HER2-positive gastric and gastroesophageal junction (GEJ) cancers have poor prognosis despite standard trastuzumab-based chemotherapy. Immune checkpoint inhibitors (ICIs) may enhance therapeutic efficacy when combined with trastuzumab.

Primary pulmonary lymphoepithelioma-like carcinoma (PLELC) is a rare subtype of non-small cell lung cancer characterized by pronounced regional clustering and high PD-L1 expression. Although early studies suggest that first-line immunotherapy combined with chemotherapy has application potential, we still lack large-sample systematic reviews and cross-high-incidence-area real-world validation.

Medication-related osteonecrosis of the jaw (MRONJ) is a serious complication associated with antiresorptive and antiangiogenic therapies, particularly following tooth extraction. Platelet-rich fibrin (PRF) has been proposed as a biologically active adjunct capable of enhancing tissue repair and potentially reducing the risk of MRONJ. This systematic review and meta-analysis evaluated the effectiveness of PRF in preventing MRONJ and improving postoperative healing in patients undergoing tooth extraction while receiving these medications.

Doxorubicin (DOX)-induced cardiotoxicity remains a major limitation of cancer therapy. Incretin-based therapies are established cardiometabolic agents with pleiotropic cardiovascular effects; however, their potential role in mitigating DOX-related cardiac injury has not been systematically synthesized. We conducted a PRISMA 2020-compliant systematic review to evaluate the effects of incretin-based therapies on DOX-induced cardiotoxicity, with a focus on functional, structural, biomarker, and mechanistic outcomes. PubMed/MEDLINE, Embase, Web of Science, and Scopus were searched through 20 October 2025. Eligible studies included in vivo rodent models of DOX cardiotoxicity and any clinical studies directly evaluating incretin-based therapy during DOX exposure; in vitro studies, non-DOX models, combination-treatment studies, studies not focused on cardiotoxicity, gene therapy-based interventions, and reviews/editorials were excluded. Risk of bias and certainty of evidence were assessed using the SYRCLE tool and GRADE adapted for preclinical research. Thirteen rodent studies were included, and no eligible human study was identified. Investigated agents included liraglutide (n = 4), exenatide/exendin-4 (n = 4), semaglutide (n = 2), and tirzepatide (n = 3). In chronic cumulative-dose DOX models, incretin-based therapies were generally associated with preservation of left ventricular systolic function, with between-study improvements of approximately 7-20 percentage points in left ventricular ejection fraction, along with reductions in injury biomarkers. These effects were accompanied by attenuation of oxidative stress, inflammation, apoptosis, and, in some studies, ferroptosis. In contrast, findings were less consistent in acute single-dose models. Co-treatment during DOX exposure showed the most reproducible protective signal, whereas isolated pretreatment with liraglutide or tirzepatide and post-treatment with exenatide did not show a clear additional benefit. The evidence base is limited by exclusive reliance on small heterogeneous animal studies, predominantly male models, variable dosing/timing protocols, and low-to-very-low certainty of evidence. Overall, incretin-based therapies show biologically plausible cardioprotective effects in preclinical DOX cardiotoxicity, but these findings should be regarded as hypothesis-generating until confirmed in carefully designed clinical studies.

MAPK-pathway inhibitors including BRAF, MEK, and type II RAF inhibitors are now integral to treatment of pediatric low-grade glioma (pLGG), BRAF V600-mutant glioma, NF1-associated tumors, and melanoma brain metastases. Intratumoral and intracranial hemorrhage has emerged as a clinically relevant safety signal, but drug-specific incidence estimates, phenotypic definitions, and contributing mechanisms remain incompletely characterized. We systematically reviewed the evidence and synthesized contributing mechanisms.

Lung cancer is typically a cancer of the elderly, with a median age at diagnosis of 71, and more than one third of the people diagnosed with lung cancer are over 75 years old. Immune checkpoint inhibitors (ICIs) have revolutionised the treatment of cancers, including lung cancer. ICIs targeting the programmed death-1/programmed death-ligand 1 (PD-1/PD-L1) axis, administered in the neoadjuvant setting, the adjuvant setting, or both, are currently the standard of care for resectable non-small-cell lung cancer (NSCLC) worldwide. These ICIs are commonly used in combination with platinum-based chemotherapy and have shown superior efficacy in patients eligible for curative surgery. The concept of immunosenescence, which refers to age-related changes in the immune system - particularly a decline in the efficiency of T-cell mediated responses - raises concerns about the benefits of ICIs in the elderly population.

Immune checkpoint inhibitors (ICIs), comprising anti-cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), anti-programmed cell death protein 1 (PD-1), and anti-programmed death-ligand 1 (PD-L1), have transformed melanoma therapy, yet the tumour microenvironment (TME), the pivotal biological interface where therapeutic efficacy, resistance, and toxicity are determined, remains incompletely characterized. This dual systematic review and meta-analysis (PROSPERO: CRD420261374242) followed PRISMA 2020 and included 58 preclinical (B16F10/C57BL/6; 46 quantitative) and 44 clinical studies (19 quantitative) to calculate pooled standardized mean differences (SMDs) for six intratumoral TME parameters. Checkpoint blockade consistently shifted the TME toward an immune-activated state, an effect that remained robust in sensitivity analyses despite substantial heterogeneity (I-squared heterogeneity statistic (I2) = 68-88%). Preclinically, ICIs significantly increased CD8+ T-cell infiltration (SMD = 1.45, p < 0.001), interferon-gamma (IFN-γ) (SMD = 1.78, p < 0.001), CD8/regulatory T-cell (Treg) ratio (SMD = 0.91, p = 0.005), and apoptosis (SMD = 3.54, p < 0.001) and reduced PD-L1 (SMD = -0.88, p = 0.004) and Ki-67 (SMD = -1.43, p = 0.028). Clinically, CD8+ infiltration and PD-L1 both increased (SMD = 0.72, p < 0.001; SMD = 0.67, p = 0.001), contrasting with the preclinical PD-L1 decrease. Meta-regression demonstrated superior anti-PD-L1 efficacy over CTLA-4 for effector parameters: IFN-γ +3.59 (p = 0.009), CD8/Treg +10.69 (p = 0.003), apoptosis +9.76 (p = 0.004), and Ki-67 -6.28 (p = 0.040). These findings establish the TME as a critical determinant of ICI outcomes, indicate that PD-L1 amplifies effector functions in the B16F10 model, and highlight translational gaps in TME reprogramming.

Ginsenoside Rg3, a rare protopanaxadiol-type saponin enriched during the heat processing of Panax ginseng, has attracted increasing attention as a multitarget anticancer agent. This systematic review examines the anticancer potential of Rg3 through comprehensive searches of the PubMed and Web of Science databases, with a focus on peer-reviewed preclinical and clinical studies. The therapeutic efficacy of Rg3 is critically influenced by its stereochemical configuration, concentration-dependent bidirectional regulation, and pharmacokinetic constraints, including poor oral bioavailability, rapid clearance, and gut microbiota-mediated metabolism. Nanocarrier-based and targeted delivery systems have substantially improved its pharmacokinetic profile and tumor accumulation, supporting its further development for anticancer applications. Within this pharmacological context, Rg3 exhibits broad-spectrum anticancer activity across multiple solid tumors, including hepatocellular carcinoma, melanoma, lung, ovarian, breast, colon, gastric, and prostate cancers, as well as osteosarcoma, renal cancer, lung adenocarcinoma, glioblastoma, gallbladder, nasopharyngeal, cervical, and pancreatic cancers, and the hematological malignancy multiple myeloma. Mechanistically, Rg3 suppresses cancer progression through coordinated regulation of proliferation, apoptosis, autophagy, ferroptosis, angiogenesis, epithelial-mesenchymal transition, cancer stemness, immune evasion, and redox homeostasis, primarily involving the PI3K/AKT/mTOR, NF-[Formula: see text]B, MAPK, Wnt/[Formula: see text]-catenin, EGFR, and p53 pathways. These effects reflect transferable network-level mechanisms rather than tumor type-restricted actions. Moreover, Rg3 demonstrates synergistic effects with chemotherapy, radiotherapy, targeted therapy, and immunotherapy, while reversing drug resistance and attenuating treatment-related toxicity in multiple cancer models and clinical settings. Overall, this review systematically integrates current evidence on the pharmacokinetics, anticancer spectrum, molecular mechanisms, synergistic combinations, immunomodulatory effects, and clinical applications of Rg3, providing a concise framework for the rational development of Rg3-based combination strategies in precision cancer therapy.

With the increasing use of immune checkpoint inhibitors (ICIs) in the first-line treatment of driver mutation-negative non-small cell lung cancer (NSCLC), we conducted a systematic review and meta-analysis to compare efficacy and adverse effects (AEs) between PD-L1 inhibitors and PD-1 inhibitors.

Several prospective and randomized trials support immune checkpoint inhibitors (ICIs) as an emerging component of standard definitive treatment for locoregionally advanced nasopharyngeal carcinoma (LA-NPC). The key uncertainty has shifted from whether ICIs have antitumor activity to how they should be incorporated into multimodality therapy, including therapeutic modality, treatment timing, chemotherapy backbone, treatment duration, and agent selection.

This study was designed to assess the risk of programmed cell death-1 (PD-1) or programmed cell death ligand 1 (PD-L1) related rash in various situations.

The regimen of rituximab we not determined based on evidence from pharmacokinetics. However, rituximab exhibited significant pharmacokinetic variability among different clinical populations, which might be a key factor influencing individual exposure and response to this monoclonal antibody. This systematic review aimed to analyze the traditional and population pharmacokinetics of rituximab and to investigate covariates influencing its pharmacokinetics.

While poly ADP-ribose polymerase (PARP) inhibitors represent a promising treatment strategy in early phase trials of patients with high-grade glioma (HGG), the clinical outcomes exhibit variability, mainly due to drug-specific pharmacokinetics and insufficient biological stratification involving MGMT and IDH status. We aimed to investigate the safety and efficacy of PARP inhibitors in grade 3 and 4 gliomas.

Among several adverse events induced by chemotherapy for patients with far advanced and unresectable cancer, oral mucositis is one that reduces patient quality of life.

Cholangiocarcinoma (CCA) is an aggressive biliary tract malignancy often diagnosed at an advanced stage. For over a decade, gemcitabine-cisplatin (GemCis) remained the standard of care with limited survival benefit. The advent of immune checkpoint inhibitors (ICIs) has transformed the therapeutic landscape, but variability in outcomes and a rapidly expanding evidence base require systematic synthesis.

To summarize diagnostic approaches and management strategies for dry mouth associated with immune checkpoint inhibitors (ICIs) in cancer patients.

Chemotherapy-induced peripheral neuropathy (CIPN) is a common, debilitating, and treatment-limiting adverse effect of many agents used for cancer treatment. There is currently no gold-standard diagnostic criterion nor a widely accepted method for accurate and early identification of CIPN. Vibration perception threshold (VPT), which reflects large-fibre nerve function, has been proposed as a potential biomarker for CIPN.

Hyperglycaemia and/or type 2 diabetes (T2D) can have a detrimental effect on women with breast cancer (BC) undergoing or post-cytotoxic chemotherapy. This systematic review aims to evaluate the short and long-term consequences of hyperglycaemia and/or T2D on treatment outcomes in women with breast cancer receiving cytotoxic chemotherapy.

Examine the quality of evidence relating to the association of routine inflammatory biomarkers neutrophil-lymphocyte ratio (NLR), platelet-lymphocyte ratio (PLR) and monocyte-lymphocyte ratio (MLR) with symptoms, treatment toxicities, and quality of life (QoL) in people with advanced cancer.

Cancer remains a leading global health challenge, and treatment efficacy is often limited by resistance to conventional therapies and their associated toxicities. These limitations have intensified the exploration of alternative strategies, particularly natural compounds with antitumor potential such as Artemisia annua (AA). This review aimed to systematically evaluate the antitumor efficacy and mechanisms of action of AA extracts and derivatives in preclinical animal models. A structured literature search was conducted in PubMed, Scopus, and Web of Science for studies published between 2019 and August 2025, following PRISMA 2020 guidelines with the protocol prospectively registered in PROSPERO (CRD420251113840). Original in vivo investigations reporting the anticancer activity of AA or its derivatives were considered eligible. Of the 176 records initially identified, 21 underwent full-text review, and seven studies met the inclusion criteria for synthesis. Among the included studies, six of seven eligible studies (86%) reported measurable reductions in tumor size or volume, and four documented apoptosis induction. Additional mechanisms included angiogenesis inhibition and ferroptosis activation. Dihydroartemisinin was the most frequently investigated derivative, while novel compounds such as ZQJ29 also showed promising activity. Importantly, no notable systemic toxicity was reported at the administered doses among the seven included in vivo studies available. This finding reflects only the data available across the seven eligible studies, demonstrates a potentially favorable safety profile. So far, the possibility of dose- or regimen-dependent toxicities reported elsewhere in the literature is not excluded; however, further comprehensive studies are needed to confirm this. This review is the first to consolidate recent preclinical evidence highlighting ferroptosis as one of the key mechanisms of AA derivatives, thereby expanding the understanding of their multifaceted anticancer activity. Collectively, the findings underscore the therapeutic promise of AA derivatives and advocate for further investigation into their pharmacokinetics, safety, and integration into regimens with established therapies. These results demonstrate that AA compounds have significant potential as adjuncts or alternatives in cancer management and warrant rigorous evaluation in standardized clinical trials.