The standard treatment for breast cancer typically includes surgery, often followed by systemic therapy and individualized treatment regimens. However, there is growing interest in identifying pre-therapeutic biomarkers that can predict tumor response to neoadjuvant chemotherapy (NACT). This study systematically evaluated various analytical parameters, including age, TNM stage, histological type, molecular subtype, and several biomarker ratios, such as the platelet-to-lymphocyte ratio (PLR), neutrophil-to-lymphocyte ratio (NLR), lymphocyte-to-monocyte ratio (LMR), systemic immune-inflammatory index (SII), and prognostic nutritional index (PNI). We aimed to assess the predictive value of these parameters regarding the tumor’s response rate to NACT. The analysis revealed a statistically significant association between the pathological complete response—pCR (absence of any detectable cancer cells in the tissue following neoadjuvant chemotherapy (NACT))—rate and NLR in the subgroup with values between 1 and 3 (p = 0.001). The optimal cut-off for PLR was determined to be 120.45, with 80.55% of patients achieving pCR showing PLR values below this threshold (p = 0.000). Similarly, the LMR cut-off was found to be 12.34, with 77.77% of patients with pCR having LMR values below this threshold (p = 0.002). Additionally, lower pre-therapeutic values of NLR (p < 0.001), PLR (p = 0.002), SII (p = 0.001), and LMR (p = 0.001) were significantly correlated with pCR compared to the non-pCR subgroup (p < 0.005). These findings highlight the predictive potential of these biomarkers for achieving pCR following NACT. Our study supports the hypothesis that pre-therapeutic values of NLR, PLR, SII, and LMR can serve as predictive biomarkers for pCR in breast cancer patients undergoing NACT. However, the PNI did not demonstrate predictive potential in relation to pCR. These biomarkers may provide valuable insights into patient prognosis and guide personalized treatment strategies.

Introduction: Lipid metabolism plays a crucial role in breast cancer’s progression, treatment response, and prognosis. Alterations in triglycerides (TGs), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) have been implicated in tumor aggressiveness and chemotherapy outcomes. This review examines the relationship between dyslipidemia and breast cancer, with a focus on chemotherapy-induced lipid alterations and their prognostic significance. Methods: A comprehensive literature search was conducted in PUBMED, Web of Science, and Google Scholar, identifying 108 unique studies. After applying the inclusion criteria, 21 studies were selected for analysis, covering lipid profile changes before, during, and after chemotherapy, as well as their impact on treatment response and clinical outcomes. Results: Breast cancer patients exhibited lower baseline TC, TG, and LDL-C levels compared to healthy controls; however, chemotherapy significantly increased these markers while decreasing HDL-C from 1.1 to 0.9 mmol/L. The incidence of dyslipidemia rose from 42.98% pre-treatment to 58.28% post-treatment. Chemotherapy-induced lipid alterations were most pronounced in anthracycline- and taxane-based regimens, leading to a 38% increase in TGs and a 23% reduction in HDL-C. While some studies reported that lipid levels normalized post-treatment, others indicated persistent dyslipidemia up to 12 months later. High baseline HDL-C was associated with a better chemotherapy response, whereas elevated TGs and LDL-C correlated with increased tumor aggressiveness, lower pathological complete response rates, and a higher relapse risk. Patients with persistently high post-treatment TGs had significantly worse disease-free survival, with a 30% relapse rate compared to 18% in those with normal TG. Preliminary evidence suggests that lipid-lowering therapies, such as statins, may offer therapeutic benefits in breast cancer by targeting the cholesterol synthesis pathways involved in tumor growth, though further clinical trials are required. Conclusions: Dyslipidemia is a key metabolic factor influencing breast cancer’s progression, treatment response, and long-term prognosis. Chemotherapy-induced lipid alterations may persist, increasing cardiovascular risk and potentially affecting therapeutic efficacy. Routine lipid monitoring and metabolic interventions could enhance treatment outcomes and survivorship. Future research should focus on developing lipid-targeted strategies to optimize breast cancer management.

Objective: Uncovering the renoprotective and anti-inflammatory effects of atorvastatin treatment in diabetic-and-obese rats by employing traditional renal function indicators (urea and creatinine) and four prototypical cytokines (IL-1β, il-6, IL-17α, TNFα). Method: Twenty-eight male Wistar rats, aged 6 months, 350–400 g, were randomized into four groups. The first group, G-I, the denominated control, were fed standard chow over the whole course of the experiments. The rodents in G-II were exposed to a High-Fat Diet. The last two groups were exposed to Streptozotocin peritoneal injection (35 mg/kg of body weight). A short biochemical assessment was performed before diabetes model induction to ensure appropriate glucose metabolism before experiments. Following model induction, only rodents in group G-IV were gradually introduced to the same High-Fat Diet as received by G-II. Model confirmation 10 days after injections marked the start of statin treatment in group G-IV, by daily gavage of atorvastatin 20 mg/kg of body weight/day for 21 days. At the end of the experiments, the biochemical profile of interest comprised typical renal retention byproducts (urea and creatinine) and the inflammatory profile described using plasma levels of TNFα, IL-17α, IL-6, and IL-1β. Results: Treatment with Atorvastatin was associated with a statistically significant improvement in renal function in G-IV compared to untreated diabetic rodents in G-III. Changes in inflammatory activity showed partial association with statin therapy, TNFα and IL-17α mirroring the trend in urea and creatinine values. Conclusions: Our results indicate that atorvastatin treatment yields a myriad of pleiotropic activities, among which renal protection was clearly demonstrated in this model of diabetic-and-obese rodents. The statin impact on inflammation regulation may not be as clear-cut, but the potential synergy of renal function preservation and partial tapering of inflammatory activity requires further research in severely metabolically challenged models.

Background and Objectives: Post-thyroidectomy hypoparathyroidism (hypoPTH) is the most common complication of total thyroidectomy. Transient hypoPTH was defined as postoperative day 1 (POD1) intact parathyroid hormone (PTH) < 15 pg/mL and/or symptomatic hypocalcemia (<8.0 mg/dL), requiring supplementation, resolving within six months. We evaluated POD1 calcium, PTH, and their combination; identified preoperative predictors; and compared absolute with percent-change metrics. Materials and Methods: Participants comprised a retrospective single-center cohort of 380 consecutive adults undergoing total thyroidectomy between January 2023 and December 2025. Multivariable logistic regression identified preoperative predictors, and receiver operating characteristic (ROC) analysis evaluated POD1 biomarkers. Because both biomarkers are part of the outcome definition, a pre-specified sensitivity analysis re-evaluated POD1 PTH and ΔPTH against PTH-independent outcomes (POD1-calcium-defined hypocalcemia and permanent hypoPTH). Subgroups examined malignancy and central neck dissection (CND). Results: The cohort comprised 193 males (50.8%) and 187 females (49.2%), with a median age of 53 years (IQR 38–69). Indications were multinodular goiter (45.0%), differentiated thyroid cancer (37.9%), Graves’ disease (15.0%) and recurrent disease (2.1%). CND was performed in 9.5% of patients. Transient and permanent hypoPTH occurred in 132 (34.7%) and 11 (2.9%) patients. Thyroid gland weight was the sole independent preoperative predictor (OR 0.982, 95% CI 0.969–0.995, p = 0.008), with smaller glands conferring higher risk. Against the composite outcome, POD1 calcium and PTH yielded AUCs of 0.997 and 0.991 (combined 1.000), reflecting partial circularity. In the decoupled-outcome sensitivity analysis, POD1 PTH retained good-to-excellent discrimination for severe hypocalcemia (AUC 0.943) and permanent hypoPTH (AUC 0.976). Malignant cases showed a greater relative PTH decline than benign cases (−53.7% vs. −38.5%, p = 0.013) despite comparable absolute POD1 values, and CND did not increase risk. Conclusions: Combined POD1 calcium and PTH provided strong biochemical confirmation of transient hypoPTH, but the composite-outcome AUCs reflect internal definitional consistency rather than independent predictive performance; the decoupled-outcome AUCs (0.93–0.98) are the conservative benchmark. Thyroid gland weight was an inverse risk modifier with limited stand-alone utility. Multicenter prospective validation is required.

Background: The benefit of adding hyperthermic intraperitoneal chemotherapy (HIPEC) to cytoreductive surgery (CRS) in ovarian cancer with peritoneal metastasis remains debated outside selected indications. We performed a systematic review and meta-analysis to quantify survival, perioperative morbidity, and completeness of cytoreduction using study-level data. Methods: PubMed/MEDLINE, Embase, and Web of Science were searched. Eligible English-language studies included ovarian cancer patients undergoing CRS plus HIPEC and reported at least one of the following: overall survival (OS), progression-free survival (PFS), Grade III–IV complications, or CC-0 rate. Random-effects meta-analyses were conducted using inverse-variance pooling. For HR outcomes, DerSimonian–Laird τ² with Hartung–Knapp confidence intervals was applied. Proportions were pooled using logit transformation (PLOGIT) with random-effects models. Results: Twelve studies (n = 567) were included. Only two studies provided extractable HRs for OS and PFS (n = 217). CRS plus HIPEC was associated with improved OS (HR 0.68, 95% CI 0.52–0.90, p = 0.0023; I² = 0%; prediction interval 0.14–3.34) and improved PFS (HR 0.70, 95% CI 0.31–1.57, p = 0.0007; I² = 0%; prediction interval 0.18–2.66). Across 12 studies (n = 563), the pooled Grade III–IV complication rate was 0.18 (95% CI 0.14–0.22; I² = 16.3%; prediction interval 0.12–0.26). In 10 studies (n = 385), the pooled CC-0 rate was 0.87 (95% CI 0.79–0.92; I² = 46.7%; prediction interval 0.66–0.96). Conclusions: CRS plus HIPEC shows a favorable signal for OS and PFS in the limited HR-eligible evidence and appears feasible, with a pooled severe complication rate of ~18% and high CC-0 rates. Current data support HIPEC primarily as a targeted intensification strategy in carefully selected patients, while broader adoption requires additional randomized, context-specific evidence.

Background: Platinum-resistant ovarian cancer with peritoneal metastases remains a therapeutic frontier marked by limited systemic efficacy and a persistent unmet clinical need for effective locoregional strategies. Pressurized intraperitoneal aerosol chemotherapy (PIPAC) has emerged as a novel minimally invasive platform designed to enhance intraperitoneal drug distribution and overcome biological barriers to chemotherapy delivery. Methods: We performed a PRISMA-compliant systematic review and meta-analysis evaluating clinical outcomes of PIPAC in platinum-resistant ovarian cancer. Primary endpoints included histologic regression (PRGS ≤ 2), severe toxicity, and 12-month overall survival, complemented by exploratory analyses of treatment feasibility, disease burden dynamics, and bidirectional therapy strategies. Results: PIPAC demonstrated a consistent signal of biologic activity, with pooled histologic response rates indicating meaningful tumor regression despite advanced disease. Severe toxicity remained low across studies, supporting the favorable tolerability of repeated intraperitoneal treatment. Survival outcomes were clinically relevant for a heavily pretreated population, while feasibility analyses suggested that PIPAC may facilitate downstream surgical opportunities in selected patients. Exploratory findings further supported the concept of intraperitoneal disease modulation, reflected by reductions in peritoneal cancer index and integration within multimodal treatment pathways. Conclusions: Beyond a purely palliative intervention, PIPAC may represent a biologically active component of personalized treatment strategies for platinum-resistant ovarian cancer. These findings redefine the therapeutic narrative from symptom control toward disease modulation and treatment escalation, underscoring the need for prospective trials to refine patient selection and optimize multimodal sequencing.