Objective: CDK4/6 inhibitors are the standard first-line treatment for hormone receptor (HR)-positive, HER2-negative metastatic breast cancer (MBC). However, treatment response shows heterogeneity among patients. The objective of this multicentre, retrospective study is to investigate real-world parameters affecting overall survival (OS) in patients receiving CDK4/6 inhibitor therapy, particularly the effect of high oestrogen receptor (ER) expression (≥90%). Methods: A total of 603 HR-positive/HER2-negative MMK patients treated with a CDK4/6 inhibitor (ribociclib or palbociclib) from five centres were retrospectively reviewed. Age, menopausal status, metastatic status, metastatic sites, pathological subtype, HER2 status (low/negative), ER expression level (< 90% vs ≥90%), progesterone receptor (PR) status, and prior endocrine therapy (ET) or chemotherapy (CT) before CDK4/6 inhibitor were evaluated for their impact on OS using univariate and multivariate Cox regression analyses. Results: In the univariate analysis, OS was significantly longer in patients who did not receive ET prior to CDK4/6 inhibitor treatment (median OS: 51.0 months vs. 33.3 months; p< 0.01). OS was also better in patients without liver metastases (50.0 months vs. 34.0 months; p=0.019), those with bone metastases only (57.7 months vs. 40.5 months; p=0.022), and PR-positive patients (50.0 months vs. 36.0 months; p=0.037) also had better OS. OS was numerically longer in patients with ER expression ≥90% compared to those with < 90% (49.0 months vs. 41.0 months; p=0.072). In multivariate analysis, not having received ET prior to CDK4/6 inhibitor therapy (p=0.045) and high ER expression (≥90%) (p=0.031) were independently associated with better OS. Conclusion: Our study demonstrates that HR-positive/HER2-negative MBC patients who are naive to endocrine therapy prior to CDK4/6 inhibitor treatment and have high ER expression (≥90%) in their tumours derive greater OS benefit from this treatment. The ER expression level threshold of ≥90% may be proposed as a potential biomarker for predicting response to CDK4/6 inhibitor therapy. These findings necessitate further prospective studies to improve patient selection.

Background/Objectives: Claudin-18.2 (CLDN18.2) has recently emerged as a therapeutic target in gastric cancer; however, its prognostic relevance in the neoadjuvant setting remains insufficiently defined. We evaluated the clinical significance of CLDN18.2 and fibroblast growth factor receptor 2b (FGFR2b) expression in patients with locally advanced gastric cancer treated with neoadjuvant therapy. Methods: This retrospective single-center study included 64 patients with locally advanced gastric cancer who received neoadjuvant chemotherapy followed by curative surgery. Pretreatment endoscopic biopsy specimens were analyzed using immunohistochemistry to assess CLDN18.2 and FGFR2b expression. Survival outcomes were evaluated using Kaplan–Meier analysis and Cox proportional hazards regression models. Results: CLDN18.2 positivity was detected in 29.7% of patients and was not associated with baseline clinicopathological characteristics or pathological treatment response. However, CLDN18.2-positive tumors demonstrated significantly shorter relapse-free survival (median 19.0 vs. 36.6 months, p = 0.038) and overall survival (median 28.9 vs. 53.4 months, p = 0.005). In multivariable analysis, CLDN18.2 positivity remained an independent predictor of relapse-free survival. FGFR2b positivity was observed in 14.1% of patients and was evaluated descriptively due to limited case numbers. Conclusions: CLDN18.2 expression may represent a clinically relevant prognostic biomarker reflecting aggressive tumor biology in locally advanced gastric cancer treated with neoadjuvant therapy.

Medüller tiroid kanseri(MTK); parafoliküler veya C hücrelerinden köken alan tiroid bezinin nöroendokrin tümörüdür. MTK’li hastaların çoğu tanı anında metastatiktir. Multipl endokrin neoplazi tip 2(MEN 2) sendromunun bir bileşeni olarak %25’i aileseldir. Kalsitonin ve karsinoembrionik antijen (CEA) tümör belirteçleridir. Tedavi seçenekleri arasında cerrahi, radyoterapi ve lokal ablatif müdahaleler, kemoterapi, tirozin kinaz inhibitörleri, immünoterapi bulunmaktadır. Medullary thyroid cancer (MTK); It is a neuroendocrine tumor of the thyroid gland originating from parafollicular or C cells. Most patients with MTC are metastatic at diagnosis. As a component of multiple endocrine neoplasia type 2 (MEN 2) syndrome, 25% are familial. Calcitonin and carcinoembryonic antigen (CEA) are tumor markers. Treatment options include surgery, radiotherapy and local ablative interventions, chemotherapy, tyrosine kinase inhibitors, immunotherapy.

Background/Objectives: Sarcopenia predicts increased morbidity and mortality in gastrointestinal (GI) cancer. This study evaluated the longitudinal association between changes in the skeletal muscle index (SMI) and serum procollagen type III N-terminal peptide (PIIINP), together with sarcopenia and malnutrition screening tools (SARC-F, SARC-CalF, MUST), during chemotherapy for GI cancer. Methods: In this prospective single-center study, 170 patients with GI cancer were assessed at baseline and month 6; 48 died, and longitudinal analyses included the 122 survivors. SMI was derived from bioelectrical impedance analysis (Tanita SC-330) using the Janssen equation, and serum PIIINP was measured at both time points. The primary endpoint was the association between the percentage changes in SMI and PIIINP. Results: BMI, SMI, and handgrip strength decreased and SARC-F and SARC-CalF scores increased significantly (all p < 0.001); the prevalence of low muscle mass rose from 29% to 52%, and PIIINP increased significantly. The percentage changes in SMI and PIIINP were strongly inversely correlated (ρ = −0.733, p < 0.001). In the parsimonious multivariable model, the percentage change in PIIINP (β = −0.47) and month-6 albumin (β = 0.31) were independently associated with the change in SMI (R² = 0.37); the albumin association was model-dependent and not retained in the expanded model. Conclusions: In patients with GI cancer receiving chemotherapy, progressive muscle loss over six months was accompanied by a rise in the circulating collagen turnover marker PIIINP. Because the study was observational, restricted to survivors, and based on a non-muscle-specific marker, causal and muscle-specific inferences are unwarranted; PIIINP nonetheless merits further evaluation as a monitoring biomarker.

Tiroid Kanserlerinde Epidemiyoloji Emine Bihter ENİSELER Tiroid Kanserlerinde Patoloji Zübeyde YILDIRIM Tiroid Kanserlerinde Radyolojik Tanı Yontemleri Bartu ÇETİN Tiroid Nodullerine Klinik Yaklaşım Mustafa DEMİRPENCE Tiroid Kanserlerinde Cerrahi Seda BAŞTÜRK Diferansiye Tiroid Karsinomlarında Radyoaktif İyot Tedavisi Selda YILMAZ TATAR Tiroid Kanserlerine Genel Bakış Mehmet Alper YILMAZ Papiller Tiroid Kanseri Emir Gökhan KAHRAMAN Folikuler Tiroid Kanseri Emir Gökhan KAHRAMAN Tiroid Onkositik Karsinomu Gürkan GÜL Meduller Tiroid Kanseri Gürkan GÜL Anaplastik Tiroid Kanseri Kıvanç MERCAN Herediter Non-Meduller Tiroid Kanserleri Kıvanç MERCAN Tiroid Kanserlerinde Radyoterapi Endikasyonları Fatma SERT Tiroid Kanserlerinde İzlem Selda YILMAZ TATAR

Background: Platinum resistance remains a major therapeutic challenge in epithelial ovarian cancer (EOC). The tumour–stroma ratio (TSR) has emerged as a potential histopathological marker of tumour biology, but its clinical significance in different clinical settings remains unclear. We evaluated the association between stromal proportion, assessed using the TSR methodology, platinum resistance, and survival outcomes in patients undergoing primary debulking surgery (PDS) or neoadjuvant chemotherapy followed by interval debulking surgery (NACT+IDS). Methods: This retrospective study included 83 patients with epithelial ovarian cancer (EOC) who underwent either primary debulking surgery (PDS) or neoadjuvant chemotherapy followed by interval debulking surgery (NACT+IDS) between 2017 and 2024. Patients were analysed separately according to treatment strategy. Stromal proportion was assessed on primary surgical specimens in the PDS cohort and on pretreatment diagnostic biopsy specimens in the NACT+IDS cohort. For this retrospective analysis, platinum resistance was operationally defined as recurrence within six months after completion of first-line platinum-based chemotherapy. Survival outcomes were analysed using the Kaplan–Meier method, and univariable binary logistic regression was performed separately within the PDS and NACT+IDS cohorts to explore the association between stromal category and platinum resistance. Results: Platinum resistance occurred in 25.3% of patients. In the PDS cohort, stromal category was not associated with clinicopathological characteristics, platinum resistance, disease-free survival (DFS), or overall survival (OS). In the NACT+IDS cohort, patients in the stroma-high group had a numerically higher rate of platinum resistance than those in the stroma-low group (57.9% vs. 22.2%; Fisher’s exact p = 0.114). Based on univariable logistic regression analysis, the stroma-high group had higher estimated odds of platinum resistance (OR 4.81, 95% CI 0.78–29.40), although this finding did not reach statistical significance (p = 0.090). No significant association was observed between stromal category and survival outcomes in either cohort. Conclusions: In the NACT+IDS cohort, patients in the stroma-high group had a numerically higher rate of platinum resistance than those in the stroma-low group; however, this difference did not reach statistical significance. These results should be interpreted with caution due to the retrospective study design and limited sample size; however, they nonetheless support further investigation of pretreatment TSR as a simple and easily applicable histopathological parameter in EOC. Larger prospective multicentre studies are required to determine whether this exploratory signal is reproducible and clinically relevant.