Changes in survival of patients with non–small cell lung cancer in Japan: An interrupted time series study

Taniyama, Yukari; Oze, Isao; Koyanagi, Yuriko N.; Kawakatsu, Yukino; Ito, Yuri; Matsuda, Tomohiro; Matsuo, Keitaro; Mitsudomi, Tetsuya; Ito, Hidemi

doi:10.1111/cas.15646

Cited by 4 publications

(3 citation statements)

References 41 publications

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“…NSCLC is an uncompromising type of lung cancer associated with limited treatment options. Drugs that inhibit tyrosine kinases EGFR (erlotinib, gefitinib, and afatinib) or ALK (crizotinib and ceritinib) have been approved for the treatment of NSCLC harbouring genetic modifications in the genes encoding these proteins [ 36 , 37 , 38 ]. Although these drugs are associated with a median progression-free survival of 9–14 months as compared to 5–7 months for platinum-based chemotherapy [ 39 , 40 , 41 ], improvements in overall survival have not been reported.…”

Section: Discussionmentioning

confidence: 99%

Regression of Lung Cancer in Mice by Intranasal Administration of SARS-CoV-2 Spike S1

Sheinin

Jeong

Paidi

et al. 2022

Cancers

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This study underlines the importance of SARS-CoV-2 spike S1 in prompting death in cultured non-small cell lung cancer (NSCLC) cells and in vivo in lung tumors in mice. Interestingly, we found that recombinant spike S1 treatment at very low doses led to death of human A549 NSCLC cells. On the other hand, boiled recombinant SARS-CoV-2 spike S1 remained unable to induce death, suggesting that the induction of cell death in A549 cells was due to native SARS-CoV-2 spike S1 protein. SARS-CoV-2 spike S1-induced A549 cell death was also inhibited by neutralizing antibodies against spike S1 and ACE2. Moreover, our newly designed wild type ACE2-interacting domain of SARS-CoV-2 (wtAIDS), but not mAIDS, peptide also attenuated SARS-CoV-2 spike S1-induced cell death, suggesting that SARS-CoV-2 spike S1-induced death in A549 NSCLC cells depends on its interaction with ACE2 receptor. Similarly, recombinant spike S1 treatment also led to death of human H1299 and H358 NSCLC cells. Finally, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) intoxication led to the formation tumors in lungs of A/J mice and alternate day intranasal treatment with low dose of recombinant SARS-CoV-2 spike S1 from 22-weeks of NNK insult (late stage) induced apoptosis and tumor regression in the lungs. These studies indicate that SARS-CoV-2 spike S1 may have implications for lung cancer treatment.

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Section: Discussionmentioning

confidence: 99%

Regression of Lung Cancer in Mice by Intranasal Administration of SARS-CoV-2 Spike S1

Sheinin

Jeong

Paidi

et al. 2022

Cancers

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“…Protein kinases belong to an extensive superfamily, encompassing numerous kinases and isoforms. Kinase inhibitors have been employed in the treatment of various cancers including leukemia, breast cancer, melanoma, lung cancer, and renal cancer [29][30][31] . The Kinase Target analysis of SYNGR2-related genes revealed a higher enrichment score for the gene set containing ribosomal protein S6 kinase B6KB1).…”

Section: Discussionmentioning

confidence: 99%

SYNGR2 plays a tumor-promoting role in lung adenocarcinoma through PI3K-AKT signaling pathway

Liu,

Luan,

Han

et al. 2023

Preprint

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Objectives To analyze the expression level of SYNGR2 in lung adenocarcinoma, explored its prognostic and diagnostic value, and preliminarily discussed its mechanism of action. Methods The diagnostic value was assessed by generating the ROC curve using SYNGR2 expression data. COX regression and correlation analysis were conducted to establish its association with clinical features. Additionally, immunohistochemical staining was performed on samples from 20 patients with lung adenocarcinoma (LUAD) to validate the observed differences in expression levels. Furthermore, silencing of SYNGR2 in LUAD cells demonstrated inhibition of proliferation, invasion, migration, and colony formation abilities. Moreover, GO and KEGG analyses along with PPI analysis were employed to preliminarily investigate the underlying mechanism of SYNGR2 in lung adenocarcinoma. Results The results demonstrated an upregulation of SYNGR2 which was associated with shorter overall survival (OS) and progression-free survival (PFS). Furthermore, the receiver operating characteristic (ROC) curve analysis revealed a robust diagnostic value for SYNGR2. Additionally, the SYNGR2 gene exhibited a strong association with the PI3K-AKT signaling pathway. Conclusions SYNGR2 plays a tumor-promoting role in lung adenocarcinoma and may act through PI3K-AKT signaling pathway.

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“…In our research, we investigated the NCAPD3 expression in normal and NSCLC tissues according to histological type (categorized as LUAD or LUSC) and different tumor stages (classified as stage I-IV). Wherein, cancer stage I denotes that localized cancer confined to the primary site; stage II represents that cancer spread to regional lymph nodes; stage III indicates cancer spread to adjacent tissues; and stage IV indicates further spread to distant organs [ 16 ].…”

Section: Methodsmentioning

confidence: 99%

Knockdown of NCAPD3 inhibits the tumorigenesis of non-small cell lung cancer by regulation of the PI3K/Akt pathway

Yang,

Zheng,

Luo

et al. 2024

BMC Cancer

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Background Accumulating evidence indicates that aberrant non-SMC condensin II complex subunit D3 (NCAPD3) is associated with carcinogenesis of various cancers. Nevertheless, the biological role of NCAPD3 in the pathogenesis of non-small cell lung cancer (NSCLC) remains unclear. Methods Immunohistochemistry and Western blot were performed to assess NCAPD3 expression in NSCLC tissues and cell lines. The ability of cell proliferation, invasion, and migration was evaluated by CCK-8 assays, EdU assays, Transwell assays, and scratch wound healing assays. Flow cytometry was performed to verify the cell cycle and apoptosis. RNA-sequence and rescue experiment were performed to reveal the underlying mechanisms. Results The results showed that the expression of NCAPD3 was significantly elevated in NSCLC tissues. High NCAPD3 expression in NSCLC patients was substantially associated with a worse prognosis. Functionally, knockdown of NCAPD3 resulted in cell apoptosis and cell cycle arrest in NSCLC cells as well as a significant inhibition of proliferation, invasion, and migration. Furthermore, RNA-sequencing analysis suggested that NCAPD3 contributes to NSCLC carcinogenesis by regulating PI3K/Akt/FOXO4 pathway. Insulin-like growth factors-1 (IGF-1), an activator of PI3K/Akt signaling pathway, could reverse NCAPD3 silence-mediated proliferation inhibition and apoptosis in NSCLC cells. Conclusion NCAPD3 suppresses apoptosis and promotes cell proliferation via the PI3K/Akt/FOXO4 signaling pathway, suggesting a potential use for NCAPD3 inhibitors as NSCLC therapeutics.

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Changes in survival of patients with non–small cell lung cancer in Japan: An interrupted time series study

Cited by 4 publications

References 41 publications

Regression of Lung Cancer in Mice by Intranasal Administration of SARS-CoV-2 Spike S1

Regression of Lung Cancer in Mice by Intranasal Administration of SARS-CoV-2 Spike S1

SYNGR2 plays a tumor-promoting role in lung adenocarcinoma through PI3K-AKT signaling pathway

Knockdown of NCAPD3 inhibits the tumorigenesis of non-small cell lung cancer by regulation of the PI3K/Akt pathway

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