Lung Cancer

P=N/A, N=310, Active, not recruiting, McMaster University | Recruiting --> Active, not recruiting | N=200 --> 310 | Trial completion date: Dec 2030 --> Dec 2027 | Trial primary completion date: Dec 2030 --> Dec 2027

P1/2, N=288, Recruiting, BicycleTx Limited | Trial completion date: Oct 2026 --> Oct 2025

P2, N=109, Completed, Pfizer | Active, not recruiting --> Completed

P=N/A, N=120, Completed, Massachusetts General Hospital | Active, not recruiting --> Completed

P2, N=60, Active, not recruiting, Xiangya Hospital of Central South University | Phase classification: P1 --> P2 | N=40 --> 60

P1, N=138, Recruiting, BeiGene | Trial completion date: Dec 2026 --> Feb 2028 | Trial primary completion date: Dec 2026 --> Feb 2028

P1, N=150, Recruiting, Daiichi Sankyo | Not yet recruiting --> Recruiting

P1/2, N=203, Recruiting, Phanes Therapeutics | N=61 --> 203 | Trial completion date: Jun 2025 --> Aug 2028 | Trial primary completion date: Jan 2025 --> Dec 2027

P2, N=182, Active, not recruiting, Maia Biotechnology | Recruiting --> Active, not recruiting | Trial completion date: Dec 2024 --> Oct 2026 | Trial primary completion date: Jun 2024 --> Aug 2025

Importantly, restoration of IFN signaling through re-expression of endogenous STING, enforced expression of IFN response factor 7 or administration of recombinant type I IFN re-established antitumor immunity, inhibiting metastatic SCLC in vivo. These data show the potential of augmenting the innate immune response to block metastatic SCLC.

Furthermore, GCC2 inhibition compromised Golgi structural integrity in cancer cells, indicating a functional role of GCC2 in regulating intracellular trafficking and signaling to promote lung cancer progression. Together, these findings suggest GCC2 as a potential therapeutic target for the treatment of NSCLC.

No abstract available

We further discussed that the most commonly used drugs in standard regimens for mainly breast cancer, lung cancer, and acute lymphoblastic leukemia could be subject to MDR mediated by ABC transporters. Collectively, these insights will aid in conducting new studies aimed at a deeper understanding of the clinical MDR mediated by ABC proteins and in designing more effective pharmacological treatments to enhance the objective response rate in cancer patients.

Our results indicated tumor promotion of TXN in NSCLC and TXN regulated c-Myc in the interest of tumorigenesis through ERK1/2 and ERK5 signaling pathways. Targeting TXN and blocking the ERK1/2 and ERK5 pathways could potentially offer new therapeutic strategies for NSCLC.

Additionally, in vitro sensitivity to cisplatin and mTOR inhibitors was evaluated in SCLC cell lines harbouring RICTOR amplification and other mTOR pathway mutations...The importance of these alterations was confirmed both by the sensitising effect of vistusertib in vitro and the RICTOR copy number/expression changes in xenografts. Our study highlights the role of mTORC2 in SCLC progression. Early detection of RICTOR amplification in primary tumours and targeting mTORC2 in these cases may represent a promising novel strategy to develop personalised therapy for metastasis prevention.

This study confirmed the SCLC subtyping based on key transcription factors. While no significant differences in OS and PFS among subtypes were found, the SCLC-I subtype showed potential benefit from platinum-based chemotherapy combined with immune checkpoint inhibitors. M stage and bone metastasis at diagnosis were identified as independent risk factors for SCLC.

Comprehensive serum biomarker analysis revealed that a lower fold change in serum IL-8 was associated with better outcomes in pre-treated patients with advanced NSCLC receiving atezolizumab.

This study provides data on the molecular epidemiology of lung adenocarcinoma in Brazil, confirming high prevalence of EGFR mutations, ALK fusions, and MET exon 14 skipping alteration. Biomarker detection is largely affected by biospecimen collection and processing, with one third of the patients eligible for non-NGS testing only, which presents reduced coverage and sensitivity for actionable drivers.

The distribution of lung tumours metastatic to the brain is dependent on the lung cancer subtype (p<0.001). The reporting of histologic subtype could be further optimized in the local environment.

Our results revealed the role of ADAR1 in cooperation with Rad18 in modulating oncogenesis and radioresistance in NSCLC for the first time, and suggested the therapeutic potential of targeting ADAR1 in overcoming radioresistance.

The predictive value of PLR was more apparent in patients treated with 1st or 2nd generation TKIs compared to those treated with osimertinib. Third generation EGFR TKIs may be more efficacious in treating patients with laboratory findings previously shown to predict poor survival. The significant changes in peripheral cell counts suggest variable tumor microenvironment changes dependent on the generation of TKI received.

Although most adverse effects are reversible, vigilance is warranted particularly for nephrotoxicity and hepatotoxicity during the administration of KRAS G12C inhibitors.

The efficacy of post-relapse EGFR-TKI treatment was independent of PD-L1 expression. The significance of PD-L1 expression in perioperative EGFR-TKI therapy should be evaluated.

Our research constructed a risk score based on FA-related and tumor stemness-related specific genes. In addition to accurately predicting the prognosis of patients with LC, the risk score may also serve as an innovative and viable predictor of immunotherapy response.

Tail effect is a golden tail of immunotherapy. This case illustrates that the tail effect of immunotherapy can offer substantial survival benefits for patients with unresectable advanced lung cancer who have failed chemotherapy.

Overlap of the Oncopig LC transcriptome with human LC transcriptome was noted. This pig model is expected to have high clinical translatability to the human LC patient.

P2, N=179, Completed, Hoffmann-La Roche | Active, not recruiting --> Completed

P1, N=22, Recruiting, TILT Biotherapeutics Ltd. | Trial completion date: Oct 2025 --> May 2026 | Trial primary completion date: Oct 2024 --> Jan 2026

The combination of RC48 with platinum+/- bevacizumab resulted in the highest ORR of 71.4% (5 out of 7 patients), with HER2 TKI following at a 50.0% ORR (4 out of 8 patients). RC48, particularly in combination regimens, demonstrates promising efficacy in advanced NSCLC with HER2 alterations. These findings underscore the need for further research to validate RC48's application in clinical practice.

In addition, lncRNA-SNHG12 increased the expression of Smad3 which was significantly upregulated in MMT through sponge of miR-181a-5p. LncRNA SNHG12 derived from CAFs-EV induced MMT in NSCLC.

The essential oil of the plant Cleistocalyx operculatus may be a potential lead for anti-inflammatory and anti-proliferative function.

P=N/A, N=300, Recruiting, Central South University

P=N/A, N=46, Not yet recruiting, Duke University | Initiation date: Oct 2024 --> Jan 2025

P=N/A, N=600, Recruiting, Maastricht Radiation Oncology | Trial completion date: Apr 2025 --> Apr 2028 | Trial primary completion date: Apr 2024 --> Apr 2026

P=N/A, N=4000, Active, not recruiting, Sophia Genetics SAS | Recruiting --> Active, not recruiting

P1, N=20, Recruiting, Sichuan Baili Pharmaceutical Co., Ltd. | Not yet recruiting --> Recruiting

P1, N=20, Suspended, Mayo Clinic | Trial completion date: Oct 2024 --> Jan 2026 | Withdrawn --> Suspended | Trial primary completion date: Oct 2024 --> Jan 2026

This review will discuss the cellular responses controlled by p53 that contribute to tumour suppression, p53 mutant lung cancer mouse models and characterisation of p53 mutant lung cancer. Furthermore, we discuss potential approaches of targeting mutant p53 for the treatment of lung cancer.

Moreover, we show that fructose, the PP end-product, as well as other non-glycolytic hexoses confer survival to cancer cells and resistance against chemotherapy via sustained NF-κB activity as well as an oxidative switch in metabolism. Given the detrimental consequence of PP gene targeting on growth and survival, we propose PP pathway interference as a viable therapeutic approach against NSCLC.

P2, N=52, Recruiting, Shanghai Chest Hospital

No abstract available

Finding and confirming these biomarkers is essential for improving early detection, tracking the course of the disease, and directing focused treatments. As research progresses, combining molecular, genetic, and environmental insights might improve lung cancer care, prevention, and early diagnosis, thereby lowering the disease's worldwide burden.