Cancer Innovation最新文献

The convergence of artificial intelligence (AI) and big data is reshaping contemporary oncology by enabling the integration of multimodal information across imaging, pathology, genomics, and clinical records. From a physician-centered perspective, these technologies can potentially be used to improve diagnostic precision, support individualized treatment planning, enhance longitudinal patient management, and accelerate both clinical and translational research. In this review, we synthesize the core AI methodologies most relevant to oncology-machine learning, deep learning, and large language models-and examine how they interact with established and emerging oncology data platforms. We further highlight practical use cases in clinical workflows and research pipelines, emphasizing opportunities for advancing precision cancer care while also addressing challenges associated with data heterogeneity, model generalizability, privacy protection, and real-world implementation. By underscoring the synergistic value of AI and big data, this review aims to inform the development of clinically meaningful, context-adapted strategies that promote translational innovation in both global and locally resourced healthcare environments.

In recent years, multidisciplinary treatment strategies have profoundly improved drug responses and survival outcomes of breast cancer (BC) patients. However, there is an urgent need for novel therapies for BC patients who are heavily treated or develop resistance to conventional treatment regimens. Radionuclide therapy (RT) and targeted radionuclide therapy (TRT) have emerged as paradigm-shifting therapeutic approaches for BC, which enable functions of both imaging and localised treatment. They utilise radionuclides that can selectively bind to biomarkers overexpressing on BC cells, allowing precise delivery and localised tumour irradiation. Moreover, several types of radionuclides possess ‘cross-fire’ effects that result in the eradication of neighbouring tumour cells lacking the biomarker expression. In the current review, we summarise the potential biomarkers for the development of RT and TRT that can be employed in the treatment of BC, including receptor markers of ER, PR and HER2, together with other markers of Trop2, PD-1, EGFR, GRPR and PSMA.

Breast cancer (BC) remains the most frequently diagnosed malignancy worldwide, with an estimated 2.3 million new cases and approximately 685,000 deaths reported in 2020. Forecasts suggest a substantial rise in global incidence, with new annual cases projected to reach 3.2 million by 2050, representing a 39% increase. Additionally, BC is expected to account for approximately 7.7% of the anticipated $25.2 trillion global economic burden associated with cancer by 2050. These trends underscore an urgent need for affordable, widely accessible and effective therapeutic strategies, particularly in low- and middle-income countries. Statins, commonly prescribed for the treatment of hypercholesterolaemia via inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, have garnered increasing interest for their potential anticancer properties. This review focuses on the mechanistic underpinnings and therapeutic implications of statin use, particularly simvastatin, in the context of BC. Statins exert their primary effect through inhibition of the mevalonate pathway, which is crucial for cholesterol and isoprenoid biosynthesis. Disruption of this pathway impairs the prenylation of key signalling proteins, including members of the Ras and Rho GTPase families, which are essential for cancer cell proliferation, survival and metastasis. Preclinical evidence has demonstrated that simvastatin can induce tumour cell apoptosis, arrest cell-cycle progression and inhibit oncogenic signalling pathways. These effects have been particularly pronounced in hormone receptor-negative and triple-negative breast cancer (TNBC) subtypes, which are often associated with poor prognosis and limited treatment options. Epidemiological and observational studies further support a potential association between statin use and reduced BC recurrence and mortality. Nevertheless, robust evidence from randomised controlled trials remains limited, and further investigation is required to establish causality and define optimal therapeutic regimens. Given their well-established safety profile, global accessibility and pleiotropic effects, statins, especially simvastatin, represent a promising class of repurposed drugs in the adjuvant treatment of BC. This review synthesises evidence from the past two decades, highlighting the need for continued clinical research to validate and optimise the use of statins as adjunctive agents in BC therapy.

DNA methylation is a crucial epigenetic regulatory mechanism that can modify chromatin structure, DNA conformation, DNA stability, and the interactions between DNA and proteins, thereby controlling gene expression. It has been shown to play a significant role in pathological processes such as fibrosis and tumorigenesis. DNA methyltransferases (DNMTs) are key players in this process. This study aims to investigate the role of DNMTs in the development of urinary system diseases, such as renal fibrosis and prostate cancer, revealing how they regulate gene expression by modulating DNA methylation levels, thereby significantly promoting the progression of these diseases. Additionally, this review explores their potential clinical applications as therapeutic targets, which may offer new research directions for understanding the pathogenesis and treatment of urinary system diseases in the future.

Current drugs against multiple human malignancies are limited, and developing new treatment strategies is improbable within a short time. So, considering the current situation, phytochemicals could be a viable option for developing chemotherapeutic agents for managing numerous types of malignancies. Therefore, we aimed to locate all phytochemicals of Eclipta prostrata and unravel their chemotherapeutic mechanisms and strategies individually. We defined 25 active compounds based on their anticancer activities after filtering through IMPPAT and literature search, and these compounds have chemotherapeutic activities against around 15 different human malignancies. In vitro and preclinical models support that the chemotherapeutic properties of phytochemicals derived from Eclipta prostrata are believed to be regulated by many pathways, including targeting signaling pathways, for example, phosphoinositide 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR), tumor necrosis factor-alpha (TNF-α), nuclear Factor-kappa B (NF-κB), mitogen-activated protein kinase (MAPK); regulated cell death such as Fas cell surface death receptor (FAS), Bid, apoptosis-inducing factor (AIF), Bcl2, Bax, Bak, Bad, caspase, and Poly (ADP-ribose) Polymerase (PARP); metastasis and angiogenesis such as matrix metalloproteinases (MMPs) (2&9), wingless/integrated (Wnt)/beta-catenin, angiogenesis (E-cCadherin & N-cadherin, vimentin), cell proliferation (cyclins-A, B1, D1, E1, and cyclin-dependent kinases (CDKs) 1, 2,4), inflammatory molecules (programmed death-ligand 1 (PD-L1), TNF-α, NF-κB, Interleukin-1 (IL-1), Interleukin-6 (IL-6), Interleukin-8 (IL-8), Interleukin-1 beta (IL-1β)), regulating tumor suppressor genes (p21, p27, p38, p51, p53), microRNA (miRNA) regulation, and some nonspecific pathways like DNA fragmentation damage and repair, autophagy (light chain 3-II (LC3-II) and mTOR), and many other pathways. Some selective phytochemicals exert synergistic activities with standard chemotherapeutic drugs and reverse drug resistance through several mechanisms. Nano-based phytochemicals target numerous cancer cells, resulting in drug accumulation and improved drug efficacy, making phytochemicals more potent chemotherapeutic agents in cancer treatment. Additionally, an in-silico pharmacokinetics study reveals that phytoestrogen possesses suitable pharmacokinetic characteristics with minor toxicity in the human body. So, direct consumption of different parts of Eclipta prostrata or specific phytochemicals from this plant can be a potential candidate drug against human malignancies.

The groundbreaking success of messenger RNA (mRNA) vaccines during the COVID-19 pandemic has significantly accelerated their application in oncology. This review comprehensively synthesizes the recent advancements in mRNA cancer vaccine development, emphasizing three critical domains: mechanistic innovations, clinical translation, and ongoing challenges. Technologically, advancements in nucleotide modification, lipid nanoparticle (LNP) delivery systems, and AI-driven neoantigen selection have significantly improved vaccine stability, immunogenicity, and personalization. Clinically, more than 150 trials have demonstrated the synergistic efficacy of mRNA vaccines (e.g., mRNA-4157/V940, BNT122) in combination with immune checkpoint inhibitors (ICIs), particularly in melanoma, with Phase III trials currently underway. Individualized neoantigen vaccines targeting patient-specific mutations have shown unprecedented response rates (> 50% in certain cohorts), while shared-antigen vaccines are progressing for high-incidence cancers. However, several critical challenges remain: (1) overcoming immunosuppressive tumor microenvironments (TME), (2) addressing systemic toxicities and LNP-related limitations, (3) scaling up cost-effective personalized manufacturing, and (4) optimizing targeted delivery. Future research directions encompass self-amplifying mRNA constructs, novel biomaterial vectors, neoadjuvant applications, and multi-omics integration for next-generation vaccine development. With rapid industrialization and evolving regulatory frameworks, mRNA vaccines are well-positioned to revolutionize precision cancer immunotherapy despite persistent translational barriers.