Non-invasive prenatal testing (NIPT) based on fetal free DNA is a non-invasive technique to screen for common fetal aneuploidies by analyzing cell-free fetal DNA (cffDNA) in the peripheral blood of pregnant women. This technique has opened a new era of prenatal screening for its high safety and reliability. In recent years, it has been shown that NIPT can not only screen for fetal aneuploidies, but may also reveal maternal genomic abnormalities. The incidental detection of maternal tumors has aroused widespread concern in the clinical settings. The aim of this review is to systematically summarize the research progress of NIPT technique in incidental detection of maternal tumors, and to discuss its clinical significance, technical challenges, and future development direction. It has been found that multiple chromosome aneuploidies (MCAs) in NIPT detection is one of the important biomarkers suggesting occult maternal malignant tumors. In this paper, the relevant progress of NIPT technique in the incidental discovery of maternal tumors were reviewed in order to provide a reference for individualized and standardized application of NIPT technique in maternal health monitoring.

Although targeted therapy has made significant advances in cancer treatment throughout these years, drug resistance still remains a major obstacle. Plenty of evidence has proved that abnormal expression of receptor tyrosine kinase AXL is associated with targeted therapy resistance and poor clinical outcomes. AXL drives drug resistance through diverse mechanisms, including altering tumor cell phenotypes, orchestrating DNA damage response process, promoting the activation of bypass signals, or interacting with other receptor tyrosine kinases. Preclinical and clinical studies have demonstrated that combined inhibition of AXL and the other target can enhance the efficacy of various targeted therapies and improve outcomes for patients with drug resistance. This review summarizes recent advances in the specific roles of AXL in targeted therapy resistance and AXL-targeted treatment strategies. It further explores the potential clinical value of combinatorial approaches involving AXL inhibition and discusses future directions for its application in developing novel targeted therapies and advancing precision oncology treatment. 
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Metabolic reprogramming is a hallmark of cancer, with the Warburg effect-driven aerobic glycolysis leading to a substantial accumulation of lactate in the tumor microenvironment. For a long time, lactate was considered a mere metabolic end product; however, recent studies have found that it acts as an important signaling molecule, profoundly influencing tumor progression by inducing a novel post-translational modification - lactylation. Lactylation, driven by lactate, occurs on both histones and non-histone proteins and is finely regulated by the 'writer' 'eraser' and 'reader' mechanisms, thereby altering the function of target proteins and gene expression. This review systematically explores the bidirectional regulatory network between glycolytic reprogramming and lactylation: on one hand, key glycolytic regulators promote lactate production, thereby increasing lactylation levels; on the other hand, lactylation can feedback to regulate the activity and expression of key glycolytic enzymes, forming a pro-tumor positive feedback loop. This interaction plays a central role in tumor proliferation, metastasis, DNA damage repair, and immune evasion. Consequently, targeting lactate production, lactate transport, or the lactylation process itself has emerged as a highly promising anti-cancer strategy and shows potential synergy with existing therapies such as immune checkpoint inhibitors. In-depth analysis of the glycolysis-lactylation axis will provide a crucial theoretical basis for developing novel cancer treatment approaches.
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First-line immunotherapy for advanced non-small cell lung cancer (NSCLC) shows significant survival benefits in patients without driver mutations, but the optimal duration of treatment remains controversial. Some studies support limiting immunotherapy to 2 years, arguing that longer treatment does not bring additional survival benefits; while other studies believe that treatment should continue until disease progression to maximize survival benefits. This article systematically reviews the current research progress on the duration of immunotherapy and discusses the potential predictive value of biomarkers such as circulating tumor DNA (ctDNA), the best efficacy response, and programmed cell death ligand 1 (PD-L1) expression levels in individualized treatment decisions. More prospective studies, especially biomarker-driven trials, are still needed to clarify the optimal duration of treatment and establish an individualized treatment strategy based on multidimensional indicators.
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mRNA-targeted tumor drugs, featuring various types and distinct antitumor mechanisms of action, have demonstrated significant potential in tumor immunotherapy. Currently, nearly one hundred registered clinical trials initiated by pharmaceutical companies or sponsors are being conducted worldwide, and these trials have shown impressive efficacy. In China, multiple registered clinical trials have been conducted in the past two years, reflecting rapid development. Although mRNA tumor drugs still face certain challenges, the advantages of mRNA technology are clear, promoting the integrated development of immunotherapy, gene therapy, and cell therapy. With ongoing technological innovation and optimization, the demand for "mRNA therapy" for tumor prevention and treatment is expected to be met. This review discusses the distinct mechanisms of action, progress in basic research, clinical advancements, challenges, and future perspectives of both prophylactic and therapeutic mRNA cancer vaccines. It aims to enhance understanding of research progress in mRNA technology for oncological drug applications and to provide insights for future research and product development of mRNA-based interventions in oncology.

The Hippo signaling pathway, as a highly conserved tumor suppressor pathway, is closely related to the occurrence and development of various malignant tumors due to the abnormal expression of its core components, mammalian STE20-like protein kinase 1/2(MST1/2), large tumor suppressor kinase 1/2(LATS1/2), and effector factor Yes-associated protein 1(YAP)/WW domain-containing transcription regulator 1(TAZ). This pathway plays a key regulatory role in pathological processes such as malignant proliferation, apoptosis, and drug resistance by regulating downstream target genes such as connective tissue growth factor(CTGF) and cysteine-rich angiogenic inducer 61(CYR61). Currently, it has been found through research that effective components of traditional Chinese medicine(TCM) and TCM formulas can exert anti-cancer effects by regulating the Hippo signaling pathway, but the specific targets and biochemical processes involved remain unknown. This article integrated the action targets and regulated biochemical processes of effective components of TCM targeting the Hippo signaling pathway in anti-tumor activities and discovered that flavonoids, terpenoids, glycosides, and other effective components of TCM and TCM formulas can regulate the Hippo signaling network, with the most significant mechanisms being the intervention of YAP/TAZ nuclear-cytoplasmic shuttling, restoration of the activity of Hippo core kinases, and blocking of crosstalk between pathways. Taking the Hippo pathway as the research object not only provides a new perspective for explaining the scientific connotation of TCM in anti-tumor activities but also lays a theoretical foundation for the development of new TCM drugs based on Hippo pathway-targeted therapy.

Chronic gastritis, a chronic and insidious inflammatory condition of the gastric mucosa, is characterized by nonspecific early symptoms and a high risk of progression to gastric cancer. Persistent inflammatory stimulation accelerates the "inflammation-cancer transformation" by remodeling the microenvironment, and suppressing this process is critical for gastric cancer prevention and treatment. Nuclear factor-κB(NF-κB) serves not only as a central hub for inflammatory regulation but also as a key node connecting pathways such as Toll-like receptor 4(TLR4), NOD-like receptor protein 3(NLRP3), mitogen-activated protein kinase(MAPK), signal transducer and activator of transcription 3(STAT3), and protein kinase B(AKT). Extensive studies have demonstrated that monomers and herbal formulas in traditional Chinese medicine(TCM) can modulate NF-κB-related signaling pathways to mitigate the progression of "inflammation-cancer transformation" of chronic gastritis, achieving multi-level, multi-target intervention in gastric cancer. Based on this, this article systematically reviewed the dynamic network of NF-κB and relevant crosstalk pathways in "inflammation-cancer transformation" and the mechanisms of TCM-based interventions, providing theoretical foundations for optimizing clinical strategies and advancing gastric cancer prevention.

Mantle cell lymphoma (MCL) is a rare B-cell lymphoma characterized by both the incurable nature of indolent lymphomas and the clinical course of aggressive lymphomas. The integration of high-dose cytosine arabinoside (Ara-C) and autologous hematopoietic stem cell transplantation (ASCT) has led to substantial improvement in the outcomes of MCL patients in the immunochemotherapy era. More recently, the widespread use of small molecule targeted agents, particularly Bruton tyrosine kinase inhibitor (BTKi), has re-shaped the therapeutic landscape of MCL patients and challenged the traditional role of high-dose Ara-C and ASCT. Novel immunotherapies including bi-specific antibodies and chimeric antigen receptor T-cell (CAR-T) therapy have emerged as important treatment options for MCL patients with relapsed or refractory disease. With advances in multi-omics profiling, the development of personalized, potentially curative strategies based on individual genetic and immune features is expected to become a major focus of future research on MCL. This article will delve into the latest research progress in the treatment and genetics and translational research on MCL patients, focusing on the latest progress of research on the treatment of newly diagnosed MCL patients, treatment of relapsed/refractory MCL patients, and the genetics and translational treatment of MCL patients, and explore the evolution and future direction of its treatment model.

Cancer treatment is a significant challenge facing global medicine, with complex molecular mechanisms and drug resistance being key factors limiting treatment outcomes. Abnormal lipid metabolism is one of the important characteristics of tumors, providing metabolic support for the growth, proliferation, migration, and invasion of tumor cells. Tumor suppressor p53 protein and sterol O-acyltransferase 1 (SOAT1) play an important role in regulating cellular lipid metabolism and are closely related to the occurrence, development, and prognosis of various tumors. p53 protein regulates tumor lipid metabolism through multiple signaling pathways, while SOAT1, as a key enzyme in cholesterol esterification, is highly expressed in many tumors and accelerates tumor progression. Recent studies have shown that there may be a functional association between p53 protein and SOAT1, coordinating the regulation of lipid homeostasis in tumor cells. This article reviews the research progress on p53 protein and SOAT1 in tumor lipid metabolism, focusing on the potential mechanisms of action of the p53-SOAT1 axis in tumor development, and prospects its application prospects as a target for cancer treatment.
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We retrospectively analyzed the clinical data and clonal architecture of two multiple myeloma (MM) patients harboring concurrent IGH::FGFR3 and IGH::CCND1 fusions, with a review of relevant literature. Fluorescence in situ hybridization (FISH) confirmed biallelic IGH translocations in both cases. Case 1, diagnosed with smoldering MM (SMM), exhibited co-positivity for both IGH translocations in 91% of bone marrow plasma cells. Case 2, with active MM, showed predominant IGH::FGFR3 positivity (93% of cells), with a minor subclone (5%) co-expressing IGH::CCND1. This study demonstrates that primary biallelic IGH translocations can lead to the coexistence of IGH::FGFR3 and IGH::CCND1, revealing a novel genetic mechanism driven by biallelic IGH translocations in the founding clone. Furthermore, it elucidates the clonal heterogeneity in biallelic IGH translocation events.

Ultraviolet (UV) radiation, one of the critical environmental carcinogenic factors, promotes skin photoaging and carcinogenesis by inducing DNA damage, oxidative stress, and chronic inflammatory cascades. N6-methyladenosine (m6A)-modifying enzymes (writers, erasers, and readers) play bidirectional regulatory roles in UV-mediated skin pathology. In photoaging, the reactive oxygen species (ROS)-m6A axis accelerates collagen degradation and epithelial-mesenchymal transition (EMT) through modulation of matrix metalloproteinases (MMPs), inflammatory mediators, DNA damage repair, apoptosis, and collagen metabolism. In skin cancers, m6A regulators promote tumor progression by influencing oncogenic signaling, proliferation, invasion, metastasis, and immune evasion. Bioactive monomeric compounds derived from traditional Chinese medicine, including polyphenols, saponins, and alkaloids, can regulate the activity of m6A enzymes to interfere with photoaging and UV-induced skin carcinogenesis. This study integrates current evidence to establish an m6A-targeted epigenetic intervention framework for UV-induced skin injury and highlights the potential of synergistic multi-component m6A-modulating therapeutic strategies as a future research priority.

Breast cancer is one of the most common malignant tumors in women worldwide, and its high incidence and mortality rate seriously threaten women's health. Studies show that the forkhead box O3a (FoxO3a) plays a key role in the occurrence and progression of breast cancer, particularly in the regulation of apoptosis. As a major member of the FoxO family, FoxO3a exerts tumor-suppressive functions by participating in apoptosis regulation and cell-cycle control. In breast cancer cells, FoxO3a acts as a downstream signaling hub of multiple upstream pathways including phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT), mitogen-activated protein kinase (MAPK), and serum- and glucocorticoid-regulated kinase 1 (SGK1). Through nucleocytoplasmic shuttling and alterations in transcriptional activity, FoxO3a precisely modulates the expression of apoptosis-related target genes such as Bcl-2-interacting mediator of cell death (Bim) and p53-upregulated modulator of apoptosis (PUMA), thereby influencing cell survival or death. In addition, multiple natural compounds and combination therapies can induce apoptosis in breast cancer cells by restoring or enhancing FoxO3a activity, and may partially overcome treatment resistance. Systematic elucidation of the complexity of the FoxO3a signaling network and its dual roles in breast cancer therapy may provide theoretical support for understanding tumor-drug resistance mechanisms and for developing precision therapeutic strategies targeting FoxO3a nodes. Future research should further clarify the functional differences among FoxO3a splice variants and FoxO family members, reveal the molecular basis of FoxO3a functional switching in the tumor microenvironment, and promote the clinical translation of biomarkers and targeted drugs.

Aiolos is a member of the Ikaros zinc-finger protein family and is encoded by the Ikaros family zinc finger 3 (IKZF3) gene. Aiolos not only plays a crucial role in controlling the normal differentiation and proliferation of lymphocytes, but studies have also found that it exhibits abnormally high expression in the early stages of the onset and development of multiple tumors. It influences the biological behavior of tumor cells not only by regulating tumor invasion and metastasis through mediating signaling pathways such as 66-kilodalton Src homology 2 domain-containing transforming protein (p66Shc), phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/Twist, cellular myelocytomatosis oncogene, interferon regulatory factor 4, B-cell receptor, and nuclear factor kappa B, but also the instability of its gene affects tumor therapy, drug resistance, and patient prognosis. This suggests that IKZF3 is a good biological indicator for tumors and may become a new therapeutic target for tumors. A systematic elaboration of the latest research progress on the IKZF3 gene structure, physiological functions, tumor regulation, and treatment resistance can provide reference and scientific basis for future tumor therapy.

Small nucleolar RNAs (snoRNAs) are a class of important non-coding RNAs traditionally involved in the modification and processing of ribosomal RNA. Recent studies have revealed that snoRNAs are aberrantly expressed in various gastrointestinal malignancies-including gastric cancer, colorectal cancer, and esophageal cancer-and contribute to tumorigenesis and progression by regulating gene expression and modulating key biological processes such as tumor cell proliferation, apoptosis, invasion, migration, metabolism, drug resistance, and stemness maintenance. Although extensive research has focused on the roles of snoRNAs in cancer, their precise molecular mechanisms and clinical utility remain incompletely understood. This review summarizes the expression profiles and functional mechanisms of snoRNAs in gastrointestinal cancers and discusses their potential as biomarkers or therapeutic targets, aiming to provide new insights for early diagnosis and precision therapy of these malignancies.

Gastrointestinal malignant tumors are a group of severely life-threatening tumors. Their incidence and mortality rates consistently rank among the top 10 cancers worldwide and are increasing year by year. Based on his long-term clinical practice, Professor Zhou Zhongying proposes the theory of "cancer toxin". The research team led by Professor CHENG Hai-bo further establishes the pathogenesis theory of cancer toxin, holding that cancer toxin is the key factor in the occurrence and development of tumors, and thus taking "anti-cancer and detoxification" as the basic therapeutic principle. With the vigorous promotion of TCM, various active ingredients of TCM are extracted and make a difference in tumor therapy. These active ingredients can inhibit tumor cells in a multi-target and multi-pathway manner. Cinobufotalin is an active ingredient extracted from the skin of Bufo gargarizans with detoxifying, anti-swelling, and pain-relieving effects and is widely used in the treatment of intermediate and advanced tumors. Clinical studies have revealed that cinobufotalin enhances tumor control rates, prolongs survival time, improves quality of life, and reduces the incidence of adverse reactions when combined with chemotherapy, radiotherapy, or targeted therapies. The mechanism studies have demonstrated that cinobufotalin plays a therapeutic role by inhibiting cell proliferation and invasion, inducing tumor cell apoptosis, modulating immune response, reversing drug resistance, etc. This paper reviews the research progress on cinobufotalin from the perspective of pathogenesis theory of cancer toxin through summarizing domestic and international reported research on clinical application and mechanism of cinobufotalin against gastrointestinal malignant tumors in recent years. The findings aim to provide a theoretical basis for research on the anti-tumor effect of cinobufotalin and a reference for standardized use and in-depth research of drugs.

Colorectal cancer(CRC), a prevalent malignancy of the digestive system, exhibits an escalating incidence and mortality rate in China. While contemporary western therapeutic approaches demonstrate efficacy in tumor suppression and symptom management, their clinical benefits are substantially limited by adverse effects, drug resistance, and high recurrence rates. Consequently, developing novel therapeutic strategies with enhanced efficacy and safety profiles has emerged as a critical research priority in oncology. TGF-β signaling pathway plays a pivotal role in modulating CRC cell proliferation, differentiation, and apoptosis, and it is intimately involved in tumorigenesis, progression, and metastasis, thereby representing a promising molecular target for CRC treatment. Traditional Chinese medicine(TCM) exhibits distinctive therapeutic advantages in CRC management through its multi-target, multi-pathway regulatory mechanisms. Notably, TCM has demonstrated significant efficacy in preventing postoperative recurrence and metastasis, mitigating treatment-related side effects, and improving patients' quality of life, establishing its integral role in comprehensive CRC therapy. Current evidence indicates that various TCM active constituents, including polyphenols, terpenoids, alkaloids, polysaccharides, flavonoids, and isothiocyanates, as well as compound formulas such as Jianpi Tongluo Formula, Jianpi Xiao'ai Formula, modified Shenling Baizhu Decoction, Qingjie Fuzheng Granules, and Chanling Ointment, can effectively modulate the TGF-β signaling pathway and its interactive networks. These therapeutic agents exert anti-CRC effects through diverse mechanisms, including apoptosis induction, EMT inhibition, macrophage polarization, stemness attenuation, immune activation, chemoresistance reversal, and cell cycle arrest. This review systematically synthesizes contemporary research advances in TCM interventions for CRC, with a particular emphasis on the mechanism underpinning TGF-β pathway modulation. Our findings provide valuable insights for the development of innovative anti-CRC agents and the optimization of clinical therapeutic regimens.

Malignant tumors, as a major public health issue facing the world, have extremely complex pathogenesis. Molecular biology features represented by acidic microenvironment and lipid metabolism disorders are closely related to tumor invasion and metastasis. Traditional Chinese medicine(TCM) holds that the diseases caused by phlegm toxicity are characterized by heaviness, turbidity, stickiness, and difficulty in resolving. Modern pharmacological research has confirmed that as a TCM for resolving phlegm and detoxifying to treat phlegm toxicity, it can not only exert anti-cancer effects by directly inhibiting tumor cell proliferation but also reshape the steady-state regulatory network of the tumor microenvironment, including downregulating the microenvironment of lactate accumulation mediated by hypoxia-inducible factor 1α(HIF-1α) and regulating fatty acid synthase(FASN)-related lipid metabolism reprogramming processes, thereby antagonizing tumor invasion and metastasis. The innovative TCM theory of cancer toxicity pathogenesis proposed by our team suggests that the pathogenic characteristics of phlegm toxicity are homologous to the pathological accumulation of abnormal metabolites in the tumor microenvironment. This study systematically reviews the relevant literature on the treatment of tumors with TCM for resolving phlegm and detoxifying, deeply analyzes the theoretical basis of TCM, summarizes the clinical experience of famous TCM practitioners, and explores the clinical efficacy of TCM for resolving phlegm and detoxifying against tumors. At the same time, this study objectively summarizes its active ingredients and anti-tumor mechanisms, so as to provide reference for the prevention and treatment of malignant tumors with TCM.