The p53 protein is a tumor-suppressing transcription factor that is critical in tumorigenesis. While TP53 mutations are rare in differentiated thyroid cancer (DTC), they are significantly more common in anaplastic thyroid cancer (ATC). This study presents original results and a meta-analysis reevaluating the prognostic value of TP53 mutations in thyroid cancer, including surrogate markers such as immunohistochemical p53 expression and serum p53-Abs levels. TP53 mutations were analyzed using SSSP and direct sequencing in a DTC group (15 patients), an ATC group (3 patients), and a control group (25 patients). The immunohistochemical p53 expression was assessed in tissue samples. A meta-analysis of 14 eligible studies identified through the PubMed, Scopus, Google Scholar, and Cochrane databases was conducted. Our results showed TP53 mutations in all ATC cases, 6.67% of DTC cases (1 out of 15), and none in the control group. Immunohistochemical p53 overexpression was observed in 4 out of 15 DTC (26.67%) and all ATC cases but absent in controls. A meta-analysis confirmed that TP53 mutations are significantly more frequent in ATC than controls (OR 8.95; 95% CI: 1.36–58.70; p = 0.02) but not in DTC vs. controls (OR 1.87; 95% CI: 0.53–6.58; p = 0.33). p53 overexpression was significantly higher in both DTC and ATC vs. controls (OR 7.99; 95% CI: 5.11–12.51; p < 0.01 and OR 64.37; 95% CI: 27.28–151.89; p < 0.01, respectively). The serum p53-Abs positivity was also elevated in patients with PTC vs. controls (OR 2.07; 95% CI: 1.24–3.47; p < 0.01). TP53 mutations are frequent events in the pathogenesis of ATC. In DTC, further prospective studies are needed to determine the prognostic value of TP53 mutations and related surrogate markers (immunohistochemical p53 expression, p53-Abs positivity).

Background/Objectives: Prognostic assessment in endometrial cancer (EC) is based on clinical and pathological features such as histological type, FIGO stage, tumor grade, LVSI, P53 status, and hormone receptor expression. Recent molecular research has distinguished four EC subtypes, with MMR status (pMMR vs. dMMR) providing clinically relevant stratification due to its predictive value for immunotherapy. The present study aims to compare dMMR and pMMR tumors in terms of the prevalence of adverse histopathological prognostic factors. Methods: This retrospective study included 179 patients with endometrioid endometrial carcinoma (EEC) treated at the authors’ institution (1 January 2023–31 August 2025). Patients were classified by MMR status (pMMR vs. dMMR) based on immunohistochemistry, and clinicopathological variables, including FIGO stage, myometrial invasion depth, tumor grade, LVSI, ER/PR expression, and P53 status, were analyzed. Normality was assessed using the Shapiro–Wilk test. Categorical variables were tested with chi-square or Fisher’s exact tests, reporting odds ratios with 95% CI, while continuous variables were compared using the Mann–Whitney test and presented as median (IQR) with the Hodges–Lehmann difference and 95% CI. Multivariable logistic regression with Wald tests was performed. Results: dMMR tumors accounted for 29.05% of all cases. Patients in the dMMR group were significantly more likely to present with FIGO stage III/IV disease (p = 0.036) and to exhibit LVSI (p = 0.008). No differences were observed between the groups with respect to tumor grade, estrogen receptor positivity, progesterone receptor positivity, or the prevalence of deep myometrial invasion. The most frequent pattern of protein loss in the dMMR population was concurrent loss of MLH1 and PMS2. Conclusions: In the studied population, dMMR tumors more frequently exhibited adverse prognostic features of EC, such as advanced stage of disease and lymphovascular space invasion. This suggests the potential for effective immunotherapy in this patient group.

Background: Chronic antibody-mediated rejection (cAMR) constitutes a serious challenge in the long-term success of organ transplantation. It is associated with donor-specific antibodies (DSAs) which activate a complement pathway in response to the presence of human leukocyte antigens (HLAs) on the graft, which results in chronic inflammation and leads to graft dysfunction. One of the recent promising methods of cAMR treatment is a recombinant humanized anti-interleukin-6 receptor (IL-6R) monoclonal antibody referred to as Tocilizumab (TCZ). The aim of the presented systematic review is to explore the existing knowledge regarding the effect of tocilizumab treatment on cAMR and to perform a meta-analysis of the available data. Methods: A systematic review was performed using the PRISMA 2020 Checklist and Flow diagram. A systematic review protocol was registered in PROSPERO: CRD42024510996. The bias assessment was obtained with Methodical Index for Non-Randomized Studies (MINORS), whereas meta-analysis was performed using MedCalc. Results: Five clinical trials with a total number of 105 patients were included in our review. The mean loss of eGFR in time was −0.141 mL/min/1.73 m² (95% CI: −0.409 to 0.126; p = 0.298) and was found to be statistically insignificant. The heterogeneity was low and was equal to I² = 0.00%. The authors demonstrated a reduction in DSA titer by TCZ (−0.266 MFI (95% CI: −0.861 to 0.329; p = 0.377)). In the majority of studies, eGFR stabilization was associated with a reduction in DSAs. Conclusions: TCZ pharmacotherapy insignificantly reduced DSA titer and eGFR. Despite promising outcomes of potential eGFR stabilization, there is a need for large randomized controlled trials comparing standard management of cAMR and tocilizumab treatment.

Background: Identification of high-risk patients with endometrial cancer (EC) remains challenging despite advances in molecular profiling. Methods: We comprehensively analyzed the RNA expression of 18 amino acid transporters (AATs) in 373 EC samples from The Cancer Genome Atlas (TCGA). Results: Our clustering analysis based on AAT expression identified a patient group with a significantly worse prognosis. Sideroflexin family (SFXN1, SFXN5), glutamine (SLC38A1, SLC38A3), glycine (SLC6A9) transporters, and the heavy-chain subunit of heteromeric AATs (SLC3A2) were elevated in poorly differentiated tumors. In contrast, the transporter of small neutral amino acids (SLC1A4) and proline/imino-acid transporter (SLC6A20) were enriched in lower-grade disease. SFXN1 and SLC38A1 were also higher in advanced (III/IV) FIGO stages. AAT expression differed across molecular subtypes, with SFXN5, SLC38A1, SLC38A3, and SLC3A2 associated with the copy-number-high profile. In survival analysis, we demonstrated that SLC38A3, SFXN4, and SLC3A2 were associated with shorter disease-free survival, and SLC38A1, SLC38A3, and SFXN1 with worse overall survival, whereas SLC1A4, SLC6A20, and the taurine transporter (SLC6A6) were related to favorable outcomes. Conclusions: These findings highlight AAT expression as a potential marker of EC aggressiveness and prognosis and suggest that integrating metabolic features with molecular classification may improve risk stratification and identify potential therapeutic targets.