Adenocarcinoma admixed with neuroendocrine carcinoma of the uterine cervix is a rare malignancy with a poor prognosis. In the literature, there are few reported cases. Herein, we report a case of a 56-year-old Turkish woman with cervical adenocarcinoma admixed with small cell neuroendocrine carcinoma. Histological examination of endocervical curettage specimens revealed a tumor composed of almost equal areas of small cell neuroendocrine carcinoma and adenocarcinoma. Neuroendocrine differentiation was confirmed by immunohistochemistry for chromogranin-A, synaptophysin, and CD 56. After the adenocarcinoma and small cell neuroendocrine carcinoma association was detected in the curettage material, both cervicovaginal smear and then total abdominal hysterectomy and bilateral salpingo-oophorectomy resection material of the patient were submitted to our pathology department. Histological features of both curettage and resection material were determined by immunohistochemical studies.

Large cell neuroendocrine carcinoma of the lung is a rare type of lung cancer. There is a limited number of studies on clinical and histopathological characteristics that are effective in survival. The aim of this study was to investigate the relationship between histopathological and clinical characteristics, mainly Ki-67 proliferation index, and survival in patients diagnosed with large cell neuroendocrine carcinoma of the lung. The data of 38 patients followed up with the diagnosis of large cell neuroendocrine carcinoma of the lung were evaluated. The mean Ki-67 value was determined to be 65.8% (±20.8). The patients' clinical characteristics and survival times were compared according to the cut-off value determined for Ki-67 index. When median overall survival times were compared, it was seen that overall survival was numerically lower in patients aged 65 years and over, in tumors located on the right side, in cases who were in the metastatic stage at diagnosis, whose Ki-67 index was 65% and above, who did not receive chemotherapy, who did not undergo curative surgery, and in patients with chronic diseases (p>0.05). In the Kaplan-Meier analysis, the median overall survival was determined to be 22.2 months (95%CI 21.7-22.7) in the patients with Ki-67<65%, while it was found to be 20.3 months (95%CI 4.5-36.2) in the patients with Ki-67≥65% (p=0.351). Our study identified subgroups with decreased survival in large cell neuroendocrine carcinoma of lung patients. Studies including a larger number of patients are needed to identify the prognostic importance of these clinical and histopathological characteristics.

Background: Atypical small acinar proliferation (ASAP) cases typically require rebiopsy, which are invasive and associated with increased risk of complications. Our aim in this study was to determine the importance of laboratory and histological findings and E-26 transformation-specific-related gene (ERG) expression in the diagnosis of malignancy. Methods: Between March 2016 and March 2022, 84 patients who were diagnosed with ASAP on biopsy or rebiopsy were included in the study. Clinical-laboratory features of age, serum prostate-specific antigen level, and histopathological features were compared and included multifocality, number of suspicious acini, nuclear enlargement, nucleolar prominence, hyperchromasia, cytoplasmic amphophilia, luminal amorphous acellular secretion, crystalloid presence, infiltrative appearance, inflammation, atrophy, α-methyl acyl-CoA racemase, p63, and/or high molecular weight cytokeratin were analyzed. In addition, ERG expression was evaluated immunohistochemically. Results: Statistically significant correlation was found between nucleolar prominence, nuclear hyperchromasia, crystalloid presence, infiltrative pattern, and prostate cancer (p < .001). In 19 of 84 cases (22.6%) ERG was positive in the nucleus. Prostate cancer was diagnosed at rebiopsy in 15 of the 19 ERG-positive cases (78.9%). A statistically significant correlation was found between ERG positivity and prostate cancer (p= .002). Conclusions: Our findings suggest that evaluation of these markers during initial transrectal ultrasound biopsies may decrease and prevent unnecessary prostate rebiopsy.

Background/Objectives: Although Ki-67 is not formally incorporated into the grading system of pulmonary neuroendocrine neoplasms (PNENs), it is widely used as an adjunct marker to reflect proliferative activity and support diagnostic stratification. Manual Ki-67 assessment is subject to interobserver variability and methodological limitations. This study aimed to evaluate the reliability and performance of two artificial intelligence (AI)-based image analysis systems in Ki-67 index assessment and to compare their results with expert pathologist evaluation in pulmonary neuroendocrine tumors. Methods: A total of 63 pulmonary neuroendocrine neoplasm cases, including typical carcinoid (n = 29), atypical carcinoid (n = 13), and large cell neuroendocrine carcinoma (n = 21), were retrospectively analyzed. Ki-67 proliferation indices were independently assessed by four pathologists within predefined hotspot regions, counting approximately 2000 tumor cells per case. The same regions were analyzed using two AI-based image analysis systems (Roche uPath Ki-67 and Virasoft Virasight Ki-67). Interobserver agreement among pathologists was evaluated using the intraclass correlation coefficient (ICC), and concordance between manual and AI-based assessments was assessed using Spearman’s correlation and linear regression analyses. To account for potential scanner/platform effects, slides were digitized using two different whole-slide scanners (VENTANA DP^® 600 and Leica Aperio AT2), and color normalization and quality control procedures were applied prior to AI-based analysis. For clinical interpretability, Ki-67 indices were stratified into categorical groups based on tumor subtype-specific thresholds (0–25%: high), and agreement between manual and AI-based categorical scoring was evaluated using Cohen’s kappa coefficient. Results: Among the 63 pulmonary neuroendocrine neoplasm cases, Ki-67 proliferation indices varied across tumor subtypes, with typical carcinoids showing low, atypical carcinoids intermediate, and large cell neuroendocrine carcinomas high proliferative activity. Interobserver agreement among four pathologists was excellent (ICC = 0.998, 95% CI: 0.996–0.998). Strong correlations were observed between manual Ki-67 assessments and AI-derived indices, with Spearman correlation coefficients of 0.961 (95% CI: 0.918–0.982) for Roche AI and 0.904 (95% CI: 0.821–0.949) for Virasoft AI, and 0.926 (95% CI: 0.842–0.968) between the two AI systems. Bland–Altman analyses demonstrated minimal mean differences and most cases within the 95% limits of agreement, indicating high concordance without systematic bias. Categorical agreement analysis, using subtype-specific Ki-67 thresholds (0–25%: high), showed excellent concordance between manual and AI-based scoring (Cohen’s kappa 0.877 for Roche AI and 0.827 for Virasoft AI; p < 0.001), confirming the clinical interpretability and reproducibility of AI-based Ki-67 assessment. Conclusions: AI-based Ki-67 index assessment shows strong concordance with expert pathologist evaluation and reflects biologically relevant differences among pulmonary neuroendocrine neoplasm subtypes. These results suggest that AI-assisted Ki-67 analysis may serve as a reproducible and objective adjunct to routine diagnostic practice in pulmonary neuroendocrine tumors.

Background and Objectives: Non-small-cell lung cancer (NSCLC) often has epidermal growth factor receptor (EGFR) mutations, which are key targets for therapy. EGFR mutation subtypes, especially exon 19 deletions and exon 21 L858R mutations, influence responses to EGFR tyrosine kinase inhibitors (TKIs) and patient survival. Despite progress in TKI treatments, resistance and different responses remain challenges. This study explores the relationship between EGFR mutation subtypes, PD-L1 expression, and patient outcomes after anti-EGFR therapy. Materials and Methods: We studied 176 cases of EGFR mutation-positive NSCLC. Next-generation sequencing was used to analyze EGFR and other mutations, while PD-L1 expression was evaluated through immunohistochemistry. We analyzed EGFR mutation subtypes, PD-L1 status, treatments, and survival outcomes. Results: Among 176 cases, 88.6% were adenocarcinomas. Within the EGFR mutation spectrum, exon 19 deletions were the most common subtype, accounting for 40.9% of cases, followed by the point mutation in exon 21, which occurred in 35.8% of cases. Less frequent alterations, making up 23.3% of all detected mutations, included mutations in exon 18, insertions, and point mutations such as S768I and T790M in exon 20, as well as changes in exon 2, exon 7, and other less frequently affected regions. Exon 19 mutations were associated with older age, female sex, adenocarcinoma, and bone metastasis (p < 0.05). TP53 was the most common concurrent mutation (44.3%). PD-L1 positivity (TPS ≥ 1%) was observed in 48.3%, with high expression (TPS ≥ 50%) in 25.9%. Exon 21 mutations were significantly linked to PD-L1 negativity (p = 0.008). The median overall survival was longest with TKI therapy (51 months), and this was also observed in PD-L1-positive patients, although the difference was not statistically significant. The median progression-free survival for patients treated with TKIs and those with EGFR mutations was 14 months. PD-L1-positive patients receiving TKIs had significantly longer survival than those who did not (51 vs. 17 months, p = 0.003). Conclusions: EGFR mutation subtypes and PD-L1 expression seem to affect treatment outcomes and survival in NSCLC. The observed links emphasize the potential value of combining molecular and immunological markers to guide therapy choices.