Ismail Erturk

Objective: Heart failure (HF) is a common and potentially fatal clinical condition. Catestatin, a peptide derived from chromogranin A (CgA), inhibits catecholamine secretion. This study aimed to evaluate differences in plasma catestatin levels between individuals without HF and patients with HF, and to investigate the relationship between catestatin and established HF markers. GB, RE, IE, BY, RA, TO, FNA, KS Methods: A total of 60 HF patients with left ventricular ejection fraction (LVEF) ≤45% and 53 control subjects matched for factors that could influence catestatin levels were included. The absence of heart failure in control participants was confirmed by clinical assessment, review of medical records and transthoracic echocardiography. Plasma samples were collected simultaneously in aprotinin-containing tubes to prevent peptide degradation. Plasma catestatin levels were measured using enzyme-linked immunosorbent assay (ELISA). Results: Catestatin levels were significantly higher in patients with HF (45.46 ± 16.69 ng/mL) compared with individuals without HF (37.15 ± 16.36 ng/mL) (t = 2.69, p = 0.008). Catestatin levels increased significantly with advancing NYHA functional class (Jonckheere–Terpstra test: J-T = 2.19; p = 0.029). Catestatin was positively correlated with NT-proBNP (r = 0.241; p = 0.010) and negatively correlated with LVEF (r = −0.19; p = 0.043). Catestatin was lower in patients with left ventricular hypertrophy than in those without, both within the patient group (41.39 ± 16.69 versus 49.64 ± 15.09 ng/mL; p = 0.04) and across the whole study population (37.41 ± 16.22 versus 44.04 ± 15.48 ng/mL; p = 0.03). The area under the ROC curve for catestatin in HF diagnosis was 0.635. Conclusion: Catestatin levels are associated with the presence and severity of heart failure. Its correlation with established parameters of severity and its progressive increase across NYHA functional classes indicate that catestatin may have value as a complementary neurohumoral marker in heart failure. Because the design was cross-sectional, no inference can be drawn regarding prognostic utility, and prospective evaluation is required.

Germline BRCA1/2-mutated (gBRCAm) hormone receptor-positive/HER2-negative (HR+/HER2-) metastatic breast cancer (MBC) is a biologically distinct subset in which the efficacy of cyclin-dependent kinase 4/6 (CDK4/6) inhibitors remains incompletely characterized. We evaluated real-world outcomes and prognostic factors in a multicenter retrospective Turkish cohort treated with a CDK4/6 inhibitor plus endocrine therapy (June 2020–September 2025). Progression-free survival (PFS) and overall survival (OS) were estimated using Kaplan–Meier and Cox methods. Among 121 patients, 30 (24.8%) had BRCA1, 88 (72.7%) had BRCA2, and three (2.5%) had dual mutations; 66.9% received first-line therapy, with ribociclib in 69.4% and palbociclib in 29.8%. Objective response rate was 69.4% and the clinical benefit rate was 82.6%. Median PFS was 17.0 months and OS 47.0 months. PFS was numerically longer in BRCA1 than in BRCA2 carriers (25.0 vs. 14.0 months), although the difference was not statistically significant in the pairwise comparison (HR 1.50, 95% CI 0.88–2.56; log-rank p = 0.135); the dual BRCA1/2 subgroup (n = 3) had the poorest outcomes and was assessed descriptively. OS did not differ significantly between BRCA1 and BRCA2 carriers (57.0 vs. 49.0 months; log-rank p = 0.520). PFS did not differ between ribociclib and palbociclib (p = 0.192); OS favored ribociclib at borderline significance (p = 0.050), but this was not confirmed in Cox regression. In multivariable analysis, ECOG ≥ 1 (HR 1.85; p = 0.010) and fulvestrant-based therapy (HR 1.74; p = 0.041) predicted shorter PFS; fulvestrant also predicted worse OS (HR 2.39; p = 0.008). CDK4/6 inhibitor-based therapy shows meaningful activity in gBRCAm HR+/HER2- MBC; the numerically poorer outcomes observed in BRCA2 carriers are hypothesis-generating and warrant validation in larger cohorts.

Background: Autologous stem cell transplantation (ASCT) is a standard treatment for relapsed or high-risk lymphoma. While disease-related factors are well-known, the impact of host-related factors like nutritional status remains less defined. We aimed to evaluate the prognostic value of the prognostic nutritional index (PNI) and other factors in lymphoma patients undergoing ASCT. Methods: We conducted a single-center retrospective cohort study including adult patients with Hodgkin and non-Hodgkin lymphoma who underwent ASCT between January 2015 and December 2023. Pre-transplant clinical, laboratory, and transplant-related variables were analyzed. The prognostic nutritional index (PNI) was calculated using serum albumin and absolute lymphocyte count and dichotomized according to the cohort median. Progression-free survival (PFS) and overall survival (OS) were evaluated using Kaplan–Meier and Cox regression analyses. We conducted a retrospective single-center cohort study including adult patients with Hodgkin and non-Hodgkin lymphoma who underwent ASCT between January 2015 and December 2023. Results: A total of 43 patients were included. Median age was 38 years, and 72.1% were male. Patients transplanted in complete remission (CR) had significantly longer PFS compared with those transplanted in partial remission (PR) (log-rank p = 0.022). Patients with higher pre-ASCT PNI demonstrated significantly improved PFS (median 45 vs. 7 months; log-rank p = 0.021). In multivariable Cox regression analysis, both higher PNI (HR 0.39; 95% CI 0.16–0.97; p = 0.043) and complete remission prior to ASCT (HR 0.41; 95% CI 0.17–0.98; p = 0.046) remained independently associated with improved PFS. Higher infused CD34⁺ (hematopoietic stem cell) dose was associated with shorter hospitalization but showed no statistically significant association with engraftment kinetics or survival. No variable was independently associated with OS, likely due to the limited number of death events. Conclusions: Pre-transplant prognostic nutritional index and disease response independently predict progression-free survival after ASCT in lymphoma. These findings highlight the complementary role of host-related and disease-related factors in transplant outcomes and suggest that PNI may serve as a practical tool for pre-transplant risk stratification and patient optimization. Given the small sample size and limited number of events, these findings should be interpreted with caution.

Background and Objectives: A combination of chemotherapy and immunotherapy may improve cancer treatment outcomes; however, determining which patient groups will benefit from immunotherapy is critical. Triple-negative breast cancer (TNBC) achieves limited benefit from immune checkpoint inhibitors (ICIs) and anti-PD-L1 blockade therapy. Materials and Methods: In this study, PD-L1 expression levels in myeloid-derived cells in the tumor microenvironment were determined in an experimental TNBC model. Results: Compared with tumor cells, granulocytes, monocytes, and macrophages had significantly higher PD-L1 expression. CD206⁺ tumor-associated macrophages (TAMs) expressed the highest level of PD-L1. PD-L1 positivity in TAMs was also significantly high in the lung, liver, lymph node, and spleen. Despite treatment initiation in late-stage tumorigenesis, the combination of paclitaxel and the anti-PD-L1 monoclonal antibody atezolizumab significantly reduced tumor growth. In addition, lung metastasis burden was reduced with combined treatment compared with chemotherapy or anti-PD-L1 monotherapy alone. Conclusions: As a result, alterations in PD-L1⁺ myeloid cells and immune infiltration can be associated with atezolizumab and paclitaxel therapy success in triple-negative breast cancer.

Introduction: Heart failure (HF) is a commonly encountered fatal clinical condition. Catestatin is a peptide produced by the breakdown of chromogranin A and inhibits catecholamine secretion. The main goal of this study is to identify the difference between catestatin levels in patients at without and with different stages of HF. It is important to determine catestatin’s relationship with pro-B-type natriuretic peptide (proBNP) and left ventricular ejection fraction (LVEF), that are used to identify HF and as well as other laboratory findings in order to better understand the contribution of catestatin. Materials-Methods: Sixty HF patients with LVEF< %45 and 53 matching control patients of factors that can impact catestatin level were included in the study. Plasma samples of these patients and controls were simultaneously collected in tube containing a drop of aprotinin (proteinase inhibitor). Plasma catestatin levels were measured by using enzyme-linked immunosorbent assay method. Results: The study findings showed that catestatin levels of HF patients (45.46±16.69 ng/ml) were significantly higher than that of patients without (37.15±16.36 ng/ml) (t=2.69, p< 0.05) and that the catestatin level increases as the HF stage progresses (J-T=2.19; p< 0.05). Catestatin level is found to be correlated positively with proBNP (r=0.241; p< 0.05), and inversely with LVEF (r=-0.19; p< 0.05). The area under the ROC curve calculated in order to demonstrate catestatin’s diagnostic adequacy in heart failure was 0.635. Discussion: Catestatin is considered an indicator of HF and it seems reasonable to use it for diagnosis and follow-up as it increases with disease severity.

Background/Objectives : Accurate prognostic assessment remains crucial in metastatic renal cell carcinoma (mRCC), especially as treatment options have expanded beyond vascular endothelial growth factor (VEGF)-targeted therapies to include immune checkpoint inhibitors (ICIs) and ICI–TKI combinations. The widely used IMDC classification shows important limitations in the modern therapeutic era, highlighting the need for complementary prognostic tools. In this context, the Meet-URO and CANLPH scores—incorporating clinical, inflammatory, and nutritional markers—have emerged as promising alternatives. To evaluate and compare the prognostic performance of the Meet-URO and CANLPH scoring systems in a real-world mRCC cohort predominantly treated with first-line tyrosine kinase inhibitor (TKI) monotherapy due to limited access to ICI-based combinations. Methods: This retrospective single-center study included 112 patients with mRCC. The Meet-URO score was calculated for all patients, while the CANLPH score was assessed in 56 patients with complete laboratory data. CAR, NLR, and PHR were computed using baseline pre-treatment measurements. Overall survival (OS) and progression-free survival (PFS), the latter defined exclusively for first-line therapy, were estimated using the Kaplan–Meier method. Correlations between inflammatory markers and survival outcomes were analyzed using Spearman’s rho. Results: Meet-URO demonstrated clear prognostic stratification across all five categories, with the most favorable outcomes in score group 2 and progressively poorer OS and PFS in higher-risk groups. CANLPH also showed meaningful survival discrimination, with the highest inflammatory group (score 3) exhibiting markedly reduced OS and PFS. CAR was the strongest individual predictor of survival, while NLR and PHR showed weaker associations. Conclusions: Both Meet-URO and CANLPH provide strong, complementary prognostic information in mRCC, even in a cohort largely treated with TKI monotherapy. Their integration into routine risk assessment may enhance clinical decision-making, particularly in resource-limited settings.

Aim: Metastatic osteosarcoma remains associated with poor survival despite multimodal therapy. High-dose chemotherapy followed by autologous stem cell transplantation (HDCT+ASCT) has been explored as a treatment intensification strategy; however, robust real-world data remain limited. This study aimed to evaluate treatment response and survival outcomes in patients with metastatic osteosarcoma treated with ICE-based HDCT followed by ASCT in a real-world setting.Materials and Methods: In this retrospective single-center cohort study, 46 patients with metastatic osteosarcoma who received ICE-based HDCT followed by ASCT were analyzed. Tumor response was assessed according to RECIST criteria. Progression-free survival (PFS) and overall survival (OS) were estimated using the Kaplan–Meier method. Univariable and multivariable Cox regression analyses were performed to evaluate associations between baseline clinical characteristics and survival outcomes.Results: The median age was 23,5 years, and 34 patients (73.9%) were male. The objective response rate (ORR) was 28.3%, and disease control (CR+PR+SD) was achieved in 52.2% of patients. Median PFS was 3.5 months (IQR: 2.6–6.0), and median OS was 10.7 months (IQR: 8.8–14.9). Survival curves demonstrated early attrition followed by a plateau phase. Exploratory analyses indicated longer OS in patients with ECOG 0–1 and lung-only metastases. No treatment-related mortality was observed.Conclusions: ICE-based HDCT followed by ASCT demonstrates measurable antitumor activity in metastatic osteosarcoma. However, given the limited median PFS and absence of a comparative control group, this approach should be considered a selective intensification strategy rather than a standard salvage therapy, and careful patient selection remains essential.

Background: Accurate prognostic assessment remains crucial in metastatic renal cell carcinoma (mRCC), especially as treatment options have expanded beyond vascular endothelial growth factor (VEGF)–targeted therapies to include immune checkpoint inhibitors (ICIs) and ICI–TKI combinations. The widely used IMDC classification shows important limitations in the modern therapeutic era, highlighting the need for complementary prognostic tools. In this context, the Meet-URO and CANLPH scores—incorporating clinical, inflammatory, and nutritional markers have emerged as promising alternatives. Objective: To evaluate and compare the prognostic performance of the Meet-URO and CANLPH scoring systems in a real-world mRCC cohort predominantly treated with first-line tyrosine kinase inhibitor (TKI) monotherapy due to limited access to ICI-based combinations. Methods: This retrospective single-center study included 112 patients with mRCC. The Meet-URO score was calculated for all patients, while the CANLPH score was assessed in 56 patients with complete laboratory data. CAR, NLR, and PHR were computed using baseline pre-treatment measurements. Overall survival (OS) and progression-free survival (PFS) the latter defined exclusively for first-line therapy—were estimated using the Kaplan–Meier method. Correlations between inflammatory markers and survival outcomes were analyzed using Spearman’s rho. Results: Meet-URO demonstrated clear prognostic stratification across all five categories, with the most favorable outcomes in score group 2 and progressively poorer OS and PFS in higher-risk groups. CANLPH also showed meaningful survival discrimination, with the highest inflammatory group (score 3) exhibiting markedly reduced OS and PFS. CAR was the strongest individual predictor of survival, while NLR and PHR showed weaker associations. Conclusion: Both Meet-URO and CANLPH provide strong, complementary prognostic information in mRCC, even in a cohort largely treated with TKI monotherapy. Their integration into routine risk assessment may enhance clinical decision-making, particularly in resource-limited settings.

Background: Ewing sarcoma (ES) is a highly aggressive malignant tumor that predominantly affects children and young adults. Despite advances in multimodal therapy, relapse and refractory disease remain the leading causes of treatment failure. High-dose chemotherapy followed by autologous stem cell transplantation (HDCT-ASCT) has been proposed as a consolidation strategy for high-risk or relapsed ES; however, its clinical value remains controversial. Methods: We retrospectively analyzed 46 consecutive patients with locally advanced or metastatic ES who underwent HDCT-ASCT after at least one prior systemic therapy line. Clinical, pathological, and transplant-related variables were evaluated for associations with overall survival (OS), post-transplant OS (OS-2), and progression-free survival (PFS). Survival was estimated using the Kaplan–Meier method, and prognostic factors were assessed by Cox proportional hazards modeling. Results: The median age at diagnosis was 23 years (range: 14–55). Median OS from diagnosis was 42 months, while post-transplant OS-2 and PFS were 8 and 5 months, respectively. Younger patients (≤23 years) had significantly longer OS (50 vs. 34 months; p = 0.027). Liver metastasis predicted inferior OS (HR = 5.411; p = 0.006), whereas lung metastasis was associated with shorter OS-2 (HR = 2.672; p = 0.025) and PFS (HR = 6.037; p = 0.016). Treatment-related mortality was low (2.1%), though hematologic toxicity was universal. Overall, HDCT-ASCT provided transient disease control, with modest benefit confined to younger, chemosensitive, and medically fit patients. Conclusions: In this real-world cohort, HDCT-ASCT was feasible and safe but offered limited survival advantage in heavily pretreated Ewing sarcoma. Prognosis was primarily influenced by age and metastatic distribution, particularly hepatic and pulmonary involvement. These findings support a risk-adapted, biology-driven approach reserving HDCT-ASCT for selected patients and highlight the need for post-transplant maintenance strategies integrating targeted or immunotherapeutic modalities.

Background: The role of high-dose chemotherapy followed by autologous stem-cell transplantation (HDCT–ASCT) in advanced Ewing sarcoma remains uncertain, with mixed prospective data and heterogeneous retrospective findings. Materials and Methods: We performed a single-center, retrospective cohort study of consecutive patients with histologically confirmed ES who received HDCT–ASCT after ≥1 prior systemic therapy line (N=46). Conditioning was ICE. Prespecified endpoints were overall survival (OS; diagnosis → death), post-transplant overall survival OS-2 (ASCT → death), and progression-free survival PFS (ASCT → progression/death). Survival was estimated by Kaplan – Meier and compared by log-rank. Prognostic factors (age at diagnosis, primary tumor site, metastatic organ involvement) were evaluated using Cox models. Results: Median age at diagnosis was 23.5 years (14–55); 69.6% were male and 21.7% had metastatic disease at presentation. Median OS was 42.0 months, median PFS and OS-2 after HDCT–ASCT were 5.0 months and 8.0 months, respectively. Younger age (≤23 years) was associated with longer OS (50.0 vs 34.0 months; p=0.027). Primary tumor site was not independently associated with PFS, OS-2, or OS. Metastatic site showed endpoint-specific effects: liver metastasis independently predicted worse OS (HR 5.411; p=0.006), while lung metastasis was associated with shorter PFS (HR 6.037; p=0.016) and OS-2 (HR 2.672; p=0.025). Post-transplant best responses were CR 8.7%, PR 17.4%, SD 15.2%, and PD 58.7%. Grade 3–4 hematologic toxicities were universal (febrile neutropenia, neutropenia, thrombocytopenia 100%; anemia 86.9%); common non-hematologic events included nausea/vomiting (82.6%), diarrhea (78.2%), and mucositis/stomatitis (65.2%). Treatment-related mortality was 2.1% (1/46). Conclusions: In this young-adult–predominant cohort, HDCT–ASCT achieved limited disease control with substantial but manageable toxicity. Prognosis was driven more by age and metastatic organ involvement than by primary site, with liver metastasis portending inferior OS and lung metastasis adversely affecting PFS/OS-2. These data support risk-adapted patient selection and exploration of post-transplant maintenance strategies in future prospective studies.