Lung Adenocarcinoma

In COAD, a subset of patients in stage II/III with CD3+RUNX3+high/CD8 + high may be spared adjuvant treatment due to excellent prognosis. However, further studies are needed to confirm and elucidate the protective role of CD3+RUNX3+ cells in COAD and LUAD.

In our cohort, KRAS mutations were more prevalent in PLMAC than PLNMAC (72% vs. 40%, P < 0.05). However, the KRAS G12C variant was significantly less frequent in PLMAC compared to PLNMAC (19% vs. 47%, P < 0.05), suggesting that patients with PLMAC are less likely to benefit from KRAS G12C-targeted therapy. These findings underscore the importance of comprehensive KRAS genotyping and highlight the need for developing additional KRAS variant-targeted therapy for patients with PLMAC.

CS/DS content increased 3.4-fold in A549 sEVs, while the ratio of the two monosulfated disaccharides changed 2-fold. These findings demonstrate the utility of N-glycoproteomics and GAG profiling for sensitively characterizing molecular differences between sEVs derived from different cell culture models, thereby providing a foundation for future EV biomarker studies.

Baohuoside I is a new pyroptosis inducer in LUAD, and combined treatment with Baohuoside I and cisplatin has a synergistic inhibitory effect on LUAD.

Additionally, farnesol impaired mitochondrial ATP synthesis by reducing mitochondrial membrane potential (MMP) to 66% and elevated ROS levels to 54% creating a disturbance in mitochondrial stability. Overall, Farnesol significantly disrupts anaerobic glycolysis in A549 cells promoting cell death through mitochondrial dysfunction, oxidative stress, apoptosis and reducing cellular acidosis.

Finally, we find that induced systemic SIAH2 expression promotes CD8 T cell infiltration into subcutaneous tumors in a syngeneic mouse model. Our work further supports the tumor suppressive role of PLK3 in lung cancer and discovered a novel involvement of PLK3 in the regulation of the immune microenvironment of lung tumors.

In an orthotopic lung cancer mouse model treated with erastin (a ferroptosis inducer) and programmed cell death protein 1 (PD-1) blockade, the role of TIMELESS in therapeutic response was assessed via flow cytometry and multiplex immunofluorescence (mIF)... TIMELESS recruits CNOT3 to accelerate TF mRNA degradation, thereby suppressing ferroptosis and promoting LUAD growth. These findings suggest that the TIMELESS/TF regulatory axis may be a promising therapeutic target for LUAD.

Failure to respond to standard antibiotic therapy and drainage should prompt consideration of an underlying malignancy. Surgical resection is essential for both definitive diagnosis and treatment.

P1/2, N=260, Completed, Amgen | Active, not recruiting --> Completed

Compared to results from established architectures such as Inception-v3 on the same WSIs, our model demonstrated significantly improved performance for most features. With further optimization, our model could support triaging for molecular testing and inform precision treatment strategies for NS-LUAD patients.

Our findings suggest that PD-L1 immunohistochemistry is effective for evaluating pleural fluid cytological specimens and that PD-L1 expression is significantly higher in lung adenocarcinoma patients with malignant pleural effusions associated with the KRAS, ALK and BRAF mutations.