Cancer Biology & Medicine最新文献

Objective: To evaluate the impact of government-organized screening on the economic burden among patients with cervical cancer and precancerous lesions, and explore mediating pathways across diagnosis, initial treatment, radiotherapy/chemotherapy, follow-up, and recurrence/progression/metastasis.

Methods: A multicentre, nationwide survey across 5 disease courses was conducted from 26 hospitals in China. Multivariable regression and structural equation modeling were used to assess the effects of government-organized screening on economic burden by comparing government-organized screening with workplace check-up, self-paid check-up, and symptom-based detection.

Results: Workplace check-up, self-paid check-up, and symptom-based detection were associated with progressively higher costs across diagnosis [β: 1.10, 95% confidence interval (CI): 0.54-1.67; β: 1.46, 95% CI: 1.00-1.92; and β: 1.68, 95% CI: 1.25-2.11, respectively], initial treatment (β: 0.36, 95% CI: 0.18-0.55; β: 0.51, 95% CI: 0.35-0.66; and β: 0.56, 95% CI: 0.42-0.70, respectively), and follow-up (β: 0.63, 95% CI: 0.38-0.88; β: 0.83, 95% CI: 0.61-1.04; and β: 0.85, 95% CI: 0.65-1.06, respectively) compared to government-organized screening (all P < 0.05). Earlier clinical staging and greater use of lower-level hospitals mediated 44.74%-54.97% of cost differences in diagnosis, 73.27%-85.04% in initial treatment, and 30.38%-54.73% in follow-up. Fifteen percent of the cost differences during initial treatment were related to lower overtreatment for precancerous lesions.

Conclusions: Government-led cervical cancer screening was associated with lower economic burden with pathways involving earlier-stage diagnosis, reduced overtreatment, and decreased reliance on higher-level hospitals, suggesting potential clinical benefits, efficient resource use, and improved equity in cancer care.

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.

Objective: Current clinical staging of pancreatic ductal adenocarcinoma (PDAC) relies predominantly on anatomical resectability, thus limiting its prognostic utility. We developed and validated a pretreatment prognostic grading system incorporating multidimensional parameters.

Methods: Patients with histologically confirmed PDAC undergoing curative-intent pancreatectomy were retrospectively enrolled. Independent prognostic determinants of overall survival (OS) and disease-free survival (DFS), identified through multivariable Cox proportional hazards regression, provided the basis for deriving the Tianjin Prognostic Score and its corresponding risk stratification scheme.

Results: Resectability status, lymph node metastasis indicated by imaging, pretreatment serum CA19-9 levels, and the prognostic nutritional score (PNS) independently predicted both OS and DFS. These parameters were integrated into the Tianjin Prognostic Score for PDAC prognosis stratification. The Tianjin-Grade system, subsequently established according to this score, segregated patients into 4 discrete prognostic cohorts with significantly divergent survival outcomes. This system exhibited significantly greater discriminatory ability for prognosis than conventional serum CA19-9 and resectability criteria. Notably, patients classified as having high risk or extremely high risk derived substantial survival benefits from neoadjuvant chemotherapy (NAC), whereas those with low or intermediate risk demonstrated comparable survival outcomes regardless of NAC administration.

Conclusions: The Tianjin-Grade system provides accurate pretreatment prognosis prediction in patients with PDAC through integration of anatomical and biological parameters, thus serving as a reliable tool for prognostic assessment. This system facilitates the development of personalized preoperative therapeutic strategies.

Over the past 2 decades, remarkable advancements in the screening, diagnosis, and treatment of non-small cell lung cancer (NSCLC) have led to improved patient outcomes. For the treatment of NSCLC with actionable gene mutations, tyrosine kinase inhibitors developed against EGFR, ALK, RET, BRAF, ROS1, NTRK, MET, and KRAS, exhibit substantial antitumor activity and have been incorporated into standard treatment regimens. Additionally, numerous novel therapies, including immunotherapy and antibody-drug conjugate therapy, have been found to benefit patients with NSCLC. This review summarizes current advancements in targeted therapy for NSCLC, according to a systematic search of the PubMed database and synthesis of cutting-edge findings presented at the 2024 American Society of Clinical Oncology Annual Meeting and 2024 World Conference on Lung Cancer.

Immune checkpoint inhibitors have markedly improved outcomes in patients with multiple advanced malignancies. However, their widespread use has markedly increased the incidence of immune-related adverse events (irAEs). irAEs can affect a wide range of organ systems and are characterized by heterogeneous onset, broad toxicity spectra, and complex management requirements, thus ultimately impairing treatment continuation and patient quality of life. This review systematically summarizes the epidemiological features, clinical progression, and current management of irAEs. Existing guidelines largely focus on acute toxicities but have not provided structured strategies for chronic, delayed-onset, or multisystem irAEs. Moreover, clinical practice is hampered by incomplete multidisciplinary collaboration, insufficient training of oncologists, and fragmented treatment pathways, all of which limit the efficacy of irAE management. We propose incorporating irAE management into core oncology training and call for the establishment of comprehensive interdisciplinary frameworks to ensure the standardized long-term use of immunotherapy.

Tumor cells undergo metabolic reprogramming to adapt to rapid proliferation and harsh microenvironments, as evidenced by aerobic glycolysis. Mitochondria serve as key coordinators of this process. Under internal and environmental stress in tumors, mitochondria reprogram metabolism by balancing energy dynamics, redirecting metabolic routes, communicating via metabolites, and preserving the quality of mitochondria, thus supporting tumor cell survival. Traditional Chinese medicine (TCM) has a key role in modulating mitochondrial reprogramming in tumor cells, possibly disrupting metabolic pathways that are necessary for survival and proliferation. However, the underlying molecular signaling and cellular biological mechanisms need to be elucidated. In this review, we focused on the Key functions of mitochondria in adapting to tumor metabolic reprogramming are the focus of this review and recent advances in and regulatory mechanisms of TCM and nano-pharmaceutical formulations in maintaining mitochondrial homeostasis are discussed. These insights may help understand the role of mitochondria in the pathogenesis of metabolic diseases, such as cancer, and identify therapeutic targets.