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.

Introduction: Bloom syndrome (BS) is a rare autosomal recessive disorder caused by a loss-of-function mutation in the BLM gene encoding an RecQ helicase involved in DNA repair and maintenance of chromosomal stability. In patients with BS, significant sensitivity to both DNA-damaging chemotherapy (CT) and ionizing radiation complicates the management of neoplasms by exacerbating comorbidities and predisposing to toxicities and poor outcomes. Case report: A 30-year-old female patient diagnosed with BS who presented with early-stage triple-negative breast cancer was treated with four cycles of doxorubicin (60 mg/m²) and cyclophosphamide (600 mg/m²) followed by weekly paclitaxel (80 mg/m²) for 12 weeks as the chemotherapy protocol and a total of 5000 cGy curative radiotherapy (RT). Due to pancytopenia 8 months after completion of therapy, bone marrow biopsy and aspiration were performed, and a diagnosis of myelodysplastic syndrome with excess blasts 2 (MDS-EB2) was made. Two courses of the azacitidine (75 mg/m²) protocol were administered every 28 days in the hematology clinic. Two weeks after CT the patient was transferred from the emergency department to the hematology clinic with the diagnosis of pancytopenia and febrile neutropenia. She died at the age of 33 due to sepsis that developed during follow-up. Conclusion: Due to the rarity of BS, there is no prospective trial in patients with cancer and no evidence base upon which to design treatment programs. For these reasons, it is strongly recommended that patients receive multidisciplinary care, with precise assessment and discussion of the indication and an adequate dose of DNA-damaging agents such as chemotherapy and ionizing radiation.

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.

Introduction. Gemcitabine is used in treatment of such cancers as pancreatic cancer and biliary tract cancer and has been shown to improve progression-free survival in patients with pancreatic cancer when administered as adjuvant chemotherapy. Low-grade elevations in liver enzymes are generally among the known toxicities of gemcitabine. However, it has also been associated with serious and fatal hepatic failure. Case report. A 71-year-old male patient with pancreatic cancer developed fatal cholestatic hepatitis after six cycles of gemcitabine given as adjuvant chemotherapy. Management and outcome. A fatal gemcitabine-associated cholestatic hepatitis in a patient receiving adjuvant gemcitabine monotherapy for pancreatic cancer. Discussion. Our case differs from those reported in the literature. In our patient, 10 days after the 6th course of gemcitabine administration, elevated liver enzymes, increased bilirubin, and jaundice were observed. Gemcitabine-induced cholestatic hepatitis was diagnosed because there was no other drug use that could have triggered this reaction. Keywords: cholestatic hepatitis gemcitabine pancreatic cancer