Immune checkpoint inhibitors (ICIs) are under extensive investigation as a treatment for triple-negative breast cancer (TNBC) in numerous trials. Given the need to evaluate their therapeutic profile, we conducted this systematic review and meta-analysis to comprehensively assess the safety and efficacy of ICI therapy for TNBC.

The widespread use of antineoplastic drugs in cancer treatment has led to significant concerns regarding the potential health risks posed to healthcare professionals involved in the preparation, administration, and handling of these chemical compounds, including genotoxicity. This systematic review investigates the genotoxicity of various anticancer drugs through the micronucleus assay in mammalian cells through a comprehensive analysis of studies retrieved from PubMed, SCOPUS, and Web of Science. A systematic search conducted in May 2025 identified 28 relevant studies, all of which employed the micronucleus assay. The results indicated that 23 of the reviewed studies observed genotoxic effects linked to several drugs. As for the quality assessment, all studies (but one) were categorized as either strong or moderate; therefore, we consider our findings to be reliable. These findings raise significant concerns regarding the potential health risks associated with oncologic drugs, warranting further investigation and regulatory oversight to ensure professionals' safety. Finally, such findings are very important for clarifying the role of the micronucleus assay as a putative biomarker for evaluating the cancer risk due to anticancer drug exposure in humans.

Chemotherapy-induced alopecia (CIA) affects approximately 65% of patients receiving chemotherapy and has a negative impact on quality of life (QoL). Scalp cooling (SC) is the only FDA-cleared intervention for CIA. This systematic review and meta-analysis evaluated SC adverse events (AEs), reasons for discontinuation, and scalp metastasis incidence.

Recent advancements highlight promising outcomes with immune checkpoint inhibitors (ICIs) when combined with concurrent chemoradiotherapy (CCRT) or chemotherapy in the treatment of locally advanced cervical cancer (LACC). This systematic review and meta-analysis aimed to assess the efficacy and safety of ICIs combined with CCRT/chemotherapy in patients with LACC.

Cisplatin causes nephrotoxicity in approximately 30% of patients. Mannitol has been proposed as a nephroprotective agent, yet the clinical evidence remains inconclusive.

Lung cancer therapy is constrained by profound intrinsic and acquired resistance to targeted therapies and immunotherapy. To overcome this, a new therapeutic paradigm is emerging that targets the unique metabolic and survival dependencies of cancer cells. Mitochondria, the central hubs of metabolism, cell death, and signaling, represent a critical vulnerability. This review provides a new conceptual framework for understanding and targeting mitochondrial pathways in lung cancer. First, this review outlines the key "mitochondrial hallmarks" of lung cancer that create therapeutic windows, emphasizing the critical role of metabolic heterogeneity. Second, it provides a novel, mechanism-based classification of mitochondrial inhibitors into four major classes: (1) electron transport chain (ETC) inhibitors, (2) metabolic enzyme modulators, (3) apoptosis pathway modulators, and (4) mitochondrial quality control (MQC) disruptors. Third, this review critically analyzes the molecular mechanisms by which these inhibitors activate regulated cell death pathways (apoptosis, ferroptosis) and, most importantly, their potential in overcoming therapeutic resistance to standard-of-care. Fourth, it explores the mechanisms of mitochondrial crosstalk within the tumor microenvironment (TME), including intercellular transfer via tunneling nanotubes. Finally, this review presents a systematic review of the clinical landscape, synthesizing data from preclinical models and ongoing clinical trials. This review concludes by highlighting key limitations and future perspectives, positioning MQC and the mitochondrial unfolded protein response (UPRmt) as next-generation targets to improve patient outcomes.

Cancer remains a major global health challenge, which drives the ongoing search for effective and less toxic treatment options. Due to its demonstrated anticancer properties, Artesunate (ART), a well-established antimalarial agent, has gained increasing attention as a promising candidate for oncological applications. This systematic review provides a comprehensive evaluation of ART's therapeutic potential by examining its anticancer efficacy, underlying molecular mechanisms, synergistic capacity, and pharmacological toxicity. An extensive search of the PubMed and Web of Science databases identified relevant peer-reviewed experimental and clinical studies that investigated ART's anticancer activity. The data were systematically extracted with an emphasis on research methodologies, treatment regimens, and mechanistic pathways. Evidence from in vitro and in vivo studies confirms ART's broad efficacy against a range of malignancies, including hematological cancers such as lymphoma, acute myeloid leukemia, and multiple myeloma, and various solid tumors such as lung, pancreatic, colorectal, hepatocellular, breast, ovarian, bladder, gastric, cervical, glioblastoma, melanoma, retinoblastoma, and esophageal cancers. ART exerts its anticancer effects through multiple pathways, including ROS-mediated programmed cell death, ferroptosis induction, mitochondrial dysfunction, the inhibition of proliferation, and the disruption of key signaling networks such as NF-κB, STAT3, and Wnt/β-catenin cascades. Additionally, ART has been shown to enhance the efficacy of conventional chemotherapeutic agents like cisplatin and gemcitabine while also reducing associated toxicities and overcoming drug resistance. These attributes highlight ART's considerable potential as a versatile anticancer agent that exhibits multiple - mechanisms of action and favorable compatibility with existing therapies. However, further rigorous clinical studies are essential to fully establish its therapeutic utility and facilitate its integration into modern oncology practice.

This systematic review and meta-analysis evaluated whether compression therapy prevents chemotherapy-induced peripheral neuropathy (CIPN) in breast cancer patients receiving taxanes.

Betulinic acid (BA), a naturally occurring pentacyclic triterpenoid, exhibits remarkable bidirectional regulatory effects on apoptosis, demonstrating pro-apoptotic activity in cancer cells while protecting normal cells from oxidative stress and apoptosis. This systematic review synthesizes decade-long research to elucidate BA's multifaceted mechanisms across apoptosis-related pathways. In malignant cells, BA induces caspase-dependent apoptosis through both extrinsic pathways mediated by FADD via death receptor activation and intrinsic mechanisms involving ROS accumulation, Bcl-2 family-mediated mitochondrial dysfunction, and ERS-triggered PERK activation. Concurrently, it suppresses PI3K-Akt and NF-κB survival signaling while activating AMPK/mTOR-autophagy crosstalk and p53-dependent DNA damage responses. Paradoxically, BA protects normal tissues by enhancing antioxidant defenses through Nrf2/SOD activation, inhibiting pro-inflammatory TNF-α/NF-κB signaling, and stabilizing mitochondrial integrity. Key to its therapeutic potential is the context-dependent modulation of critical nodes that balance apoptosis initiation and cytoprotection. Structural derivatives and nano-formulations further enhance BA's tumor selectivity and bioavailability. By mapping BA's pleiotropic interactions within apoptotic networks, this review highlights its unique capacity to function as a precision therapeutic agent, offering dual cytostatic and cytoprotective benefits. These insights position BA as a promising candidate for cancer therapy development, warranting further investigation into pathway crosstalk and clinical translation strategies.

Trastuzumab deruxtecan (T-DXd) is a novel antibody-drug conjugate uesd for the treatment of HER2- positive (HER2+)breast cancer. This systematic review aimed to evaluate the efficacy and safety of T-DXd in advanced HER2-positive breast cancer.

This scoping review evaluates the safety and feasibility of combining immune checkpoint inhibitors (ICIs) with radiotherapy (RT) in metastatic cancers. The analysis focuses on key variables that may influence toxicity, including the site of irradiation, the radiation dose, and treatment timing. The primary endpoint was the incidence of grade ≥ 3 adverse events. Following PRISMA guidelines, we conducted a systematic review of 59 studies published between January 2000 and January 2025, selected through a three-step screening process. The dataset included 37 prospective and 22 retrospective studies, encompassing 2 phase III trials and a total of 3593 patients. The median incidence of grade ≥ 3 adverse events ranged from 9.7% to 11% for anti-PD1 agents, 10.5% to 19% for anti-PD-L1 agents, and 20% to 25% for anti-CTLA-4 agents. No clinically significant increase in toxicity was observed when RT was combined with ICI, compared to ICI alone. Available evidence suggests that concurrent ICI and RT is a safe strategy in metastatic cancer, without requiring immunotherapy discontinuation or treatment modification during irradiation.

The role of body composition, specifically sarcopenia and adiposity, in predicting chemotherapy toxicities and outcomes in non-metastatic pancreatic cancer remains unclear. This review assesses the association between body composition metrics and chemotherapy-related outcomes.

Cancer remains a primary global health concern, with treatment-related side effects and malnutrition posing significant challenges to patient care and recovery. In recent years, there has been growing interest in the therapeutic potential of functional food components, especially whey proteins (WPs), due to their notable antioxidant, immunomodulatory, and anticancer properties. This systematic review explores the effects of WPs across various cancer types and assesses their value as supportive nutritional agents. A thorough literature search was conducted in PubMed, Scopus, and Web of Science databases, identifying 24 relevant studies published between 2000 and 2024. The selection process followed PRISMA guidelines. The evidence, drawn from both laboratory and clinical research, suggests that WPs may exert anticancer effects by inhibiting tumor cell growth, promoting apoptosis, enhancing antioxidant defenses, modulating immune activity, and influencing signaling pathways such as the PI3K/Akt, mTOR, and Wnt/β-catenin pathways. Colorectal, breast, and liver cancers emerged as the most extensively studied types. Additionally, the form of WP used-whether concentrate, isolate, or hydrolysate-appeared to influence both biological activity and clinical outcomes. Clinical findings suggest that WP supplementation may support nutritional status, mitigate the adverse effects of chemotherapy, and enhance the quality of life in cancer patients. While the preclinical data are compelling, further high-quality randomized controlled trials are needed to confirm these benefits and determine optimal use in clinical practice. This review highlights WPs as promising, well-tolerated nutritional agents with potential to enhance current cancer care strategies.

Hypoxia, oxidative stress, and impaired protein folding contribute to tumor progression and therapy resistance. Endoplasmic Reticulum Oxidoreductin 1 Alpha (ERO1α) is a key enzyme regulating redox homeostasis in the endoplasmic reticulum by reoxidizing protein disulfide isomerase, facilitating disulfide bond formation, and generating reactive oxygen species. Elevated ERO1α levels are associated with increased tumor aggressiveness, metastasis, and poor clinical outcomes. Despite growing evidence of its tumor-promoting functions, no clinically approved ERO1α inhibitors exist. This systematic review provides a comprehensive and integrative analysis of current research on ERO1α in breast cancer, emphasizing its roles in hypoxia response, angiogenesis, immune modulation, and ferroptosis resistance. We discuss mechanistic links, including VEGF-A maturation and PD-L1-mediated immune evasion, and highlight recent advances in small-molecule ERO1α inhibitors and preclinical therapeutic strategies. By consolidating molecular insights and translational considerations, this review underscores ERO1α as both a promising therapeutic target and potential prognostic marker, offering guidance for future drug development and targeted interventions in redox-dependent cancer pathways.

PARP inhibitors (PARPi) improve ovarian cancer (OC) outcomes, but resistance remains a major challenge without reliable prognostic biomarkers. This study identified epigenetic hallmarks of PARPi resistance by integrating 27 studies (22 preclinical, 5 clinical) from the past 15 years, and validating candidate genes using web-based bioinformatics tools and public microarray/RNA-seq datasets from non-relapsed, primary OC tissues. We hypothesised that early aberrant expression of these epigenetically altered, PARPi resistance-related genes in tumours may be linked to disease progression (PFS) and could serve as early biomarkers to be associated with PARPi resistance during first-line treatment. We confirmed epigenetic involvement in PARPi resistance across 36 genes linked to epigenetic modifications. Of these, 10 genes (n = 614-1435)-including RNASEH2B (HR=1.41), VHL (HR=1.26), ATM (HR=1.22), XRCC1 (HR=1.20), NRP1 (HR=1.16), KAT2B (HR=1.16), EZH2 (HR=1.15), CREBBP (HR=1.14), FZD10 (HR=0.87), and CARM1 (HR=0.86)-showed significant prognostic value for PFS (all: p < 0.05). This 10-gene signature remained collectively significant (HR 1.27, p = 0.014). RNA-seq validation showed differential expression of these genes, with highest fold-change overexpression in tumours for FZD10 (4.20), EZH2 (3.56), and CARM1 (1.61), and lowest in ATM (0.22), KAT2B (0.33), and NRP1 (0.44). GO and KEGG analyses revealed these genes are enriched in key resistance pathways, including impaired DNA repair, reduced replication stress, immune evasion, and stemness maintenance. This review with bioinformatic validation identified a 10-gene epigenetic signature associated with PARPi resistance and disease progression. These clinically actionable genes, aberrantly expressed before treatment, may serve as early biomarkers for risk stratification. Further validation in PARPi-sensitive and -resistant ovarian cancer cohorts is needed.

This meta-analysis compared the efficacy and safety of degarelix and GnRH agonists in prostate cancer treatment.

Advances in early cancer detection and treatment have significantly improved survival rates, resulting in over 18.1 million cancer survivors in the USA. Many of these survivors experience chronic pain, fatigue, and neuropathic symptoms related to cancer or its treatments. Emerging evidence suggests that autonomic nervous system dysfunction plays a crucial role in these symptoms. Heart rate variability (HRV), a measure of autonomic function, has shown potential in predicting the onset and progression of these cancer-related symptoms. This systematic review aimed to assess the association of HRV with pain, fatigue, and neuropathy in cancer patients and survivors.

To systematically review and meta-analyze the available literature on otoprotective measures for cisplatin-induced ototoxicity in head and neck squamous cell cancer (SCC), with a focus on interventions capable of reducing toxicity while preserving oncologic outcomes.

To summarize and assess the existing evidence on the effectiveness and safety of immune checkpoint inhibitors (ICIs) treatments in patients diagnosed with hepatocellular carcinoma (HCC).

Hand-foot syndrome (HFS) is a dermatological side effect of chemotherapies such as capecitabine and pegylated liposomal doxorubicin. Over recent years, numerous randomised controlled trials (RCTs) have investigated various pharmacological strategies to prevent HFS. Although urea cream and celecoxib have shown promising results, the efficacy of topical diclofenac remains unclear. To provide a comprehensive comparison of pharmacological interventions for HFS prevention in cancer patients undergoing chemotherapy, we conducted a network meta-analysis (NMA).