Cancer3.AI › Latest Research

Latest Research

All publications from the Cancer3.AI database, newest first.

ICD: C33-C34 WHO Vol. 5 Thorax (Respiratory & Mediastinum)
2026-04-10

Independent Validation of the LIONS PREY in Patients Undergoing Navigational Bronchoscopy.

Büscher E, et al

Researchers conducted an independent external validation of the LIONS PREY (Lung lesION Score PREdicts malignancY) model, a risk prediction tool designed to estimate the likelihood that a pulmonary lesion is cancerous in patients undergoing navigational bronchoscopy. The study retrospectively analyzed 193 lung lesions from patients evaluated at a tertiary academic center between December 2019 and March 2024, comparing LIONS PREY against two widely used models, Brock and Herder. LIONS PREY achieved an impressive area under the curve (AUC) of 0.94, far outperforming the Herder model (AUC 0.72) and the Brock model (AUC 0.62), while correctly classifying 85% of lesions compared to approximately 70% for the other two tools. These results are clinically significant because more accurate risk stratification can help physicians decide which patients truly need invasive procedures and which can be monitored safely, potentially reducing unnecessary interventions. The findings strongly support the adoption of LIONS PREY in high-risk lung cancer screening and bronchoscopy settings where existing models have historically underperformed.

Respiration; international review of thoracic diseases

Source →
ICD: C33-C34 WHO Vol. 5 Thorax (Respiratory & Mediastinum)
2026-04-10

Copper homeostasis dysregulation and cuproptosis in respiratory diseases.

Gao Y, et al

Researchers have published a comprehensive review examining the emerging role of cuproptosis — a newly discovered form of programmed cell death driven by copper accumulation — in serious respiratory diseases including pulmonary fibrosis, chronic obstructive pulmonary disease (COPD), and lung cancer. The review details how disruptions in the body's normal copper regulation lead to toxic copper buildup inside cells, ultimately damaging the mitochondrial respiratory chain and triggering this distinct form of cell death. By mapping the molecular mechanisms behind cuproptosis, the authors identify potential new therapeutic targets that could be exploited to develop treatments for conditions that currently have limited options. This work is significant for clinicians because it opens the door to copper-targeted therapies — such as drugs that modulate copper levels — as a novel strategy against hard-to-treat lung diseases. The synthesis of current research provides a foundation for future clinical studies and may ultimately lead to improved outcomes for patients suffering from these chronic and often life-threatening conditions.

Experimental lung research

Source →
ICD: C33-C34 WHO Vol. 5 Thorax (Respiratory & Mediastinum)
2026-04-10

Amoeboid-mesenchymal transition and the proteolytic control of cancer invasion plasticity.

Olson AW, et al

Researchers investigated how cancer cells switch between different modes of invasion through body tissues, focusing on whether a specific enzyme called MMP14 (MT1-MMP) is required across all invasion strategies. The prevailing belief had been that so-called amoeboid cancer cells—which squeeze and wriggle through tissue gaps—do not need to dissolve the surrounding protein scaffold (extracellular matrix), unlike mesenchymal cells that chemically digest their way through. Using 3D tumor models, CRISPR gene editing, single-cell RNA sequencing, and live human breast tissue explants, the team discovered that both amoeboid and mesenchymal cancer cells actively tunnel through collagen barriers and both rely on MMP14 to do so. When MMP14 was genetically removed, cancer cells lost the ability to invade regardless of changes in matrix density, cell stiffness, metabolic conditions, or the presence of cancer-associated fibroblasts—and cells forced to move without MMP14 suffered damage to their nuclear envelope and DNA. Spatial transcriptomic and immunohistological analysis of human breast cancer tissue confirmed that MMP14 is expressed in actively invading tumor cells surrounded by degraded collagen, establishing this enzyme as a critical and universal driver of cancer invasion in patients.

Proceedings of the National Academy of Sciences of the United States of America

Source →
ICD: C33-C34 WHO Vol. 5 Thorax (Respiratory & Mediastinum)
2026-04-10

Real-World Evidence of Treatment Outcomes in Small Cell Lung Cancer: A Bayesian Mixed Effects and Competitive Risk Approach.

Marzano L, et al

Researchers from Karolinska University Hospital in Stockholm analyzed real-world treatment data from 421 patients with small cell lung cancer (SCLC) treated between 2016 and 2022, applying advanced Bayesian statistical modeling and competitive risk analysis to uncover factors influencing survival and treatment complications. The study found that patients who developed neutropenia—a reduction in white blood cells caused by chemotherapy—actually had longer overall survival, suggesting it may serve as a marker of effective drug exposure. Higher doses of etoposide were strongly associated with a greater likelihood of adverse events, yet dose reductions did not worsen survival outcomes as long as patients completed their full four-cycle chemotherapy regimen, pointing toward the potential benefit of individualized dosing strategies. Male patients experienced fewer side effects and showed better responses to first-line treatment compared to female patients, highlighting a clinically meaningful sex-based difference in treatment tolerance. Notably, high-risk patients—those with poor performance status or aged over 75—who discontinued therapy early had survival outcomes similar to those who received no treatment at all, raising important questions about the risk-benefit balance of chemotherapy in this vulnerable subgroup. These findings support a more personalized approach to SCLC treatment and emphasize the value of real-world data in informing clinical decisions beyond what controlled trials can capture.

JMIR cancer

Source →
ICD: C33-C34 WHO Vol. 5 Thorax (Respiratory & Mediastinum)
2026-04-10

Associations of State Mandatory Paid Sick Leave Policies With Cancer Outcomes in the United States.

Kohut-Jackson A, et al

Researchers examined whether state-level mandatory paid sick leave (PSL) policies in the United States are associated with improved cancer outcomes, analyzing data from over one million adults diagnosed with cancer between 2010 and 2019 using the SEER registry. Using a difference-in-differences statistical approach, the study compared cancer stage at diagnosis and one-year overall survival before and after PSL policy implementation in states that enacted such policies versus those that did not. The findings revealed that mandatory PSL policies were associated with a statistically significant 0.83 percentage point decrease in late-stage (stage IV) cancer diagnoses and a 0.63 percentage point increase in one-year survival rates. Exploratory analyses suggested that men and patients with lung cancer experienced the most pronounced improvements linked to these policies. These results indicate that workplace policies ensuring income continuity during illness can enable patients to seek timely cancer screening and treatment, ultimately leading to better health outcomes. The study underscores the importance of social and economic policy as a tool for reducing cancer mortality and late-stage diagnoses at the population level.

JCO oncology practice

Source →