Dendritic cell-derived exosomes (Dex) are small extracellular vesicles secreted by viable dendritic cells. In the two phase-I trials that we conducted using the first generation of Dex (IFN-γ-free) in end-stage cancer, we reported that Dex exerted natural killer (NK) cell effector functions in patients. A second generation of Dex (IFN-γ-Dex) was manufactured with the aim of boosting NK and T cell immune responses. We carried out a phase II clinical trial testing the clinical benefit of IFN-γ-Dex loaded with MHC class I- and class II-restricted cancer antigens as maintenance immunotherapy after induction chemotherapy in patients bearing inoperable non-small cell lung cancer (NSCLC) without tumor progression. The primary endpoint was to observe at least 50% of patients with progression-free survival (PFS) at 4 mo after chemotherapy cessation. Twenty-two patients received IFN-γ-Dex. One patient exhibited a grade three hepatotoxicity. The median time to progression was 2.2 mo and median overall survival (OS) was 15 mo. Seven patients (32%) experienced stabilization of >4 mo. The primary endpoint was not reached. An increase in NKp30-dependent NK cell functions were evidenced in a fraction of these NSCLC patients presenting with defective NKp30 expression. Importantly, MHC class II expression levels of the final IFN-γ-Dex product correlated with expression levels of the NKp30 ligand BAG6 on Dex, and with NKp30-dependent NK functions, the latter being associated with longer progression-free survival. This phase II trial confirmed the capacity of Dex to boost the NK cell arm of antitumor immunity in patients with advanced NSCLC.

https://tandfonline.com/doi/pdf/10.1080/2162402X.2015.1071008

Dendritic cell-derived exosomes as maintenance immunotherapy after first line chemotherapy in NSCLC

Lung cancer is the most frequent cancer with an aggressive clinical course and high mortality rates Most cases are diagnosed at advanced stages when treatment options are limited and the efficacy of chemotherapy is poor The disease has a complex and heterogeneous background with non-small-cell lung cancer (NSCLC) accounting for 85% of patients and lung adenocarcinoma being the most common histological subtype Almost 30% of adenocarcinomas of the lung are driven by an activating Kirsten rat sarcoma viral oncogene homolog (KRAS) mutation The ability to inhibit the oncogenic KRAS has been the holy grail of cancer research and the search for inhibitors is immensely ongoing as KRAS-mutated tumors are among the most aggressive and refractory to treatment Therapeutic strategies tailored for KRAS+ NSCLC rely on the blockage of KRAS functional output, cellular dependencies, metabolic features, KRAS membrane associations, direct targeting of KRAS and immunotherapy In this review, we provide an update on the most recent advances in anti-KRAS therapy for lung tumors with mechanistic insights into biological diversity and potential clinical implications

https://www.mdpi.com/1422-0067/21/12/4325/pdf

Targeting KRAS Mutant Non-Small-Cell Lung Cancer: Past, Present and Future.

Lung cancer is the leading cause of death in individuals with malignant disease. Non-small-cell lung cancer (NSCLC) is the most common type of lung cancer, and chemotherapy drugs such as cisplatin are the most widely used treatment for this disease. Baicalein is a purified flavonoid compound that has been reported to inhibit cancer cell growth and metastasis and increase sensitization to chemotherapeutic drugs via different pathways. Therefore, we assessed the effects of baicalein on the proliferation, apoptosis and cisplatin sensitivity in the NSCLC A549 and H460 cell lines and determined the pathways through which baicalein exerts its effects. Baicalein was slightly toxic to normal human bronchial NHBE cells but inhibited growth, induced apoptosis and increased cisplatin sensitivity in A549 and H460 cells. Baicalein down-regulated miR-424-3p, up-regulated PTEN expression and down-regulated expression of PI3K and p-Akt in A549 and H460 cells. Dual-luciferase reporter assay demonstrated that PTEN is a target gene of miR-424-3p, and overexpression of miR-424-3p or silencing of PTEN partially attenuated the effects of baicalein on A549 and H460 cells. Taken together, we concluded that baicalein inhibits cell growth and increases cisplatin sensitivity to A549 and H460 cells via down-regulation of miR-424-3p and targeting the PTEN/PI3K/Akt pathway.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/jcmm.13556

Baicalein inhibits cell growth and increases cisplatin sensitivity of A549 and H460 cells via miR‐424‐3p and targeting PTEN/PI3K/Akt pathway

Lung cancer (LC) is the leading cause of cancer-related deaths worldwide. MicroRNAs (miRNAs) are highly evolutionarily conserved noncoding small RNAs, which were first identified in Caenorhabditis elegans. There are 1100 or more miRNAs have been identified in Homo sapiens. Let-7 miRNA is involved in the regulation of gene expression in cells. Several novel factors and feedback loops involved in the regulation of the synthesis of let-7 have been identified and additional let-7 target genes have been found. Let-7 has also been shown to be significantly correlated with the occurrence and development of cancer and the results of preliminary studies suggest that it is involved in the regulation of oncogenic pathways in numerous types of tumors, such as, LC. As let-7 is a potential molecular target for tumor therapy, a mass of studies have been conducted focus on the relationship between let-7 and LC. With the mechanism becoming revealed, more and more groups are looking for the anti-tumor role of let-7 family in anti-tumor therapy development. In this review, we summarize the newest investigations on let-7 and LC, the regulation of let-7 and its targets gene have been discussed, and the attempts for new therapy for LC have also been summarized.

MicroRNA let-7: Regulation, single nucleotide polymorphism, and therapy in lung cancer

Lung cancer is one of the most common malignant tumors, and it has the highest death rate. Oncothermia is a feasible and successful treatment for lung cancer. Results show a remarkable survival benefit for patients, with a good quality of life. The treatment has no, or in some cases mild, side-effects and could decrease the adverse effects of the complementary treatment. Applying oncothermia together with other treatment methods could increase the effects and result in better performance. A comparison of studies demonstrates a good correspondence in the data, which strengthens the reliability of the studies, and clearly shows the feasibility of the application of oncothermia to treating all kinds of pulmonary malignancies including non-small-cell and small-cell primary tumors, and all of the metastatic diseases of the pulmonary system.

Current Status of Oncothermia Therapy for Lung Cancer

Maintenance strategies in stage IV non-small-cell lung cancer (NSCLC): in which patients, with which drugs?

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Maintenance strategies in stage IV non-small-cell lung cancer (NSCLC): in which patients, with which drugs?