Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype lacking oestrogen, progesterone, and HER2 receptors, thus limiting the effectiveness of targeted therapies. Triazole compounds have emerged as promising anticancer agents because of their structural versatility, chemical stability, and ability to interact with multiple biological targets. This review summarises the chemistry, biological significance, and therapeutic potential of triazole derivatives against TNBC. It highlights key anticancer mechanisms, including apoptosis induction, cell cycle arrest, inhibition of angiogenesis and metastasis, and modulation of major oncogenic signalling pathways. The review also compares synthetic and naturally derived triazole compounds, emphasising structure-activity relationships and evidence from preclinical studies. In addition, it discusses the contribution of computational approaches, including molecular docking, virtual screening, and predictive modelling, to accelerate triazole-based drug discovery. Overall, this review underscores the potential of triazole pharmacophores as effective therapeutic candidates for TNBC and provides directions for future research to overcome therapeutic resistance.

NOTCH2NLA is a newly identified gene that has recently emerged as a potential key regulator in cancer biology. Although evidence suggests its biological significance, its roles across different cancer types and clinical relevance remain poorly characterized. This study aims to comprehensively investigate the functional value of NOTCH2NLA across multiple cancer types.

Using advanced bioinformatics tools and publicly available datasets, we analyzed the expression profiles of NOTCH2NLA, assessed its prognostic value for survival outcomes, and examined its role in immune regulation and cancer-related signaling pathways. Genetic alterations and immune infiltration patterns were further explored to evaluate its potential role in tumor development.

NOTCH2NLA exhibited differential expression patterns across various cancer types, with its expression levels significantly correlated with patient survival. Additionally, NOTCH2NLA was found to interact with immune cells, modulate immune infiltration, and participate in key biological processes essential for cancer progression.

The findings suggest that NOTCH2NLA plays a multifaceted role in cancer biology, particularly through involvement in immune-related pathways. These results underscore the importance of further exploring how NOTCH2NLA contributes to immune evasion and tumor progression.

This study provides comprehensive insights into the pan-cancer functions of NOTCH2NLA and supports its potential as a promising target for personalized cancer therapies.

The core ethical principles of autonomy, beneficence, non-maleficence, and justice are not new topics of discussion in pediatric and adult medicine. However, these principles become far more complex in pediatrics, where parental authority must serve as a proxy for the child's welfare. This case analysis examines the application of the Best Interests Standard (BIS) in pediatric palliative care through the story of a 9-year-old boy with relapsed metastatic medulloblastoma and significant social challenges. As the child's condition declined and curative options were no longer beneficial, the ethical focus shifted from preserving future-oriented interests to meeting immediate experiential needs for comfort, safety, and relief of suffering. Resource limitations, notably in rural areas with scarce pediatric palliative services, intensified the ethical tensions and decision-making. This case illustrates how assessments of best interests evolve with changing clinical circumstances and why, near the end of life, comfort-focused care often becomes the most ethically appropriate option.

Most cancer therapeutics that show preclinical promise fail in clinical trials, underscoring the need for complementary disease models. Over the past two decades, zebrafish models have matured from a tool for studying vertebrate development into a versatile platform spanning the translational cancer pipeline. Transgenic and transplantation zebrafish models have dissected fundamental mechanisms of tumor initiation and metastasis. Beyond mechanistic insight, phenotypic chemical and genetic screens provide a rapid, whole-organism filter to prioritize and repurpose therapeutic candidates, several of which have reached the clinic. Most recently, zebrafish patient-derived xenografts have begun to predict individual patient treatment responses within clinically actionable timeframes. Tracing this evolution, we argue that zebrafish models are not a replacement for other systems but earn their translational value when applied to the questions they answer best and when embedded in co-clinical workflows alongside oncology teams.

Gastrodin (GAS), a natural polyphenolic compound derived primarily from Gastrodia elata, exhibited a wide spectrum of pharmacological activities, with growing evidence supporting its anticancer potential. This review summarized preclinical findings on the anticancer effects of GAS across multiple cancer types, including brain, breast, colorectal, liver, oral, and skin cancers. The literature was systematically collected from major databases such as PubMed, Scopus, Web of Science, and Google Scholar, focusing on studies published from 2013 onward. Evidence indicates that GAS exerted anticancer effects via multiple cellular and molecular mechanisms, including apoptosis, ferroptosis, cell cycle arrest, inhibition of glycolysis, suppression of oncogenic signaling pathways (e.g., NF-κB, PI3K/Akt), immune modulation, and attenuation of inflammation and oxidative stress. Preclinical in vitro and in vivo studies demonstrated significant tumor growth suppression and the ability of GAS to overcome drug resistance. Pharmacokinetic studies revealed favorable drug-like properties, while toxicological evaluations highlighted its high safety margin with minimal adverse effects. Despite promising findings, the lack of clinical trials and standardized protocols remained a major limitation. Collectively, GAS represents a promising natural product candidate with potential as an adjunct or alternative anticancer therapy, warranting further translational and clinical investigation.

Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of non-Hodgkin lymphoma. Its high genomic and transcriptomic heterogeneity leads to significant differences in clinical phenotypes and prognosis. Traditional bulk sequencing techniques cannot fully resolve heterogeneity at the single-cell level and fail to reveal the interactions and dynamic changes between cells. The breakthrough progress of single-cell sequencing (SCS) technology has provided a new perspective for elucidating the pathogenesis of DLBCL. SCS technology accurately identifies hetero- geneous cell subpopulations at the single-cell level, systematically dissects cellular interactions within the tumor microe- nvironment (TME), reveals the complex changes of tumor cells, optimizes the prognostic evaluation system, and explores new breakthroughs in the study of novel therapeutic targets. This article systematically reviews the cutting-edge progress of SCS technology in DLBCL research, provides a theoretical basis for promoting precise treatment of the disease, and looks forward to the clinical application prospects of multi-omics and spatial transcriptomics technologies.

With the development of new drug research and transplantation techniques, significant progress has been made in the treatment of acute myeloid leukemia (AML). However, most patients still suffer from clinical relapse. Bone marrow mesenchymal stem cells (BM-MSCs), as crucial cellular components of the bone marrow microenvironment, contribute to AML drug resistance and relapse by promoting the proliferation of AML cells and reducing their sensitivity to chemotherapeutic agents. This article reviews the specific mechanisms through which AML cells reprogram BM-MSCs to mediate drug resistance and relapse, as well as recent research advances in targeting BM-MSCs for AML treatment, providing a theoretical basis for AML therapy from the perspective of regulating the bone marrow microenvironment.

Multiple myeloma (MM) has strong heterogeneity and is still an incurable tumor. The new immunotherapy represented by bispecific antibody (BsAb) and chimeric antigen receptor T-cell immunotherapy (CAR-T) has shown significant efficacy in MM treatment. However, these therapies directly utilize T cell activity, and the efficacy is affected by the functional state of T cells. T cell exhaustion (Tex), one of the important characteristics of MM, is closely related to the progression, drug resistance, recurrence, and poor prognosis of MM. Therefore, Tex is the key factor limiting the efficacy of BsAb and CAR-T technologies. This article reviews the latest research progress on the mutual influence between Tex and these therapies.

The rapid and accurate diagnosis of lymphoma is essential for understanding its pathogenesis, progression, and treatment outcomes. Compared to traditional diagnostic methods, artificial intelligence (AI) demonstrates superior data processing efficiency, delivering precise and consistent results. Meanwhile, three-dimensional (3D) histopathology provides a more comprehensive and detailed perspective of the disease. Consequently, the application of AI and 3D histopathology in lymphoma diagnosis is increasingly prevalent, addressing several challenges in current clinical practice. These technologies mitigate limitations related to diagnostic techniques and sample collection, reducing diagnostic turnaround time, and enhance accuracy. This review highlights recent advancements in AI and 3D histopathology for lymphoma diagnosis, while also discusses the remaining limitations and challenges in their implementation.

Primary thyroid lymphoma (PTL), a rare malignancy originating from thyroid lymphoid tissue, is strongly associated with Hashimoto's thyroiditis where accelerated lymphocyte proliferation and chronic antigen stimulation constitute key pathogenic mechanisms. The predominant pathological subtypes of PTL include diffuse large B-cell lymphoma and mucosa-associated lymphoid tissue lymphoma (MALTL). Current research on molecular alterations primarily focuses on MALTL, particularly pathogenic mutations in CD274 and TNFRSF14 . Diagnostic imaging modalities such as ultrasonography and computed tomography contribute significantly to PTL identification and differential diagnosis, while core needle biopsy remains the gold standard for definitive diagnosis. Therapeutic advancements demonstrate that combination therapies incorporating targeted agents with radiochemotherapy can improve clinical outcomes, with surgical intervention serving as a viable option for early-stage patients. This article reviews the latest research advances in PTL.