Cytojournal最新文献

Objective: Cervical cancer ranks as the fourth most prevalent cancer among women globally; it originates in the cervix and has a significant association with human papillomavirus (HPV) infection. The purpose of this study was to investigate the diagnostic utility of cell block (CB) preparations from liquid-based cytology samples in identifying cervical lesions among Turkish patients with HPV. This approach was intended to supplement conventional Pap smear tests and HPV testing.

Material and methods: A retrospective analysis was conducted on 60 HPV-positive cervical smear samples processed through the ThinPrep Pap test. CBs were prepared from liquid-based residues, stained with hematoxylin and eosin, and analyzed. Cytological diagnoses were compared with histopathological findings from colposcopy-guided biopsies. The relationships between the Pap smear, CB, and biopsy results were statistically analyzed.

Results: Pap smear cytology identified 1.6%, 16.6%, 43.3%, and 3.3% as high-grade squamous intraepithelial lesion (HSIL), low-grade squamous intraepithelial lesion (LSIL), atypical squamous cells of undetermined significance, and atypical squamous cells - HSIL cannot be excluded + LSIL, respectively. The CB evaluations classified 6.6% of the samples as cervical intraepithelial neoplasia (CIN)1, 1.6% as CIN2, and 1.6% as squamous cell carcinoma (SCC), with 78.3% deemed negative. Histopathological biopsy revealed CIN1 in 11.7%, CIN2 in 1.7%, and CIN3 in 8.3% of the patients. High concordance was observed between the Pap smear and CB diagnoses for negative and low-grade lesions, although discrepancies occurred in higher-grade lesions. HPV testing revealed 65% high-risk positivity, predominantly for HPV16 and HPV18. Significant correlations were found among HPV subtype positivity, CB, and biopsy diagnosis (P < 0.05).

Conclusion: CB preparations provide enhanced diagnostic accuracy for high-grade lesions and SCC, thus complementing Pap smear cytology and HPV testing. This approach supports their integration into the routine cervical cancer screening protocols in Türkiye. Further global, multicenter studies are recommended to validate these findings.

Objective: Pancreatic cancer is the cancer type with the highest mortality rate worldwide, and despite advances in treatment, molecular biomarkers are needed for both early diagnosis for developing targeted therapies and improving survival rates in this challenging malignancy. In our study, the contributions of programmed death-ligand 1 (PD-L1) expression to the determination of pancreatic cancer subtypes and patient prognosis and its impact on survival were investigated.

Material and methods: Paraffin-embedded tissues from 92 patients diagnosed with pancreatic cancer were included in this study. Tumor-infiltrating lymphocytes (TILs) and lymphocytes in the stromal area within the tumor borders were scored as stromal TILs; lymphocytes in tumor islands were scored as intratumoral TILs. Staining in each area was scored as a percentage, and staining with a score of 5 or more in tumor and immune cells for PD-L1 was scored as positive.

Results: After staining, a score of 5 or more with tPD-L1 staining was used to identify one patient as having micropapillary adenocarcinoma, three patients as having ductal adenocarcinoma, and four patients as having signet ring cell carcinoma. When the clinical parameters and outcomes were compared, a statistically significant difference was found between the histopathologic type of signet ring cell carcinoma and poor differentiation and positivity of PD-L1 expression (P < 0.05). Survival was significantly influenced by tumor location, histopathological subtype, degree of differentiation, PD-L1 expression, and tumor size, with tumor size being the most critical factor (P < 0.05).

Conclusion: Our findings suggest that PD-L1 positivity is notably prevalent in signet ring cell carcinoma of the pancreas and is strongly associated with poor survival outcomes. Given these results, further studies with larger patient cohorts are warranted to validate these observations and explore potential therapeutic implications.

Objective: Ischemia-reperfusion (I-R) injury in the myocardium is a considerable challenge in cardiovascular medicine, posing a severe threat to life. Given that galectin-3 possibly regulates myocardial I-R damage, this study aims to investigate the detailed mechanisms underlying galectin-3's effects on myocardial I-R injury.

Material and methods: The expression levels of galectin-3 in vivo and in vitro myocardial I-R models were determined by Western blot and quantitative real-time polymerase chain reaction. The effects of galectin-3 on inflammatory factors and oxidative stress factors in myocardial I-R were measured with an enzyme-linked immunosorbent assay, and the extent of myocardial tissue damage was assessed using hematoxylin-eosin staining. The influence of galectin-3 on peroxisome proliferator-activated receptor g (PPARg) signaling pathway-related proteins in myocardial I-R was determined by Western blot.

Results: Myocardial I-R damage was associated with increased galectin-3 expression, and the blood levels of creatine kinase-myocardial band and creatine kinase were favorably correlated with the messenger RNA levels of galectin-3 in mice with cardiac I-R damage. The inhibition of galectin-3 alleviated oxidative stress and inflammatory response, and galectin-3 promoted reactive oxygen species production in myocardial I-R cells. Furthermore, the cardiac I-R damage mouse model exhibited decreased expression of proteins linked to the PPARg signaling pathway, but galectin-3 inhibition enhanced the expression of these proteins.

Conclusion: Galectin-3 plays a crucial role in exacerbating myocardial I-R injury, and its up-regulation is associated with increased oxidative stress, inflammatory responses, and inhibition of the protective PPARg signaling pathway. The alleviation of these harmful effects by galectin-3 inhibition suggests that targeting galectin-3 is a potential therapeutic method for reducing myocardial I-R injury.

Objective: Burns refers to a severe form of trauma that often leads to localized and systemic inflammatory responses, oxidative stress, and immune dysfunction. Patients with severe burns are highly susceptible to the development of postburn sepsis, a condition influenced by multiple factors, such as bacterial infection of the burn wound, alterations in immune status, and excessive release of inflammatory mediators. This study aimed to investigate the mechanisms by which hydrogen gas treatment exerts its effects on postburn sepsis, with a focus on its influence on inflammatory responses, oxidative stress, and wound healing.

Material and methods: This work employed in vitro assays with Sprague-Dawley (SD) rat skin fibroblasts (RSFs) to assess the effects of burn serum and hydrogen gas on cell proliferation through methylthiazolyldiphenyltetrazolium bromide assays and on apoptosis through flow cytometry with Annexin V-fluorescein isothiocyanate/propidium iodide staining. In addition, an enzyme-linked immunosorbent assay was performed to quantify inflammatory cytokines and oxidative stress markers in fibroblasts treated with burn serum. Western blotting (WB) analysis was conducted to investigate signaling pathway modulation. The severe burn sepsis models of SD rats were segregated into three experimental groups: a healthy normal control group, a burn sepsis control group, and a burn sepsis + hydrogen gas (2%) treatment group. Wound healing was monitored, with wound contraction rates recorded and histological assessments conducted using hematoxylin and eosin and Masson's trichrome staining to evaluate tissue repair and collagen deposition.

Results: In vitro assays showed that burn serum reduced fibroblast proliferation and increased apoptosis (P < 0.01), which hydrogen gas mitigated by rescuing cell viability and reducing apoptosis (P < 0.01). Enzyme-linked immunosorbent assay revealed burn serum-induced increases in the levels of inflammatory cytokines and oxidative stress markers, with decreases in antioxidant enzymes (P < 0.01), which hydrogen gas reversed (P < 0.05). WB analysis suggested hydrogen gas's anti-inflammatory and proliferative effects by modulating signaling pathways (P < 0.01). In vivo, hydrogen gas treatment considerably improved wound healing, with accelerated contraction and enhanced collagen deposition. Plasma and skin tissue analyses indicated systemic and local anti-inflammatory and antioxidant effects from hydrogen gas.

Conclusion: Hydrogen gas treatment demonstrates potential therapeutic efficacy in the management of postburn sepsis by modulating inflammatory responses, reducing oxidative stress, and promoting wound healing. These findings provide scientific evidence supporting hydrogen gas as an adjunctive treatment strategy for postburn sepsis.

The application of artificial intelligence (AI) in cancer pathology has shown significant potential to enhance diagnostic accuracy, streamline workflows, and support precision oncology. This review examines the current applications of AI across various cancer types, including breast, lung, prostate, and colorectal cancer, where AI aids in tissue classification, mutation detection, and prognostic predictions. The key technologies driving these advancements include machine learning, deep learning, and computer vision, which enable automated analysis of histopathological images and multi-modal data integration. Despite these promising developments, challenges persist, including ensuring data privacy, improving model interpretability, and meeting regulatory standards. Furthermore, this review explores future directions in AI-driven cancer pathology, including real-time diagnostics, explainable AI, and global accessibility, emphasizing the importance of collaboration between AI and pathologists. Addressing these challenges and leveraging AI's full potential could lead to a more efficient, equitable, and personalized approach to cancer care.

Objective: Thyroid nodules are frequently encountered in medical practice. Fine needle aspiration cytology (FNAC) is used to rule out malignant nodules, but few studies have questioned the accuracy of FNAC in larger thyroid nodules compared to smaller ones. We, therefore, aim to compare the diagnostic performance of FNAC based on nodule size and whether larger nodule size increases the possibility of obtaining indeterminate or non-diagnostic results.

Material and methods: Adult patients with thyroid nodules who underwent thyroid biopsy and surgery from 2016 to 2022 were included in the study. We assessed the proportion of benign, malignant, indeterminate, and non-diagnostic FNAC in relation to the nodule size. We then divided cytology into true positive (malignant FNAC and histology), and true negative (benign FNAC and histology) and examined whether the proportion of true FNAC would be affected by different thyroid nodule cutoffs. The study used mean and frequency to describe continuous and categorical variables. t-test and Chi-square tests were used to compare statistics.

Results: Three hundred and forty-five patients were included in the study. The majority were female (86.7%) and older than 40 years. Half had a benign histology; the other 50% were malignant. The majority (49.3%) had indeterminate thyroid cytology. The proportion of indeterminate or non-diagnostic FNAC was the same (58%) in nodules ≥4 cm and <4 cm. The proportion of true FNAC was similar between different nodule size categories. It was 35% in ≥4 cm, and 34.3% in <4 cm nodules.

Conclusion: The study found that the diagnostic performance of FNAC in thyroid nodules did not significantly differ based on nodule size, with similar rates of indeterminate or non-diagnostic results across different size categories. The proportion of true positive FNAC results also remained consistent regardless of nodule size.

Objective: This study investigates the diagnostic concordance between bronchoalveolar lavage (BAL) cytology and the histologic analysis of transbronchial lung biopsy (TBLB) specimens in patients with suspected pulmonary diseases to highlight the strengths and limitations of these complementary diagnostic tools.

Material and methods: We conducted a comprehensive retrospective cross-sectional analysis on patients suspected of pulmonary diseases who underwent both BAL and TBLB from 2018 to 2022. We assessed diagnostic agreement using kappa statistics and calculated the overall concordance rates. The analysis was stratified based on malignant versus infectious etiologies to elucidate performance differences between the two methods.

Results: Our study included a cohort of 189 patients, comprising 104 individuals with suspected malignancy and 85 with suspected infections. Among the malignancy group, BAL yielded positive results for cancer in 49 patients, whereas TBLB confirmed malignancy in 64 patients, demonstrating an overall agreement of 70.19% (kappa = 0.52, 95% confidence interval [CI]: 0.38-0.66). Conversely, within the infectious cohort, BAL identified micro-organisms in only five patients, while TBLB diagnosed infection in 22 patients, achieving an overall agreement of 77.65% (kappa = 0.29, 95% CI: 0.17-0.41).

Conclusion: Our findings underscore the critical role of BAL cytology in the diagnosis of pulmonary carcinoma and infectious processes while also revealing its limitations in detecting interstitial lung diseases. The TBLB procedure emerges as an indispensable technique for accurate histopathological evaluation in lung cancer diagnostics. The integration of BAL and TBLB not only enhances diagnostic yield but also provides a more comprehensive understanding of pulmonary pathologies. Notably, we found moderate agreement between BAL and TBLB in neoplastic cases and fair agreement in non-neoplastic conditions, suggesting a nuanced interplay between these methodologies that could inform clinical practice and improve patient outcomes. This study advocates a combined approach in diagnostic frameworks to optimize the management of patients with suspected pulmonary diseases, paving the way for more precise and effective diagnoses in the field of cytology.

The mainstay of treatment for ovarian cancer is surgery. To prevent under-treatment and overtreatment and to choose the best surgical strategy for patients with ovarian tumors, intraoperative pathological assessment is essential. Frozen sections (FSs) have been historically used for intraoperative evaluation. In 1927, cytology was introduced by Dudgeon and Patrick as a new method of intraoperative pathological examination. Diagnosis can be made in minutes by making smears from the lesion, staining them quickly, and analyzing them under a microscope. Following a comprehensive search of the literature, using pertinent keywords in PubMed, and reviewing the data, it was discovered that intraoperative cytology (IOC) had been reported to have a diagnostic accuracy in ovarian lesions comparable to that of FSs. Few of the studies have confirmed that IOC has several benefits over FSs. There are drawbacks as well, which one should be mindful of. In this review, every aspect that is connected to IOC is covered in detail, along with the potential for raising the standard of IOC to make it more applicable in the present times.

Objective: Idiopathic pulmonary fibrosis (PF) is a chronic and life-threatening lung disease. This study aimed to investigate the role of zinc finger and BTB domain containing 16 (Zbtb16), a transcription factor, in the progression of PF by analyzing its expression and regulatory effects in mouse and cell models.

Material and methods: The gene expression profiles in bleomycin-induced (BL-I) PF lung tissues of mice were analyzed using the gene expression omnibus database. The mouse model of BL-I PF and cell model of transforming growth factor-β1 (TGF-β1)-induced mice lung epithelial cell (LEC) fibrosis was constructed. Zbtb16 expression was evaluated by reverse transcription quantitative polymerase chain reaction, Western blot, or immunohistochemistry. Tissue sections were assessed by hematoxylin and eosin, Masson, and terminal deoxynucleotidyl transferase dUTP nick-end labeling staining. The levels of protein, inflammation factors, and albumin were measured through Western blot or enzyme-linked immunosorbent assay.

Results: Bioinformatics analysis found that Zbtb16 was the highest differentially expressed marker in BL-I PF mice. Zbtb16 was highly expressed in the mice and cell model. Zbtb16 silencing could reduce lung tissues' collagen deposition, pulmonary edema, and pulmonary apoptotic cells; improve vascular permeability; and decrease fibrosis markers and inflammation factors expressed in model mice. Zbtb16 silencing could reduce fibrosis markers and inflammation factor levels in the cell model (P < 0.05). Kyoto encyclopedia of genes and genomes and gene set enrichment analyses suggested that Zbtb16 might regulate BL-I PF in mice through the phosphoinositide 3-kinases (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway (PAmT-P). Co-immunoprecipitation showed the combination of AKT and Zbtb16. PAmT-P in the mice model and cell model was visibly activated (P < 0.05), and Zbtb16 silencing could inhibit it (P < 0.05). Moreover, the rescue experiments showed that the AKT activator SC79 could reverse the effect of TGF-β1 + small interfere RNA-Zbtb16 on LECs.

Conclusion: This study identified Zbtb16 as a key regulator of PF progression, mediating its effects through the PAmT-P. Zbtb16 silencing alleviated fibrosis and inflammation in vivo and in vitro, providing a promising target for therapeutic intervention in PF.

Objective: Matrix Gla protein (MGP) has been found to be strongly associated with cancer progression. However, its role in intrahepatic cholangiocarcinoma (ICC) remains unclear, particularly within the tumor immune microenvironment. MGP may promote immune evasion by activating the nuclear factor-kappa-light-chain-enha ncer of activated B-cells (NF-κB) signaling pathway, which increases the expression of programmed death-ligand 1 (PD-L1) and contributes to CD8⁺ T-cell exhaustion. This research mainly aims to examine the regulatory role of MGP in immune evasion in ICC.

Material and methods: ICC xenograft mouse models and human ICC cell line (HuCCT1) cell models were established to evaluate MGP expression patterns. MGP knockdown or overexpression in HuCCT1 cells was co-incubated with antigen-specific CD8⁺ T cells, and flow cytometry was used to detect markers of CD8⁺ T-cell exhaustion. The effects of MGP modulation on PD-L1 expression were assessed by immunohistochemistry and immunofluorescence. Western blotting was employed to analyze the impact on NF-κB signaling. In addition, MGP overexpression and p65 knockdown in HuCCT1 cells were co-transfected to study their combined effects on PD-L1 expression and CD8⁺ T-cell exhaustion markers. Cell proliferation and apoptosis were evaluated through colony formation assays and flow cytometry.

Results: Compared to adjacent tissues and human intrahepatic cholangiocellular epithelial cells, MGP was significantly overexpressed in ICC tumor tissues and HuCCT1 cells (P < 0.001). MGP overexpression led to NF-κB signaling phosphorylation (P < 0.001), elevated PD-L1 expression (P < 0.001), and heightened levels of CD8⁺ T-cell exhaustion markers (P < 0.001). Conversely, p65 knockdown mitigated the effects of MGP overexpression on HuCCT1 cell proliferation (P < 0.01) and CD8⁺ T-cell exhaustion (P < 0.01 and P < 0.001), while also significantly reducing PD-L1 expression (P < 0.01).

Conclusions: MGP promotes CD8⁺ T-cell exhaustion and facilitates immune evasion in ICC through NF-κB pathway activation.