Background: Cuproptosis is a new form of cell death induced by intracellular copper overload. With the deepening of research, the research of cuproptosis in the field of cancer has become a hot topic. The bibliometric analysis of cuproptosis research can provide valuable insights into the development of this field.Method: In this study, the Web of Science Core Collection database was used to obtain literature, and the screened data were imported into CiteSpace software for analysis. We use this data for visualization analysis and made knowledge maps including authors, countries, institutions, journals, and keywords.Results: 1140 literature was obtained from Web of Science from 2001 to 2024. The results indicate a consistent upward trend in the number of publications in this field. Moreover, a particularly significant surge in the frequency of citations has been observed since 2022. Through a systematic analysis, we found that in the current field of cancer research on cuproptosis, breast cancer, lung cancer, hepatocellular carcinoma and colorectal cancer have more research results.Conclusion: This article describes how copper ions regulate cell death, particularly in cancer therapy, and requires an in-depth understanding of the complexity of copper metabolism and its specific mechanisms of action in cell death. The work provides a panoramic view of the research landscape on cuproptosis in cancer, highlighting its potential as a therapeutic target and the need for further exploration into its mechanisms and clinical applications. With the depth of research, it is expected that cuproptosis will continue to be a hotspot in cancer treatment research. In addition, it provides a solid theoretical foundation and experimental basis for the development of new anti-tumor therapeutic strategies.

DDX41 is one of the most frequently altered genes in familial acute myeloid leukemia/myelodysplastic syndrome (AML/MDS). Mutation of DDX41 has been widely reported in various types of myeloid neoplasms. This systematic review and meta-analysis were conducted to assess the clinical characteristics and relationship between DDX41 mutations and OS in myeloid neoplasm patients. We thoroughly searched the PubMed, the Cochrane Library, Embase, Web of Science, MEDLINE, and Google Scholar databases. Two reviewers separately reviewed and extracted the data. Twenty studies totaling 9,058 patients have been integrated into the meta-analysis. The extensive pooled analysis showed a significant association between DDX41 mutations and improved OS (HR 0.70, 95% CI 0.52–0.93, P = 0.01). Subgroup analysis confirmed that DDX41 mutation operated to be a reliable positive indicator of OS when subdivided by different types of myeloid neoplasms. In terms of the clinicopathological value, DDX41 mutations were significantly correlated with the male sex and older age. AML prevalence, bone marrow, or white blood cell counts did not correlate with any findings. The top three genetic variants were p.M1I, p.D140fs, and p.R525H. Co-mutations in patients with DDX41 mutations most commonly include the following: additional sex combs-like 1 ( ASXL1 ), DNA methyltransferase 3 A ( DNMT3A ), tumor protein p53 ( TP53 ), ten-eleven translocation 2 ( TET2 ) and serine/arginine-rich splicing factor 2 ( SRSF2 ). Our results substantiate that DDX41 mutations were associated with significantly good OS and provide more insight into the clinicopathological characteristics of DDX41 mutations in individuals with myeloid neoplasms.

Background: Lactylation, a post-translational modification (PTM), has gained attention for its role in disease pathogenesis, particularly in cancer and immune regulation. Initially viewed as a glycolysis byproduct, lactate is now recognized as a precursor for histone lysine lactylation (Kla), which regulates gene transcription and epigenetic processes. Dysregulation of lactylation is linked to malignancies, inflammation, and metabolic diseases. Despite growing research, a systematic bibliometric analysis of lactylation remains absent. This study addresses this gap by analyzing lactylation research from 2019 to 2024, focusing on its disease-related mechanisms and therapeutic potential.Method: Data were extracted from the Web of Science Core Collection (2019–2024), yielding 198 relevant articles after screening. Bibliometric analysis was conducted using Microsoft Excel, VOSviewer, Scimago Graphica and CiteSpace. Excel tracked publication trends, VOSviewer generated author density maps, and CiteSpace visualized collaboration networks, co-cited references, and keyword clusters. Scimago Graphica generated Map of country cooperation networks. The study identified research trends, collaborative patterns, and emerging hotspots in lactylation research.Result: Lactylation research has surged exponentially since 2022, with China as the primary contributor (92.42% of publications). Dominant keywords converge on lactylation’s role as a direct epigenetic regulator of gene activation, enabling transcriptional reprogramming in diseases; Lactylation drives bladder cancer progression via immunosuppressive genes, mediates myoblast differentiation for muscle repair, and disrupts signaling through non-histone targets; Emerging focus on “differentiation” and “metabolic regulation” highlights its potential as a cellular reprogramming target, crucial for advancing regenerative medicine and combating inflammation-linked pathologies.Conclusion: This study provides the first bibliometric analysis of lactylation research, highlighting its rapid growth and global significance. China leads the field, with extensive contributions from its institutions. Lactylation’s role in disease mechanisms, particularly cancer and immune regulation, underscores its therapeutic potential. Emerging research on differentiation and metabolic regulation offers new directions for future studies. Further investigation into lactylation’s molecular mechanisms and therapeutic applications is essential for advancing disease diagnosis and treatment.

PANoptosis is an inflammatory programmed cell death pathway possessing critical characteristics of apoptosis, pyroptosis, and necroptosis. It is regulated by PANoptosome complexes, involves interaction between these three key programmed cell death pathways, yet is distinct from any alone. PANoptosis holds vital significance in liver-related diseases, particularly hepatocellular carcinoma (HCC). This article summarizes research on the mechanism and treatments of PANoptosis in HCC. Current research has partially elucidated PANoptosis-related mechanisms in HCC and identified several molecules modulating it. Therapeutic strategies targeting PANoptosis hold significant promise. Investigations into these critical molecules have led to the development of traditional targeted drug therapies and emerging strategies like nanotechnology-based immunocombination therapies. However, there are still challenges in the mechanistic and pharmacological studies of PANoptosis in HCC, including the bidirectional regulation of key apoptotic factors, specific molecular mechanisms, and preclinical models. This article offers a new orientation for studying the pathogenesis and potential therapeutic strategies for HCC.