ArchiveImmunotherapy, particularly immune checkpoint inhibitors (ICIs) programmed death-ligand 1/programmed death-1 (PD-L1/PD-1) and cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4), has heralded a new era of tumor treatment. Although ICIs have clinical benefits, their complex heterogeneity and diverse resistance mechanisms critically limit their efficacy. Neoantigens, arising from tumor-specific alterations, offer novel targets for individualized immunotherapy, because of their high immunogenicity and tumor specificity. In the past decade, neoantigen-based tumor vaccines have been demonstrated to be a promising immunotherapy strategy to prime the tumor-specific immune response. These therapeutic vaccines include peptide vaccines, nucleic acid vaccines, and dendritic cell (DC) vaccines, and are categorized according to the neoantigen source and delivery method. In vivo, neoantigens are processed and presented by antigen-presenting cells (APCs) via the peptide-Major Histocompatibility Complex (pMHC) for T cell recognition, thereby triggering specific immune responses. Because DCs, the most potent APCs, play crucial roles in antitumor immunity, neoantigen-based DC vaccines provide a promising therapeutic strategy. A series of global clinical trials are exploring the safety, feasibility, and efficacy of neoantigen-based DC vaccines in tumors. This review focuses on current progress in clinical research on neoantigen-based DC vaccines in the treatment of solid tumors.
A significant number of anticancer drugs fail to treat primary and metastatic brain tumors primarily because of the complex blood-brain barrier (BBB) and overexpression of ATP-binding cassette (ABC) transporters, which decrease drug penetration into the central nervous system and ultimately into tumors. It is noteworthy that the ABC transporters, ABCB1 [known as P-glycoprotein (P-gp)] and ABCG2 [known as breast cancer resistance protein (BCRP)], are overexpressed in brain tumors, including common gliomas. The co-presence of these transporters may negate the inhibition of either transporter, particularly if both transport the same anticancer drug. The cellular export of drugs by ABC transporters has been implicated in mediating resistance to anticancer drugs. However, the clinical relevance as a therapeutic target in human tumors remains a matter of contention. Although effective and clinically approved ABC transporter inhibitors could potentially overcome drug resistance, none are currently approved. Furthermore, the ABC transporter inhibitors in clinical trials produced low or no clinical efficacy, significant toxicities, and unsuitable pharmacokinetic profiles. Therefore, innovative approaches are needed to efficaciously and simultaneously inhibit these transporters to surmount anticancer drug resistance. This review emphasizes the clinical significance of ABC transporters in diminishing the efficacy of brain tumor treatments. The molecular alterations in BBB following brain tumor development, which are linked to various cancer therapies, are discussed. The overexpression of ABCB1 and ABCG2 at the BBB is discussed, potential strategies to decrease the export of chemotherapeutics by these transporters and the associated challenges and failures are discussed, and the implementation of novel approaches is considered.
The occurrence and progression of liver cancer are closely associated with mitochondrial dysfunction. Mitochondria exhibit characteristics, such as decreased oxidative phosphorylation efficiency, abnormal accumulation of reactive oxygen species in liver cancer and promoting tumor proliferation and drug resistance through the Warburg effect, as the core of energy metabolism and apoptosis regulation. Mutations in mitochondrial DNA (mtDNA) and dysregulation of mitochondrial autophagy (mitophagy) further enhance the invasive and metastatic capabilities of liver cancer. Current targeted therapeutic strategies focus on modulating the activity of respiratory chain complexes, regulating calcium homeostasis, repairing mtDNA, and activating mitochondrial apoptotic pathways. Although these approaches have shown therapeutic effects, challenges persist, such as tumor heterogeneity, insufficient drug specificity, and drug resistance. Future research needs to integrate the concept of precision medicine by focusing on breakthroughs in the molecular mechanisms underlying mitochondrial dysfunction, development of targeted delivery systems, optimization of combination therapy regimens, and screening of biomarkers to provide new pathways for individualized treatment. With advances in technology, targeting mitochondrial dysfunction is expected to become an important breakthrough for improving the prognosis of liver cancer.
This study aimed to analyze the temporal trends in cancer mortality in China from 2013–2021 and project the future trends through 2030.
This study was based on the China Causes of Death Surveillance Dataset, which covers 2.37 billion person-years. Age-standardized mortality rates (ASMRs) were calculated using Segi’s world standard population and the trends were evaluated via Joinpoint regression. Bayesian age-period-cohort models were used for mortality projections. Contributions of demographic changes (population size and age structure) and risk factors to the mortality burden were quantified using the decomposition analysis.
The combined ASMRs for all cancers decreased annually by 2.3%, driven by significant declines in esophageal (4.8%), stomach (4.5%), and liver cancers (2.7%). In contrast, the pancreatic and prostate cancer ASMRs increased by 2.0% and 3.4% annually, respectively. Urban areas demonstrated a more rapid decline in the combined ASMRs for all cancers [average annual percent change (AAPC) = −3.0% in urban areas vs. −2.0% in rural areas], highlighting persistent disparities. Population aging contributed 20%–50% to death increases between 2013 and 2021. The combined ASMRs for all cancers, like the findings of temporal trend analyses, will continue to decrease and the regional (urban and rural) difference is projected to simulate that of the temporal trend through 2030. In fact, cancer deaths are projected to reach 2.4 million by 2030.
The cancer burden in China is facing the dual challenges of population aging and urban-rural disparities. It is necessary to prioritize rural screening, control risk factors, such as smoking and diet, and integrate more efficacious cancer prevention and control programmes into the policy to reduce mortality in the future.
This study aimed to assess the global, regional, and national burden of early-onset gastric cancer (EOGC) and the attributable risk factors from 1990–2021 with projections extending to 2040.
The EOGC burden was quantified using incidence, prevalence, mortality, and disability-adjusted life years (DALYs) with calculation of age-standardized rates. The risk factor contributions were analyzed and disparities were evaluated using the slope index of inequality. Future trends for 2021–2040 were estimated using a Bayesian age-period-cohort model.
There were approximately 125,000 new cases of EOGC globally in 2021 with an estimated 336,000 individuals living with EOGC and 78,000 associated deaths, contributing to 3.86 million DALYs. The highest EOGC incidence rates existed among individuals 45–49 years of age. The global age-standardized incidence, prevalence, mortality, and DALY rates demonstrated an overall decline between 1990 and 2021. Smoking and high-salt dietary intake were the leading risk factors for DALYs with regional and gender-based variations. Smoking accounted for > 10% of DALYs in Central Europe and East Asia, while high-salt dietary intake accounted for approximately 8% of DALYs. Despite the overall decline in the EOGC burden, disparities across geographic regions widened. Projections indicated a continued gradual reduction in EOGC burden through 2040.
Although the global burden of EOGC has decreased, significant disparities persist across geographic regions, age groups, and genders. Public health interventions should combine smoking prevention strategies (e.g., youth education and tobacco taxation) with cessation programs with dietary salt reduction initiatives.
The aim of the current study was to identify independent prognostic factors, evaluate differential adjuvant chemotherapy efficacy across clinicopathologic subgroups, and define adjuvant chemotherapy-sensitive populations.
A retrospective analysis of 168 AAC patients undergoing curative pancreaticoduodenectomy (2011–2020) was performed. Cases were classified into intestinal (28.0%), pancreatobiliary (30.4%), and mixed subtypes (18.5%) per NCCN (v2.2025) criteria. Independent prognostic factors for AAC patients were identified through uni- and multi-variable Cox proportional hazards modeling and subgroup analyses were stratified by age range, gender, differentiation, T stage, N stage, BVI, TDs, and PNI.
The pancreatobiliary signature (HR = 2.884, P < 0.001) and BVI (HR = 2.330, P = 0.001) were independent poor prognostic factors. Adjuvant chemotherapy improved overall survival (OS) in the following AAC patients: T3–T4 stage (HR = 0.485, P = 0.050); N1–N2 stage (HR = 0.365, P = 0.008); and TD-positive (HR = 0.401, P = 0.026). The median OS increased from 22.3–51.3 months with adjuvant chemotherapy in TD-positive patients (P = 0.019). TD positivity conferred a worse prognosis in BVI-negative subgroups (OS: HR = 3.840, 95% CI: 2.058–7.166, P < 0.001; and progression-free survival (PFS): HR = 2.950, 95% CI: 1.550–5.617, P = 0.002).
The pancreatobiliary signature and BVI constitute critical high-risk pathologic features in AAC. TD status identified high-risk cohorts, thus enabling postoperative risk-stratified treatment strategies. In patients negative for pancreatobiliary signature or BVI, TD positivity predicted significantly worse survival.
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