As acute enterovirus⁃induced infections, herpangina(HA) and hand⁃foot⁃mouth disease(HFMD) are simi⁃lar in many aspects. Although these diseases vary with time and region, many studies have shown that the viruses caus⁃ing HA and HFMD are consistent, and there is no notable difference in partial VP1 gene sequences between different vi⁃ruses. HA and HFMD also resemble each other in epidemiological features. Both infections show significant summer⁃time seasonality, have a strong connection with certain environmental conditions and are most prevalent in young chil⁃dren and infants. Herpangina is thought to be a mild disease, defined as vesicular enanthem and then ulcers of the fau⁃ces and soft palate with presentation of feve r, sore throat, and decreased appetite. HFMD, which could lead to severe symptoms, is also characterized by oral ulcers, although they are chiefly on the buccal mucosa and tongue, and typical vesicular rashes, which are most commonly found on the hands, feet, knees and buttocks. While HA is generally be⁃ lieved to be self⁃limited and has a favorable prognosis, HA with certain clinical characteristics, such as diarrhea, vomit⁃ing, limb jitter and sleepiness, can evolve into HFMD, according to some literature in recent years. However, HA is an independent risk factor for HFMD, and severe cases only present with herpes appearing at the isthmus of the fauces at an early stage, which indicates a strong correlation between them. Clinical manifestations of HA should be considered by medical staff to identify potential children with HFMD as early as possible to prevent its further development or transformation.

Exploration of the underlying mechanisms of tumor occurrence and development, as well as evaluation of the efficacy of anticancer drug treatments, relies on various research models both in vivo and in vitro. Over the past few decades, with the rapid advancement of biomedical technology, significant achievements have been made in this field. Gene detection technology has progressed from a single-gene perspective to multi-gene approaches, resulting in rapid development of bioinformatics and transformation of the conceptual understanding of malignant tumors. Moreover, in vitro cell research models have evolved from monolayer two-dimensional and primary cultures to three-dimensional configurations, which better imitate the cellular interactions and functions within tumor tissues. Furthermore, in vivo animal research models have transitioned from traditional carcinogen induction and cell or tissue xenografts to genetically engineered animal models or xenograft models, enabling targeted investigation into the roles of relevant genes in the occurrence and development of tumors. Clinical research has shifted from simple retrospective to prospective studies, including phase Ⅰ/Ⅱ/Ⅲ clinical trials, investigator-initiated clinical trials, and real-world clinical trials. The major shortcomings of current malignant tumor research models include their singularity, insufficient simulation of the tumor microenvironment, disparities between animal models and human tumors, and the lack of consideration for personalized medicine. Further research and optimization of the models are still needed in the future, along with more effective integration of different models to form an optimized comprehensive experimental model system. This review systematically examines and comprehensively overviews the evolution of malignant tumor research models with the aim of providing more references to researchers engaged in oncology research.