Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the gastrointestinal tract, primarily driven by activating mutations in KIT (CD117) and platelet-derived growth factor receptor alpha (PDGFRA). The introduction of tyrosine kinase inhibitors (TKIs), especially imatinib, has significantly transformed GIST treatment. However, the emergence of both primary and secondary resistance to imatinib presents ongoing therapeutic challenges. This review comprehensively explores the mechanisms underlying imatinib resistance and evaluates subsequent TKI therapies. Sunitinib, regorafenib, and ripretinib are currently approved as standard second-, third-, and fourth-line therapies, each demonstrating efficacy against distinct mutational profiles. Avapritinib, notably effective against PDGFRA D842V mutations, represents a milestone for previously untreatable subgroups. Several alternative agents—such as nilotinib, masitinib, sorafenib, dovitinib, pazopanib, and ponatinib—have shown varying degrees of success in refractory cases or specific genotypes. Investigational compounds, including crenolanib, bezuclastinib, famitinib, motesanib, midostaurin, IDRX-42, and olverembatinib, are under development to address resistant or wild-type GISTs. Despite progress, long-term efficacy remains limited due to evolving resistance. Future strategies include precision medicine approaches such as ctDNA-guided therapy, rational drug combinations, and novel drug delivery systems to optimize bioavailability and reduce toxicity. Ongoing research will be crucial for refining treatment sequencing and expanding therapeutic options, especially for rare GIST subtypes.

Colorectal cancer remains among the most prevalent gastrointestinal malignancies worldwide, imposing a substantial clinical burden and highlighting the urgent need for precision and personalized treatment strategies. Conventional drug delivery approaches are limited by low selectivity, restricted bioavailability, and systemic toxicity, thereby limiting therapeutic efficacy. Antibody–drug conjugates, as advanced delivery plat-forms, have the advantages of highly specific antibody recognition, versatile cytotoxic payloads, and continuously evolving linker technologies. This combination provides novel opportunities to increase efficacy, reduce toxicity, and enable individualized precision therapy. Recent advances have demonstrated the potential of ADCs in CRC, yet challenges such as resistance, toxicity, and clinical translation persist. Multidisciplinary efforts among the pharmaceutical industry and molecular biology and clinical medicine fields will be essential to accelerate the development of more precise and personalized CRC therapies. This review summarizes the current research progress on ADCs as a treatment option for CRC, discusses innovations in delivery system design, examines the key challenges of personalization, and highlights future directions to better integrate ADCs into effective treatment paradigms.

Angiomyofibroblastoma (AMFB) is a rare benign soft tissue tumor that primarily arises in the vulvovaginal region of women of reproductive age. Due to its rarity, AMFB is often overlooked in the differential diagnosis, and as such, it is not frequently encountered in clinical practice. Here, we present the case of a 29-year-old female with a pelvic retroperitoneal tumor, confirmed postoperatively as AMFB based on histopathological and immunohistochemical findings. Additionally, we highlight the utility of next-generation sequencing (NGS) as a valuable tool in the differential diagnosis of such rare tumors. Due to the tumor was located at the narrow part of the pelvis and was adjacent to important tissues and organs such as the uterus and bladder, we performed surgical resection using the Da Vinci robotic system after obtaining the patient’s informed consent. The procedure was successful, with no complications observed during the three-month postoperative follow-up. Furthermore, we reviewed the literature on AMFB, focusing on reported cases to identify and summarize patient characteristics, clinical presentations, histological features, and diagnostic challenges associated with this rare tumor. We aim to offer a reference for clinicians facing similar cases, aiding in accurate diagnosis and management, while addressing the challenges posed by the rarity and diagnostic complexity of angiomyofibroblastic tumors, ultimately improving clinical outcomes and advancing knowledge.

Liver metastasis is the leading cause of mortality in colorectal cancer (CRC) patients, and there is an urgent need for biomarkers to improve the diagnosis and prognosis of CRC. However, the molecular mechanisms driving metastatic progression remain incompletely understood, necessitating the discovery of novel therapeutic targets. GEO datasets and machine learning algorithms (Lasso regression, SVM, and RF) were employed to screen for upregulated genes in CRC liver metastasis. Protein-protein interaction (PPI) networks were constructed using STRING. Single-cell RNA sequencing (scRNA-seq) and ATAC-seq were performed to analyze immune infiltration and chromatin accessibility in metastatic tissues. Functional enrichment analysis of RNA-seq data was conducted to explore DAPK1-related pathways. Finally, CRISPR/Cas9-mediated knockout of DAPK1 in LoVo cells was used to validate its role in invasion and migration. In this study, we identified DAPK1 as a metastasis-specific upregulated gene in CRC. scRNA-seq of CRC metastases highlighted a significant correlation between DAPK1 expression and macrophage infiltration. Furthermore, ATAC-seq analysis demonstrated increased chromatin accessibility of DAPK1 in CRC liver metastasis. CRISPR/Cas9-mediated knockout of DAPK1 in LoVo cells markedly suppressed their invasion and migration. By combining machine learning and multi-omics bioinformatics approaches, we identified DAPK1 as a novel biomarker for CRC liver metastasis, which has potential implications for prognosis and therapeutic targeting. These findings highlight DAPK1 as a critical driver of metastatic progression and provide a theoretical foundation for the treatment of CRC.