Purpose: This study aims to compare the clinicopathological and prognostic features of women aged 40 years and younger and 65 years and older with breast cancer. Methods: Between January 2011 and December 2021, 136 female cases aged 40 years and younger and 223 female cases aged 65 and over were identified among all cases (1395 cases) registered as breast cancer in the file archives of Afyonkarahisar Health Sciences University Faculty of Medicine, Department of Medical Oncology for the study. A Chi-square (× 2) test was used for categorical variables, and an independent sample t-test for continuous variables. Log-rank test and Kaplan–Meier plots were used for survival analysis. For the statistical evaluation, p < 0.05 was considered significant. Results: Both overall survival (p < 0.01) and breast cancer-specific survival (BCSS) (p = 0.01) were significantly worse in the older group. BCSS were significantly worse in the older group in Luminal B (HER2−) (p = 0.013) and HR− HER2+ (p = 0.015) subtypes detected. In multivariate Cox regression analysis, only the presence of metastases at diagnosis or follow-up (p < 0.001) and ECOG PS 2–3 status (p = 0.001) were associated with an increased risk of breast cancer-specific death. Conclusion: To our knowledge, no study directly compares these two groups. In our study, similar to many studies, more aggressive tumor features were found in young patients, but unlike many studies, mortality was found to be significantly higher in older patients. The presence of metastasis and poor ECOG PS were found to be the most influential factors in breast cancer-specific death risk.

Background: Metastatic gastric cancer (GC) and gastroesophageal junction (GEJ) cancer are associated with a poor prognosis. Recent advancements in treatment have incorporated trastuzumab, anti-PD-1 agents, and anti-claudin therapies alongside chemotherapy (ChT), significantly improving outcomes. Contemporary studies predominantly employ doublet ChT as the backbone for these regimens, although historically triplet ChT regimens have been favored, particularly in younger patients requiring rapid tumor shrinkage. Objective: The aim of this study was to compare the efficacy of mFOLFOX-6 and mDCF regimens in the treatment of advanced GC and GEJ adenocarcinoma. Design: This was a retrospective multicenter study. Methods: Patient data were obtained from the databases of 25 hospitals across Turkey. Demographic and clinicopathological characteristics were documented. Overall survival (OS) and progression-free survival (PFS) were analyzed using the Kaplan–Meier method, and group discrepancies were assessed with log-rank test. Results: A total of 493 patients were included in the analysis, with similar baseline characteristics between the two groups. The objective response rate was 36.3% in the mDCF group and 38% in the mFOLFOX-6 group ( p = 0.7). The median PFS was 6 months for mDCF and 7 months for mFOLFOX-6 ( p = 0.2), while the median OS was 12 months for mDCF and 11 months for mFOLFOX-6 ( p = 0.4). Grade 3–4 neutropenia occurred in 27.6% of patients treated with mDCF versus 17.8% with mFOLFOX-6 ( p = 0.01). Likewise, grade 3–4 anemia was more frequent in the mDCF group (9.5%) compared to the mFOLFOX-6 group (4.8%; p = 0.04). Conclusion: Modified FOLFOX-6 demonstrated comparable efficacy to mDCF in the treatment of advanced GC and GEJ adenocarcinoma. Moreover, mFOLFOX-6 was associated with a lower incidence of hematological adverse effects.

There are conflicting data regarding the prognostic effect of microvascular density (MVD) in breast cancer and its molecular subtypes. It is thought that high levels of FOXP3 + T cells in breast cancer are associated with poor prognosis. However, data regarding FOXP3 show significant variability in the literature. In our study, we aim to measure MVD and FOXP3 + T cells in breast cancer cases and investigate their relationship with each other and their effects on breast cancer patients’ clinical and prognostic features. In our study, the results of 207 female breast cancer patients whose excisional tumoral tissue was obtained are presented. The study evaluated the findings under a light microscope using antibodies against CD34 for measuring MVD and FOXP3 for measuring FOXP3-positive T cells. CD34 ≥ 17 was categorized as high MVD, and CD34 < 17 was classified as low MVD. FOXP3 + cell count ≥ 20/mm2 was categorized as high FOXP3 positivity and < 20/mm2 as low FOXP3 positivity. The SPSS program (version 22) was used to evaluate the results statistically, and p < 0.05 was considered significant. The median age was 54.0 (27–86) years, and the median follow-up period was 60.0 (IQR: 42.6–86.5) months. In the high MVD group, a higher progesterone receptor (PR) positivity rate was detected (p = 0.035). High FOXP3 positivity was significantly associated with high nuclear grade (p = 0.003). High FOXP3 positivity was significantly associated with PR negativity and high Ki67 values ​​(p = 0.009, p = 0.012, respectively). No statistically significant correlation was found between MVD elevation and FOXP3 positivity (r = 0.063, p = 0.36). A weakly significant positive correlation was detected between high Ki67 and FOXP3 positivity (r = 0.0146, p = 0.04). A weak inverse correlation was detected between high FOXP3 positivity and PR percentage values ​​(r=-0.182, p = 0.01). While there was no significant difference in disease-free survival in cases with high MVD and high FOXP3 + T cells compared to groups with low levels, the results were not mature enough because the median values ​​in overall survival could not be reached. A significant correlation was found between high FOXP3 positivity and some aggressive tumor features; no effect on survival was detected. In contrast to literature data on luminal A breast cancer, high MVD in the luminal B (HER2-) subgroup was associated with a lower risk of recurrence. Our study is the first in the literature to evaluate the relationship between MVD measured using CD34 and FOXP3 positive T cells in breast cancer. Our study found no correlation between MVD and FOXP3 positivity, while literature data show significant correlations in some other cancers.

Background and Objectives: Non-small cell lung cancer (NSCLC) accounts for approximately 85% of all lung cancers and remains a leading cause of cancer-related mortality worldwide. EGFR-targeted tyrosine kinase inhibitors (TKIs) have substantially improved outcomes in EGFR-mutant NSCLC; however, primary and acquired resistance continues to limit their long-term efficacy. HER3 (receptor tyrosine-protein kinase ErbB3), a member of the ErbB receptor family, has been implicated in TKI resistance through heterodimerization with EGFR and HER2, leading to downstream PI3K/AKT pathway activation. Despite its biological plausibility as a resistance mediator, the clinical significance of HER3 expression as a prognostic and predictive biomarker in EGFR-mutant NSCLC has not been thoroughly characterized in real-world cohorts. Materials and Methods: This retrospective, single-center study included 52 patients diagnosed with EGFR-mutant NSCLC who received TKI therapy at Afyonkarahisar Health Sciences University between January 2011 and September 2023. HER3 protein expression was evaluated by immunohistochemistry (IHC) on formalin-fixed, paraffin-embedded tumor tissue sections using the Huabio anti-HER3 antibody (clone PD00-44, 1:2000 dilution). Staining in more than 30% of tumor cells was considered HER3-positive; membranous staining intensity was scored on a 1–3 scale. Progression-free survival (PFS1, PFS2) and overall survival (OS) were analyzed using the Kaplan–Meier method and log-rank test. Statistical significance was set at p < 0.05. Results: Of 52 patients (55.8% female; mean age 64.5 years), 59.6% received chemotherapy and 40.4% received an EGFR TKI as first-line treatment; erlotinib constituted 71.2% of targeted therapies. In the first-line TKI group, HER3-negative patients had a numerically longer median PFS1 compared with HER3-positive patients (14.0 vs. 7.1 months; p = 0.285); however, this difference did not reach statistical significance and should be interpreted with caution given the small sample size. In contrast, among patients receiving first-line chemotherapy, HER3 staining status did not meaningfully affect PFS1 (4.1 vs. 2.5 months; p = 0.063). In second-line treatment, HER3-positive patients who received TKI after prior chemotherapy demonstrated a PFS2 comparable to or slightly exceeding that of HER3-negative patients (21.8 vs. 19.8 months; p = 0.49), suggesting that the sequencing of chemotherapy before TKI may attenuate the adverse effect of HER3 positivity. Median OS was 15.1 months in HER3-negative patients and 12.7 months in HER3-positive patients (p = 0.824); this numerical difference of approximately 3 months did not reach statistical significance and should therefore be interpreted cautiously. Among patients receiving TKI in the first line, HER3-positive patients had a shorter median OS than HER3-negative patients (9.6 vs. 14.2 months), whereas those receiving TKI in the second line showed a trend toward longer OS in HER3-positive patients (20.5 vs. 17.2 months). Conclusions: HER3 expression was associated with reduced first-line TKI efficacy in EGFR-mutant NSCLC, suggesting a possible role for HER3 in primary TKI resistance; however, these findings are exploratory and did not reach statistical significance. The observation that HER3-positive patients who received chemotherapy before TKI demonstrated outcomes comparable to HER3-negative patients raises the hypothesis that treatment sequencing may potentially influence the impact of HER3 positivity, though this requires prospective validation before any clinical conclusions can be drawn. These results suggest that HER3 expression may warrant further investigation as a candidate biomarker for treatment sequencing decisions and as a potential therapeutic target in EGFR-mutant NSCLC. Prospective studies evaluating chemotherapy–TKI sequencing and HER3-directed agents such as patritumab deruxtecan (HER3-DXd) in HER3-positive patients are needed to confirm these preliminary observations.

Nivolumab is currently widely used in the treatment of lung cancer. Studies have been conducted using flat doses of 240 mg and 3 mg/kg. In fact, studies involving a small number of patients have begun to explore low-dose immunotherapies. The literature on the optimal dose of immunotherapy, the use of weight based, or fixed doses is very recent and has become a one of the subject of ongoing research. This multicenter study included 716 patients with NSCLC. Patients receiving standard doses of 3 mg/kg and 240 mg of nivolumab were divided into subgroups based on their weight. Patients weighing 80 kg have already received a flat dose. However, patients weighing < 80 kg who received a flat dose were considered to be receiving high-dose therapy. Conversely, patients weighing more than 80 kg who received a flat dose were maintained on a low dose. Therefore, overall survival, progression-free survival, and toxicity were examined according to weight-based usage. The median progression free survival (PFS) for those receiving a 3 mg/kg dose was 6 months, whereas it was 9.8 months for those receiving a flat dose (p < 0.001). The median (metastatic overall survival) OS for those receiving a 3 mg/kg dose was 12 months, whereas it was 14 months for those receiving a 240 mg dose (p = 0.03). This study was based on real-world data. Therefore, our results may be instructive regarding the nivolumab dose, which is a commonly used treatment for NSCLC patients. Our results suggest that a flat dose may be preferred in all groups and as a subgroup, especially in patients weighing < 80 kg.