Skin rash is the most common adverse effect in patients with cancer receiving epidermal growth factor receptor inhibitors (EGFRIs), which can impair quality of life and lead to treatment discontinuation. Numerous primary studies have explored factors that may predict the development of skin rash. However, the wide range of variables and substantial heterogeneity among these studies limit the availability of high-quality, synthesised evidence. A comprehensive scoping review is therefore warranted to systematically map and synthesise the risk factors for EGFRI-induced skin rash in patients with cancer.

Despite advancements in multimodal therapies, oral squamous cell carcinoma (OSCC) continues to exhibit poor clinical outcomes, particularly in advanced and recurrent cases. Recent studies have identified the calcium-binding protein S100A2 as a critical mediator of OSCC progression and resistance to therapy. Our prior work demonstrated that cytoplasmic overexpression of S100A2 in oral cancer patients is associated with tumor recurrence and reduced survival. Given its reported role in promoting epithelial-to-mesenchymal transition (EMT), cellular proliferation, and invasiveness, we investigated the in vitro functional impact of S100A2 inhibition in OSCC.

Breast cancer (BC) is a complex illness that affects millions of women globally. As its incidence rises, new treatment strategies are needed. Veratrum viride, a traditional medicinal herb, is known for its therapeutic potential, yet its molecular mechanism of action against BC remains unclear. The purpose of this preliminary investigation is to assess V. viride's anti-breast cancer potential by identifying its active compounds and using bioinformatics techniques to clarify their multi-target mechanisms.

Both CDK2 (cyclin-dependent kinase 2) and EGFR (epidermal growth factor receptor) play significant roles in the development and progression of colorectal cancer. In vitro studies of several hydroxyxanthone derivatives for the treatment of WiDr cancer cell lines have revealed potential anticancer activity against colorectal cancer. The present study aims to identify hydroxyxanthone derivatives as potential drug candidates for colorectal cancer treatment through an in silico approach.

Cervical cancer is the second leading cause of mortality in women globally, with its incidence increasing due to multidrug resistance (MDR) and adverse side effects associated with chemotherapeutic agents. Hence, this study was carried out to investigate the selective cytotoxicity and apoptotic induction potential of Buddleja polystachya leaf diethyl ether (BPL-DE) extract on cervical cancer HeLa cell lines.

The aim of the study was to determine how the chemotherapeutic alkylating agent dacarbazine, together with the application of the miR-204-5p mimic in vivo, affects the presence of disseminated melanoma cells in distant organs - the lungs and liver.

Malignant pleural effusion (MPE) portends poor prognosis in advanced cancer. Strategies that integrate potent tumor killing with immunosuppressive microenvironment reprogramming are crucial for the treatment of MPE. Studies show that irradiated tumor cell-derived microparticles (RT-MPs) possess natural tumor-targeting cytotoxicity and innate immune activation properties. To further boost the tumoricidal effects of RT-MPs, we developed innovative chemoradiotherapy-integrated tumor cell-derived microparticles (CR-MPs) by loading RT-MPs with chemotherapeutic agents, including methotrexate (MTX), monomethyl auristatin E (MMAE), or doxorubicin (DOX). CR-MPs exhibited superior tumoricidal activity over both RT-MPs and free drugs against a range of tumors. Specifically, MTX-loaded CR-MPs (CR-MPs@MTX) triggered mitochondrial oxidative stress and immunogenic ferroptosis in tumor cells, while directly reprogramming macrophages toward the M1 phenotype and stimulating dendritic cells via cGAS-STING/NF-κB pathway activation. In murine MPE models, CR-MPs effectively suppressed tumor progression, extended survival, and demonstrated favorable biosafety. When combined with immunotherapy, this approach achieved a cure rate of up to 70%, induced durable immunological memory, and retained efficacy against chemotherapy-resistant tumors. This study establishes CR-MPs as a novel platform with robust therapeutic efficacy against MPE, highlighting their translational potential as a precision concurrent chemoradiotherapy strategy for MPE management in clinical settings.

Although cisplatin (CDDP) is widely employed in combination immunotherapy, no CDDP-based regimen has shown a survival benefit when treating the ovarian cancers. This is mainly because the impact of CDDP on immunotherapy is not fully understood. A critical gap concerns how CDDP reshape the tumour microenvironment, especially through extracellular vesicles (EVs)-mediated communication. In this work, using human and murine ovarian cancer cells as a model, we demonstrate that CDDP boosts the secretion of EVs from cancer cells, while exerting no such effect on non-cancerous cells. These CDDP-induced tumour-derived EVs, in turn, drive the differentiation of CD4+ T cells towards immunosuppressive regulatory T cells (Treg cells), which are known to limit the efficacy of immunotherapy. Based on next-generation sequencing, a significant enrichment of miR-181a-5p was identified in CDDP-induced tumour-derived EVs, and further functional studies confirmed that this microRNA promoted Treg cell differentiation via suppressing sirtuin 1 (SIRT1), a key regulator of the transcription factor forkhead box protein P3 (FOXP3). Importantly, inhibition of miR-181a-5p abrogated the Treg-promoting effect of CDDP-induced tumour-derived EVs, a finding further validated in vivo, where blockade of miR-181a-5p not only impaired Treg differentiation but also restored T-cell-mediated antitumour immunity and restrained tumour growth. Together, these findings uncover a previously unrecognised mechanism by which CDDP exacerbates immunosuppression via miR-181a-5p-enriched EVs and suggest that targeting this pathway could improve the therapeutic efficacy of combination immunotherapy in ovarian cancer.

This network meta-analysis evaluated the efficacy of 5-hydroxytryptamine-3 (5-HT3) receptor antagonists, with or without Dexamethasone (D), for preventing chemotherapy-induced nausea and vomiting (CINV) in patients undergoing highly emetogenic chemotherapy (HEC) who were limited to these regimens.

Cancer stem cells (CSCs) contribute to an immunosuppressive microenvironment through complex mechanisms and tumor-immune interactions. However, the key determinants of CSC characteristics in driving tumor progression, immune suppression, and response to ICIs remain unclear and require systematic investigation. This study developed a quantitative systems pharmacology (QSP) model covering various CSC properties, thereby capturing the temporal dynamics and CSC-immune interactions in triple-negative breast cancer (TNBC). Using the unified longitudinal dataset of tumor growth, CSC frequency, and immune cell dynamics that we obtained from BALB/c mice bearing wild-type or Cd274-knockout 4T1 cells under various inoculation conditions, which provides multi-dimensional insights into CSC-related biology, the QSP model was calibrated and validated. Simulations and sensitivity analysis indicated that TNBC tumors with strong stemness exhibited significantly accelerated tumor growth and reduced infiltration of cytotoxic immune cells such as cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells. These were associated with CSCs' enhanced self-renewal capacity, stemness maintenance, secretion of transforming growth factor beta (TGF-β) and vascular endothelial growth factor (VEGF), and PD-1/PD-L1-mediated immunosuppression. ICIs showed minimal efficacy in tumors with enhanced stemness, which was also linked to the aforementioned characteristics. Both the administration sequence and initiation timing of ICIs differentially influenced the therapeutic outcomes. These findings elucidate the roles of CSCs in TNBC progression, tumor immunity, and ICI efficacy while identifying the key underlying CSC characteristics, suggesting the potential value of assessing CSC biomarkers or abundance before ICI treatment and support the development of ICIs and anti-CSC combination therapies.

Pancreatic ductal adenocarcinoma (PDAC), one of the most lethal malignancies, exhibits a 5-year survival rate below 10% and extremely poor clinical prognosis. Over 90% of PDAC patients harbor KRAS gene driver mutations, which promote tumor proliferation, invasion, and immunosuppression of the tumor microenvironment through constitutive activation of downstream RAF/MEK/ERK and PI3K/AKT/mTOR signaling pathways. Although the therapeutic potential of targeting KRAS has been recognized for decades, its smooth protein structure and lack of traditional drug-binding pockets led to its long-standing classification as an "undruggable" target, resulting in limited efficacy of early targeted agents. Recent breakthroughs with next-generation KRAS inhibitors have transformed the therapeutic landscape for pancreatic cancer. This review synthesizes evidence from basic research and clinical translation to provide a theoretical foundation and practical guidance for the precision treatment of KRAS-mutant pancreatic cancer.

Patient-derived cells (PDCs) and patient-derived organoids (PDOs) are complementary preclinical models widely used in translational cancer research. However, their molecular and functional differences have not been systematically characterized. This study established and analyzed paired PDC and PDO models derived from the same gastric cancer ascites to delineate platform-dependent molecular and functional profiles.

The longitudinal patterns of patient-reported outcomes and their association with mortality in routine oncology care are largely unexplored.

Immune checkpoint inhibitors (ICPis) are associated with islet function impairment (IFI), manifesting as hyperglycemia, diabetes mellitus (DM), or diabetic ketoacidosis (DKA). Delayed detection and management may lead to irreversible β-cell damage and life-threatening complications. We conducted a systematic review and meta-analysis to assess the risk of IFI associated with ICPis.

In this paper, we report a case of sequential immune-related adverse events induced by envafolimab in a patient with small cell lung cancer (SCLC), including immune checkpoint inhibitor-associated diabetes mellitus (ICI-DM), diabetic ketosis (DK), and pneumonitis (CIP). A 63-year-old male with limited-stage SCLC received 4 cycles of etoposide plus carboplatin chemotherapy followed by radiotherapy, concurrent with maintenance immunotherapy using envafolimab. Eight months after initiating immunotherapy, the patient developed symptoms of dry mouth and excessive thirst. The clinical presentation was consistent with ICI-DM, though all diabetes-associated autoantibodies were negative. After achieving glycemic control with insulin, envafolimab was resumed. At 15 months, metastasis to the left submandibular region was identified and managed with localized iodine-125 seed implantation; envafolimab monotherapy was continued as maintenance treatment. Nineteen months after initiation of immunotherapy, the patient presented with chest tightness, shortness of breath, and dyspnea. Further diagnostic evaluation confirmed CIP and radiation pneumonitis, which improved following glucocorticoid therapy. Envafolimab was consequently suspended, and topotecan therapy was initiated for one month as second-line therapy, but was ultimately discontinued due to financial constraints. Six months after discontinuing topotecan, the patient was readmitted due to a progressively enlarging left submandibular metastases. Laboratory findings upon admission revealed DK, which had occurred due to self-discontinuation of insulin and a switch to oral hypoglycemic agents one week ago. During hospitalization, recurrent syncope of unknown origin occurred. After clinical improvement with supportive care, anti-tumor therapy with anlotinib was initiated as third-line therapy. Following envafolimab immunotherapy, the patient sequentially developed ICI-DM, DK and CIP. With prompt intervention, severe complications such as diabetic ketoacidosis (DKA), hyperosmolar hyperglycemic state, and respiratory failure were successfully avoided. This case underscores the importance of early recognition and management of immune-related adverse events (irAEs). The occurrence of DK after self-discontinuation of insulin highlights the necessity for long-term insulin therapy in ICI-DM. The patient remains alive with an overall survival exceeding 27 months, suggesting that ICI-DM may represent a potential prognostic biomarker for favorable outcomes in patients receiving immunotherapy.

The efficacy of immune checkpoint inhibitors (ICI) combined with chemotherapy as a neoadjuvant/adjuvant therapy for locally advanced penile squamous-cell carcinoma (PSCC) remains unclear.

Gastrointestinal stromal tumor (GIST) is the most common mesenchymal tumor of the gastrointestinal tract, with its pathogenesis primarily linked to activating mutations in the KIT or platelet derived growth factor receptor alpha (PDGFRA) genes. Surgical resection remains the standard curative treatment for localized GIST; however, ~50% of patients eventually develop recurrence or metastasis. Since the introduction of imatinib in the early 21st century, the management of metastatic GIST has shifted from solely surgical intervention to a systemic, chronic disease management model centered on tyrosine kinase inhibitors (TKIs). However, during the course of treatment, most patients develop drug resistance. Despite the transformative impact of TKIs, some critical clinical challenges remain unresolved. Intratumoral heterogeneity, in particular, poses a significant obstacle, as tumors often comprise diverse populations of cells with varying genetic and molecular profiles. This diversity means that while some subclones may initially respond well to TKI therapy, others harboring inherent or acquired resistance mutations can continue to proliferate, ultimately leading to treatment failure. Additionally, the limited durability of TKIs responses, even in tumors initially sensitive to treatment, remains a pressing concern. Moreover, the lack of curative systemic options for advanced GIST, along with adverse drug reactions, underscores the unmet needs within this patient population. These challenges underscore the necessity of this review, which discusses current standard drug treatment strategies for advanced GIST, including sequential TKIs therapy and investigations into mechanisms of drug resistance. Finally, the review explores precise and actionable future directions for GIST drug development and clinical management, including mutation-stratified therapeutic sequencing, rational TKI-based combination regimens, and circulating tumor DNA (ctDNA)-guided real-time treatment monitoring and resistance surveillance.

To evaluate the efficacy, safety, and treatment burden of intravitreal ranibizumab (RBZ) combined with a dexamethasone (DEX) intravitreal implant compared to ranibizumab monotherapy for macular edema (ME) secondary to non-ischemic retinal vein occlusion (RVO).

Previous research has demonstrated the effectiveness of lenvatinib and programmed death-1 (PD-1) blockades in the treatment of sarcoma. However, there is limited information regarding the efficacy and safety of combining lenvatinib with PD-1 blockades as a re-challenge therapy in patients with metastatic soft tissue sarcoma (STS) following prior treatment failure with tyrosine kinase inhibitors (TKIs).

Skp1 is a potential pharmacological target for cancer treatment. However, the few Skp1 inhibitors reported to date have exhibited limited structural diversity and target specificity. This highlights the need for new chemical scaffolds that could potentially be developed into potent and specific Skp1 inhibitors.