Loss of skeletal muscle mass (SMM) is common during systemic cancer treatment, but the magnitude and variability across cancer and treatment types remain uncertain. We aimed to describe changes in SMM during systemic cancer treatment supported by pooled quantitative estimates.

Essential oils (EOs) and their bioactive constituents have attracted growing interest as potential anticancer agents because they can target multiple pathways involved in tumor progression. However, the literature on their anticancer activity is highly heterogeneous and often limited by methodological weaknesses that reduce the reliability and translational value of the reported findings. This systematic review critically assessed the anticancer activity of EOs and EO-derived compounds by considering only studies that met defined methodological criteria. A PubMed search identified 872 articles published between 2015 and 2026, of which 97 were retained after screening based on EO chemical characterization, evaluation of cancer selectivity using non-tumoral control cells, and direct assessment of EO-driven anticancer effects. Across different tumor models, EOs and their constituents consistently showed selective cytotoxic or antiproliferative activity, commonly associated with oxidative stress, mitochondrial dysfunction, apoptosis, cell-cycle arrest, and modulation of oncogenic pathways. Some studies also reported reduced migration, invasion, and tumor-promoting signaling, while nanoformulation improved stability and efficacy in selected models. Overall, despite encouraging preclinical evidence, the translational potential of EO-based anticancer strategies remains limited by recurrent methodological shortcomings and insufficient in vivo validation. Standardized experimental criteria will be essential to improve reproducibility and support future clinical development.

In recent years, Marine Natural Products (MNPs) have emerged as a significant source for anticancer drug discovery, as many natural products can offer structural diversity, unique mechanisms of action, and relatively low toxicity. This article provides a systematic review of MNPs with reported anticancer activities from 2020 to 2024. These compounds are classified into seven major categories: terpenoids, alkaloids, sterols, polyketides, peptides and proteins, polysaccharides, and macrolides. For each category, we elaborate on the marine sources, structural identification, in vitro anticancer activity, and preliminary structure-activity relationships. We found that sponges and marine-derived fungi are the most abundant sources of highly active compounds. Furthermore, knowledge graph-based analysis reveals that oxygen- and nitrogen-containing heterocycles constitute the core pharmacophores, and target prediction further indicates that MNPs exert anticancer effects through coordinated modulation of a multi-target network involving kinases, proteasomes, and nuclear receptors. This review contributes significantly to a deeper understanding of recent advances (2020-2024) in MNPs and provides critical guidance for promoting the development of innovative anticancer drugs derived from marine resources.

Although immune checkpoint inhibitors combined with chemotherapy improve survival in advanced gastric cancer (AGC), comparative evidence across first-line regimens remains insufficient. This study aimed to systematically evaluate their relative efficacy and safety.

Oral mucositis (OM) is a serious complication of antineoplastic therapy and its clinical presentation can range from small erythematous lesions to large, debilitating ulcerative areas. This adverse effect results from the non-specificity of chemotherapeutic agents. This study aims to determine whether corticosteroid protocols reduce the incidence or severity of OM during antineoplastic treatment.

Immune checkpoint inhibitors (ICIs) have advanced the treatment for triple-negative breast cancer (TNBC), but evidence in older adults remains limited. This study assessed the efficacy and safety of ICIs in elderly patients through a systematic review and meta-analysis of randomized clinical trials METHODS: A systematic search identified trials evaluating ICIs in TNBC. Data from nine studies were pooled using random-effects models. Subgroup analyses examined progression-free survival (PFS) and overall survival (OS) in PD-L1-positive tumors and adults aged ≥65 years.

Triple-negative breast cancer (TNBC), an aggressive subtype lacking oestrogen and progesterone receptors and amplification of HER2 receptors, accounts for 12% to 17% of breast cancers. Adjuvant and neoadjuvant chemotherapy improve survival; however, 30% to 40% of early-stage TNBC cases progress to metastatic disease. Recent evidence suggests that combining immune checkpoint inhibitors (PD-1/PD-L1 inhibitors) with chemotherapy may improve pathological complete response and event-free survival.

Neoadjuvant therapy (NAT) is standard treatment for triple-negative breast cancer (TNBC) but toxicity is a major concern. This study aimed to assess the incidence and risk of grade ≥ 3 adverse events (AEs) associated with NAT in nonmetastatic TNBC. We performed a systematic review and meta-analysis registered in PROSPERO (CRD42024562785). Four databases were searched for randomized controlled trials (RCTs) from 2010 to 2025 reporting grade ≥ 3 AEs in TNBC. Pooled prevalence and risk ratios (RRs) were estimated using random-effects models. Six RCTs including 3316 patients were analyzed. Neutropenia was the most common severe AE, with pooled prevalence of 33.5% for ICIs, 23.7% for PARP inhibitors, and 16.0% for platinum regimens. PARP inhibitors significantly increased neutropenia (RR 1.84) and anemia (RR 2.08), while thrombocytopenia risk was also higher (RR 3.56). ICIs were associated with more febrile neutropenia (14.9%) but without a significant risk increase. ALT elevation was more frequent with platinum regimens (6.4%). Fatal AEs were rare (<1%). NAT improves outcomes in TNBC but is associated with substantial severe toxicity. PARP inhibitors carry the greatest hematologic risks, ICIs add immune-related AEs, and platinum regimens showed the lowest AE burden. Biomarker-driven patient selection and vigilant monitoring are essential to optimize safety.

With the advances in molecular diagnostics and newer treatment approaches, the overall survival and quality of life of patients have increased significantly. However, many anticancer drugs often cause ovarian damage or toxicity, leading to premature ovarian insufficiency, infertility, and serious long-term psychosocial issues, making oncofertility an unmet need in current oncology practice. This manuscript addresses questions such as, "What are the molecular pathways of anticancer drug-induced ovarian toxicity in reproductive-aged females and their clinical applications?" and "How do oncofertility care models and regulation frameworks support fertility preservation in clinical oncology?" Our goal is to provide a clear, comprehensive understanding of how major classes of anticancer drugs cause ovarian damage and to identify potential interventions to improve overall quality of life. From 2770 records, 52 studies were included. Mechanistic evidence shows distinct pathways: alkylating agents trigger oocyte apoptosis through TAp63α activation; platinum drugs and anthracyclines cause mitochondrial dysfunction and oxidative stress; and taxanes interfere with oocyte meiotic spindles. Clinically, this results in measurable loss of ovarian reserves like anti-Mullerian hormone (AMH) and antral follicle count (AFC), and decreased oocyte quality. Existing fertility preservation strategies, such as oocyte/embryo and ovarian tissue cryopreservation, are effective, and gonadotropin-releasing hormone (GnRH) agonists may offer additional protection. Ovarian toxicity from anticancer drugs represents a significant, drug-specific survivorship challenge. Understanding these mechanisms is crucial for risk assessment. To minimize the long-term impact on patients' quality of life, it is essential to incorporate proven fertility-preservation techniques into routine oncology care.

The shift of cancer care to the home setting via oral anticancer therapy has introduced significant challenges to continuity of care and patient safety. Despite its promise, there remains a lack of comprehensive research that characterizes the components of pharmacist interventions and evaluates their impact on clinical outcomes and quality indicators across the continuity of care.

Glioblastoma (GBM) is the most aggressive primary brain tumor with a poor prognosis. The current standard regimen of surgery combined with concurrent temozolomide chemoradiotherapy has limited efficacy. Multiple targeted therapies have been evaluated in randomized controlled trials (RCTs), but results are inconsistent and lack systematic comparisons. This review used network meta-analysis (NMA) to assess the relative efficacy and safety of different targeted drugs vs. standard treatment.

The discovery of Cisplatin marked the beginning of the metallodrug era in oncology. Despite their clinical success, platinum-based compounds present important limitations, including drug resistance and systemic toxicity. These challenges have stimulated interest in alternative metal complexes capable of interacting with biomolecular targets beyond DNA, particularly proteins involved in cancer-related pathways. To systematically identify and categorize protein targets associated with the antitumor activity of metal complexes in preclinical studies, emphasizing their functional classification and biological relevance. A systematic search was conducted in Web of Science, Wiley, Scopus, and ScienceDirect for studies published between January 2015 and March 2025. Original studies evaluating the antitumor activity of metal complexes with experimental or computational evidence of protein-directed mechanisms were included. Reviews, editorials, theoretical studies without experimental support, and studies focused exclusively on serum albumin binding were excluded. Of the 873 records identified, 59 studies met the inclusion criteria. Reported targets were organized according to Gene Ontology-based biological processes, revealing recurrent associations with redox regulation, apoptosis and cell-cycle control, and DNA replication and repair, with fewer studies addressing angiogenesis and drug-resistance mechanisms. Across categories, mechanistic evidence is predominantly derived from in vitro assays and computational analyses, with limited demonstration of selective intracellular target engagement. Current evidence indicates that metal complexes frequently perturb survival-related cellular networks, particularly those associated with redox balance and stress-response pathways. However, the available literature remains largely preclinical and mechanistically heterogeneous, highlighting the need for more rigorous target-validation strategies to clarify the therapeutic relevance of proposed protein targets.

Chemotherapy and targeted therapies, including anthracycline-based regimens or their combination, have significantly improved cancer patient survival; however, they are associated with cancer therapy-related cardiac dysfunction (CTRCD), which may not be adequately detected using conventional two-dimensional echocardiography.

Immune checkpoint inhibitors (ICIs) have become a standard treatment for recurrent or metastatic (R/M) head and neck squamous cell carcinoma (HNSCC), yet survival outcomes remain highly heterogeneous, and reliable host-related prognostic biomarkers are lacking in the immunotherapy era. Growing evidence suggests that nutritional status and body composition may influence immune competence, treatment tolerance, and survival, although data specific to ICI-treated HNSCC are fragmented. We conducted a systematic review and meta-analysis in accordance with PRISMA 2020 guidelines to evaluate the prognostic impact of pretreatment CT-based sarcopenia defined by skeletal muscle index (SMI) and the prognostic nutritional index (PNI) on overall survival (OS) in patients with HNSCC treated with ICIs. PubMed and Embase were searched, and hazard ratios (HRs) with 95% confidence intervals (CIs) were pooled using random-effects models. Study quality was assessed using the Newcastle-Ottawa Scale. Nine studies met the inclusion criteria, of which four evaluated CT-based sarcopenia and five evaluated PNI. In analyses restricted to multivariable-adjusted estimates, pretreatment sarcopenia was significantly associated with poorer OS (HR 2.05, 95% CI 1.48-2.84), with no evidence of heterogeneity. In a prespecified secondary meta-analysis, low PNI was also associated with inferior OS (HR 3.67, 95% CI 2.52-5.32). Sensitivity analyses confirmed the robustness of the pooled estimates. Overall methodological quality was moderate to high. Together, these findings indicate that structural muscle depletion and immune-nutritional impairment represent complementary dimensions of host vulnerability in ICI-treated HNSCC. These readily available host-related markers may support prognostic stratification and hypothesis generation.

Time toxicity-the time patients spend receiving treatment, managing side effects, attending follow-ups and undergoing rehabilitation-is increasingly recognised as an important burden of cancer care. While time toxicity has been studied in routine clinical settings, it has rarely been quantified among patients with cancer enrolled in pharmacotherapy clinical trials. This systematic review aims to quantify time toxicity in this population.

Background/Objectives: Dietary antioxidants are frequently utilized by breast cancer (BC) patients to mitigate treatment-related toxicities and enhance quality of life. However, their clinical efficacy remains highly controversial due to conflicting epidemiological and clinical data. This review aims to critically evaluate the molecular mechanisms, clinical outcomes, and translational challenges of antioxidant supplementation in BC management. Methods: A comprehensive evaluation of current literature-encompassing observational cohorts, randomized controlled trials, and mechanistic in vitro/in vivo models-was conducted. The analysis focused on the pharmacological interactions of diverse bioactive compounds (polyphenols, vitamins, carotenoids) with BC progression and standard antineoplastic regimens. Results: Current evidence demonstrates a paradoxical, double-edged role of antioxidants in oncology. While specific interventions (e.g., Coenzyme Q10, melatonin) effectively ameliorate treatment-induced toxicities without compromising therapeutic efficacy, the concurrent administration of antioxidants during cytotoxic chemotherapy can inadvertently neutralize essential reactive oxygen species (ROS), correlating with increased disease recurrence and mortality. Furthermore, clinical translation is severely hindered by the intrinsic hydrophobicity of natural compounds, the lack of whole-food matrix standardization, and dose-dependent hepatotoxicity. Emerging targeted delivery systems, such as lipid nanoformulations, show significant potential in overcoming these pharmacokinetic barriers. Conclusions: The therapeutic viability of antioxidant supplementation in BC is not universal; it is heavily dictated by intrinsic tumor biology, specific treatment modalities, and chronopharmacology. These findings underscore a critical biological imperative to transition from generalized dietary guidelines toward a rigorous paradigm of precision nutritional oncology, strictly avoiding concurrent antioxidant supplementation during active oxidative therapies.

The objective is to assess the effectiveness and safety of combining PD-1 inhibitors with CTLA-4 inhibitors for melanoma treatment, drawing on current meta-analysis findings and evaluating the supporting evidence. We used medical subject words and free text words (such as "PD-1 inhibitor", "CTLA-4 inhibitor", "melanoma") as search keywords to search the literature in six literature databases from the establishment of the database to 11 April 2025. Using the PICO (Participant, Intervention, Control, and Outcome) framework, we identified 27 unique associations between combination treatment efficacy outcomes and 70 unique associations between adverse event outcomes, which were re-evaluated using a random effects model. A total of 10 meta-analysis were included, including 36 randomized controlled trials and two retrospective studies. According to the evaluation meta-analysis of AMSTAR 2 (A MeaSurement Tool to Assess Systematic Reviews, version 2), all 10 meta-analysis were of very low quality. The association of outcome indicators was re-analyzed based on the random effects model, of which 26 associations showed high efficacy of combination therapy and 66 associations showed poor safety of combination therapy. In conclusion, a PD-1 inhibitor combined with a CTLA-4 inhibitor is a very effective method for the treatment of melanoma, but the incidence of various types of adverse reactions is high, and the evidence is not reliable. Therefore, future studies need higher quality evidence.

Methotrexate (MTX) is a long-standing drug used to treat leukemia (at high doses to inhibit DNA/RNA synthesis) and rheumatoid arthritis (at low doses for anti-inflammatory effects). Its characteristic narrow therapeutic range, in terms of efficacy and safety associated with MTX, are important factors to consider when deciding whether to prescribe it. A major challenge in its use is interindividual variability which is largely attributed to germline genetic polymorphisms in genes encoding proteins that control the pharmacokinetics or pharmacodynamics of MTX.

Advances in cancer survival have made fertility preservation an essential clinical need for young female patients. While traditional chemotherapy's gonadotoxicity is well established, the effects of newer systemic therapies (immune checkpoint inhibitors, poly [adenosine diphosphate-ribose] polymerase inhibitors, and cyclin-dependent kinase 4/6 inhibitors) on female fertility remain unclear. This systematic review aims to compare the impact of these agents on ovarian function and fertility outcomes.

To systematically evaluate and update the evidence about photobiomodulation therapy (PBMT) as a therapy for the prevention and/or treatment of oral mucositis (OM) induced by antineoplastic therapies.