Background: Advanced-stage ovarian cancer presents a significant therapeutic challenge, with primary cytoreductive surgery (PCS) followed by chemotherapy and neoadjuvant chemotherapy (NACT) with interval debulking surgery (IDS) as the two main treatment modalities. This study aims to compare the clinical outcomes, surgical complexity, and survival rates between these approaches and to assess the impact of molecular markers such as BRCA and HRD status. Methods: This retrospective, single-center observational study included 100 patients diagnosed with stage III-IV high-grade serous ovarian cancer. The patients were divided into two cohorts based on their treatment strategy: PCS followed by adjuvant chemotherapy or NACT followed by IDS. Clinical outcomes, recurrence-free survival (RFS), progression-free survival (PFS), and overall survival (OS) were analyzed, along with the impact of genetic biomarkers. Results: No statistically significant differences were observed in OS and PFS between the two treatment approaches. Patients who underwent NACT followed by IDS had lower surgical complexity scores and reduced perioperative morbidity. The HRD-positive patients exhibited improved responses to PARP inhibitors, reinforcing the significance of molecular profiling in therapeutic decision-making. The KELIM scores demonstrated prognostic relevance, particularly in the patients receiving neoadjuvant chemotherapy. Conclusion: Both PCS and NACT-IDS are viable treatment options for advanced ovarian cancer, with similar survival outcomes. The choice between strategies should be tailored based on patient-specific factors, including tumor burden, performance status, and molecular profile. The integration of biomarkers such as BRCA mutations and HRD status into clinical practice can further refine treatment selection and improve personalized management strategies.

Background/Objective: Breast cancer (BC) management has traditionally relied on static clinicopathologic and immunohistochemical biomarkers (hormone receptor status, HER2 expression, and proliferative activity assessed at diagnosis). However, these biomarkers are typically evaluated at a single time point and may not reflect therapy-induced molecular evolution. This study evaluates whether longitudinal molecular profiling before and after treatment better characterizes tumor dynamics and provides clinically actionable insights into treatment response, resistance, and prognosis. Methods: Thirty-two patients with invasive breast carcinoma were analyzed using histopathology, immunohistochemistry, tissue-based next-generation sequencing, and plasma circulating tumor DNA (ctDNA) analysis. Paired tumor tissue and plasma samples were collected before and after treatment when available. Changes in biomarker expression, molecular subtype, and genomic alterations were assessed to characterize molecular plasticity under therapeutic pressure. Results: The cohort had a median age of 54 years (range 29–86), predominantly invasive ductal carcinoma (>85%), and high-grade disease. Hormone receptor-positive tumors accounted for 78.1%. Molecular subtypes were Luminal A (34.4%), Luminal B HER2− (40.6%), Luminal B HER2+ (6.3%), HER2-enriched (6.3%), and triple-negative breast cancer (12.5%). Initial tissue sequencing identified PI3K/AKT pathway alterations in 28.1% of cases. Post-treatment analyses revealed substantial molecular discordance, including progesterone receptor loss (33.3%), HER2 status changes (33.3%), and Ki67 variability (77.8%). Plasma ctDNA analysis was informative in 53.1% of patients and identified additional clinically relevant alterations, including FGFR1 amplification and BRCA1/2 variants not detected in tissue. Conclusions: BC molecular profiles are dynamic and frequently altered by therapy. Longitudinal molecular assessment reveals clinically actionable changes overlooked by static subtyping, supporting a dynamic model of molecular classification, highlighting the potential value of adaptive molecular subtyping to improve treatment stratification and resistance monitoring.

Anorectal melanoma (ARM) is an extremely rare and aggressive malignancy. There is no standard therapeutic management, mainly due to scarcity of data and randomized control trials regarding the optimal surgical strategy. We present the case of a male patient aged 65 years in our hospital,...

The splenic rupture is one of the major causes of hemorrhagic shock with great mortality even in the case of early diagnosis and proper treatment. We present here the case of a patient aged 84 years who came to the intensive care unit of ‘Sf. Ioan’ Clinical Emergency Hospital from Bucharest...

Backgound/Objective: Breast cancer (BC) management has traditionally relied on static clinicopathologic and immunohistochemical biomarkers (hormone receptor status, HER2 expression, and proliferative activity assessed at diagnosis. However, these biomarkers are typically evaluated at a single time point and may not reflect therapy-induced mo-lecular evolution. This study evaluates whether longitudinal molecular profiling before and after treatment better characterizes tumor dynamics and provides clinically ac-tionable insights into treatment response, resistance, and prognosis. Methods: Thirty-two patients with invasive breast carcinoma were analyzed using his-topathology, immunohistochemistry, tissue-based next-generation sequencing, and plasma circulating tumor DNA (ctDNA) analysis. Paired tumor tissue and plasma sam-ples were collected before and after treatment when available. Changes in biomarker expression, molecular subtype, and genomic alterations were assessed to characterize molecular plasticity under therapeutic pressure. Results: The cohort had a median age of 54 years (range 29–86), predominantly invasive ductal carcinoma (>85%) and high-grade disease. Hormone receptor–positive tumors accounted for 78.1%. Molecular subtypes were Luminal A (34.4%), Luminal B HER2− (40.6%), Luminal B HER2+ (6.3%), HER2-enriched (6.3%), and triple-negative breast cancer (12.5%). Initial tissue sequencing identified PI3K/AKT pathway alterations in 28.1% of cases. Post-treatment analyses revealed substantial molecular discordance, including progesterone receptor loss (33.3%), HER2 status changes (33.3%), and Ki67 variability (77.8%). Plasma ctDNA analysis was informative in 53.1% of patients and identified additional clinically relevant alterations, including FGFR1 amplification and BRCA1/2 variants not detected in tissue. Conclusion: BC molecular profiles are dynamic and frequently altered by therapy. Longitudinal molecular assessment reveals clinically actionable changes overlooked by static subtyping, supporting a dynamic model of molecular classification, highlighting the potential value of adaptive molecular subtyping to improve treatment stratification and resistance monitoring.