Introduction In the treatment of metastatic non-small cell lung cancer (mNSCLC), targeted therapies are utilized in the presence of driver mutations. Tyrosine kinase inhibitors (TKIs) have contributed positively to survival outcomes in this patient group. In driver mutant mNSCLC patients, caution is warranted for the development of small cell lung cancer (SCLC) differentiation following progression under TKI therapy. SCLC is associated with an aggressive course and shorter survival. The cornerstone of SCLC treatment is conventional chemotherapy. In this study, we aimed to present the development of SCLC differentiation in driver mutant mNSCLC patients who received at least one line of TKI therapy as a single-center experience. Patients and methods Between April 2013 and January 2024, the medical records of 144 patients diagnosed with mNSCLC and found to harbor driver mutations were retrospectively reviewed at Necmettin Erbakan University Faculty of Medicine Hospital, Oncology Clinic. All patients had received at least one line of TKI. The analysis included evaluation of driver mutations, treatments administered, and the rate of SCLC differentiation in this patient population. Results A total of 144 patients were included in the study. Among them, 122 patients (84.9%) had an EGFR mutation, 21 patients (15.1%) had an ALK mutation, and 1 patient had a ROS1 mutation. TKI therapy was administered as first-line treatment in 50% of the patients, as second-line in 40.3%, and as third-line in 6.3%. Biopsies were performed in 22 out of 144 patients after disease progression. Of these, 21 biopsies were from patients with EGFR mutations, and 1 was from a patient with an ALK mutation. Biopsies were conducted after first-line therapy in 8 cases, after second-line therapy in 11 cases, and after third-line therapy in 3 cases. SCLC differentiation was observed in 3 out of 22 patients (13.6%), all of whom had EGFR mutations. Additionally, 2 of these 3 patients developed SCLC differentiation following first-line TKI therapy, while 1 developed it after second-line TKI therapy. Discussion The rate of SCLC differentiation in NSCLC is generally low and is considered rare. It is estimated that the rate of SCLC differentiation in NSCLC ranges between 1% and 3%. In our clinic, when evaluating driver mutant mNSCLC patients who received at least one line of TKI therapy, SCLC differentiation was observed in 3 patients (13.6%). The limitations of our study include its retrospective nature and the small sample size. However, the findings suggest that SCLC differentiation is a potential occurrence in driver mutant mNSCLC patients treated with TKIs. Therefore, careful monitoring and the detection of possible differentiation are essential in the follow-up of these patients.

Background and Objectives: Gastric cancer is an aggressive malignancy characterized by high recurrence rates, even following curative resection. The Albumin–Bilirubin (ALBI) score was originally established to assess hepatic functional reserve in patients with hepatocellular carcinoma (HCC). By reflecting both systemic inflammation and nutritional status, the ALBI score has demonstrated significant prognostic utility across a spectrum of solid malignancies. The present study aimed to evaluate the prognostic significance of the ALBI score in gastric cancer patients receiving adjuvant therapy after curative-intent resection. Materials and Methods: This retrospective study included 168 patients with gastric cancer who underwent curative-intent resection followed by adjuvant therapy between November 2008 and January 2021. ALBI scores were calculated from pre-treatment serum albumin and bilirubin levels. Patients were dichotomized into ALBI Grade 1 and ALBI Grade 2 based on an optimal ROC-derived cut-off value of −2.60. Survival outcomes, including overall survival (OS) and recurrence-free survival (RFS), were estimated using the Kaplan–Meier method and compared via the log-rank test. Independent prognostic factors were identified using univariate and multivariate Cox proportional hazards regression models. Results: Of the 168 patients, 56.5% were classified as ALBI Grade 1 and 43.5% as ALBI Grade 2. ALBI Grade 2 was associated with significantly shorter median RFS (18.7 vs. 72.2 months; p = 0.001) and OS (40.7 vs. 104.3 months; p = 0.003). Multivariable analysis identified ALBI Grade 2 as an independent predictor for both poor OS (HR: 1.699, p = 0.010) and RFS (HR: 1.767, p = 0.004). Pathological stage III disease was also a significant independent prognostic factor for OS (HR: 3.024) and RFS (HR: 3.049) (all p = 0.010). Additionally, elevated CEA correlated with shorter RFS (p = 0.023). Conclusions: The ALBI score is a prognostic marker for both overall and recurrence-free survival in gastric cancer patients receiving adjuvant therapy. A lower ALBI score is associated with longer survival outcomes. The ALBI score may support postoperative risk stratification and individualized follow-up planning.

Background and Objectives: Metastatic renal cell carcinoma (mRCC) remains a lethal disease despite advances with immune checkpoint inhibitors such as nivolumab. However, a substantial proportion of patients exhibit primary resistance or early progression, highlighting the need for reliable and easily accessible prognostic biomarkers. The C-reactive protein–albumin–lymphocyte (CALLY) index is a novel immunonutritional biomarker integrating systemic inflammation, nutritional status, and immune competence. Materials and Methods: In this retrospective single-center study, 91 patients with mRCC treated with nivolumab were analyzed. Patients were stratified into low and high CALLY index groups based on a receiver operating characteristic-derived cut-off (0.322). Survival outcomes were assessed using Kaplan–Meier analysis and Cox regression models. Results: Patients with a low CALLY index demonstrated significantly shorter progression-free survival (4.5 vs. 13.5 months, p < 0.001) and overall survival (9.1 vs. 25.5 months, p = 0.003). Multivariate analysis confirmed the CALLY index as an independent prognostic factor for both progression-free survival (HR: 2.63, p = 0.002) and overall survival (HR: 1.88, p = 0.035). Conclusions: The CALLY index is a simple, cost-effective, and reproducible biomarker that independently predicts survival in nivolumab-treated mRCC. It may serve as a practical tool for risk stratification and personalized treatment planning in the immunotherapy era.

Background and Objectives: Erlotinib, a tyrosine kinase inhibitor (TKI), is an established therapy for patients with metastatic non-small cell lung cancer (NSCLC) harboring epidermal growth factor receptor (EGFR) mutations. Preclinical and clinical evidence suggests that chronic stress, mediated through β-adrenergic signaling, promotes tumor progression, angiogenesis, and therapy resistance. Furthermore, interactions between β-adrenergic signaling and EGFR pathways have been hypothesized to negatively influence treatment responses. Based on this rationale, we investigated whether concomitant beta-blocker use may improve survival outcomes in EGFR-mutant NSCLC patients treated with erlotinib. Materials and Methods: This retrospective analysis included 103 patients with metastatic EGFR-mutant NSCLC who received erlotinib. Patients were classified according to concurrent beta-blocker use, defined as continuous therapy for at least six months prior to erlotinib initiation, prescribed for cardiovascular indications. Progression-free survival (PFS) and overall survival (OS) were compared between beta-blocker users and non-users. Results: Patients receiving erlotinib with concomitant beta-blocker therapy achieved a median PFS (mPFS) of 21.4 months (95% CI, 13.1–29.7), compared with 9.7 months (95% CI, 6.7–12.7) in non-users (p = 0.003). Median OS (mOS) was 32.4 months (95% CI, 14.8–50.0) in the beta-blocker group versus 19.9 months (95% CI, 14.8–25.0) in the non-beta-blocker group (p = 0.010). Multivariate Cox regression confirmed beta-blocker use as an independent prognostic factor for both PFS (p = 0.004) and OS (p = 0.014). Conclusions: Concomitant beta-blocker use was associated with significantly prolonged survival in patients with EGFR-mutant metastatic NSCLC receiving erlotinib. These findings support the hypothesis that β-adrenergic inhibition enhances the efficacy of EGFR-targeted therapy. Prospective studies are warranted to validate these results and to further elucidate the underlying biological mechanisms.

Sclerostin is a protein produced by osteocytes, kidneys, and vascular cells and has many effects on kidney and vascular structures. Soluble TNF-related weak inducer of apoptosis is a proinflammatory cytokine that may cause glomerular and tubular injury and increase sclerostin expression. This study aimed to investigate serum sclerostin and soluble TNF-related weak inducer of apoptosis levels in patients with glomerulonephritis and the effects they may be associated with.

Background: Adenocarcinoma arising from the ampulla of Vater is an extremely rare neoplasm, and there are limited data regarding frontline therapy for metastatic disease. We investigated the outcomes of first-line treatment with FOLFIRINOX by comparing it with other treatments in patients with advanced ampullary adenocarcinoma. Methods: We included 123 patients with advanced ampullary adenocarcinoma who were treated with frontline FOLFIRINOX (n = 32), fluorouracil (FU)-based chemotherapy (n = 20), and gemcitabine-based chemotherapy (n = 65) between August 2007 and January 2024 in this retrospective study. The median progression-free survival (mPFS) and overall survival (mOS) according to treatment and clinicopathological features were calculated using the Kaplan–Meier method. Results: The median age of the patients was 62 years (range, 36–78), and 75,6% of the patients had an ECOG performance status of 0–1. The mOS were 13 months (95% CI, 10.6–14.4), 11 months (95% CI, 10.6–14.4), and 12 months (95% CI, 10.6–14.4), respectively [p = 0.865]. There were no significant differences in OS among the chemotherapeutic agents according to histological subtypes. However, FOLFIRINOX and FU-based treatments appeared more effective in the intestinal subtype, while gemcitabine-based therapies were less effective. In the pancreaticobiliary subtype, FU-based therapies yielded a shorter outcome compared to FOLFIRINOX and gemcitabine-based therapies. Grade 3 or 4 hematologic toxicities were higher in patients treated with FOLFIRINOX. Conclusions: In advanced ampullary adenocarcinoma, despite higher toxicity, frontline FOLFIRINOX showed a trend toward an OS benefit in the intestinal subtype while providing a similar outcome in the pancreaticobiliary subtype.