, p=0.040), while C4 correlated with PANSSG1 (r=0.322, p=0.045) and multiple PANSS domains after 12 weeks. C3 was associated with anxiety at baseline and after 3 months (STAI-T1: r=0.376, p=0.018; STAI-S1: r=0.372, p=0.020; STAI-T2: r=0.376, p=0.018; STAI-S2: r=0.419, p=0.009), whereas C4 correlated with STAI-T1 (r=0.361, p=0.024), STAI-S1 (r=0.342, p=0.033), and STAI-S2 (r=0.338, p=0.038). Higher C3 and C4 levels were associated with CTQ subscales. C3 correlated negatively with cognitive performance (MoCA1: r=–0.339, p=0.034). However, none of the associations survived Benjamini–Hochberg false discovery rate (BH-FDR) correction (all q>0.05). Conclusion: These exploratory, within-cohort findings suggest that peripheral complement markers relate to variation in clinical severity and illness-course indicators in schizophrenia. Replication in larger, controlled longitudinal studies is warranted.

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