Classification and regression tree for estimating predictive markers to detect T790M mutations after acquired resistance to first line EGFR-TKI: HOPE-002

Tamiya, Motohiro; Fujikawa, Kei; Suzuki, Hidekazu; Yokoyama, Toshihide; Uenami, Takeshi; Tamiya, Akihiro; Sato, Yuki; Saito, Go; Uchida, Junji; Morita, Mitsunori; Hirashima, Tomonori; Fukuda, Yasushi; Kanazu, Masaki; Hosoya, Kazumi; Suzuki, Takuji; Ueno, Kiyonobu; Fujimoto, Daichi; Kumagai, Toru; Teramukai, Satoshi

doi:10.1007/s10637-021-01203-5

Cited by 4 publications

(4 citation statements)

References 28 publications

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“…This is important for improving the quality of life for LCBM patients. Nevertheless, targeted therapies and immunotherapies for LCBM still face challenges, such as still being in the animal testing stage or drug resistance, and there is still a long way to go before they can be used as effective LCBM treatments[ 38 - 40 ].…”

Section: Discussionmentioning

confidence: 99%

What enlightenment has the development of lung cancer bone metastasis brought in the last 22 years

Chen,

et al. 2024

World J Clin Oncol

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BACKGROUND Lung cancer bone metastasis (LCBM) is a disease with a poor prognosis, high risk and large patient population. Although considerable scientific output has accumulated on LCBM, problems have emerged, such as confusing research structures. AIM To organize the research frontiers and body of knowledge of the studies on LCBM from the last 22 years according to their basic research and translation, clinical treatment, and clinical diagnosis to provide a reference for the development of new LCBM clinical and basic research. METHODS We used tools, including R, VOSviewer and CiteSpace software, to measure and visualize the keywords and other metrics of 1903 articles from the Web of Science Core Collection. We also performed enrichment and protein-protein interaction analyses of gene expression datasets from LCBM cases worldwide. RESULTS Research on LCBM has received extensive attention from scholars worldwide over the last 20 years. Targeted therapies and immunotherapies have evolved into the mainstream basic and clinical research directions. The basic aspects of drug resistance mechanisms and parathyroid hormone-related protein may provide new ideas for mechanistic study and improvements in LCBM prognosis. The produced molecular map showed that ribosomes and focal adhesion are possible pathways that promote LCBM occurrence. CONCLUSION Novel therapies for LCBM face animal testing and drug resistance issues. Future focus should centre on advancing clinical therapies and researching drug resistance mechanisms and ribosome-related pathways.

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Section: Discussionmentioning

confidence: 99%

What enlightenment has the development of lung cancer bone metastasis brought in the last 22 years

Chen,

et al. 2024

World J Clin Oncol

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“…[33] In this study, sex and pathological type were not associated with clinical outcomes, whereas several previous studies have shown that sex and pathological type were associated with the clinical outcome. [34][35][36][37] The reason may be because our study was retrospective, follow-up did not strictly adhere to the prospective study protocol, and some patients were not had advanced disease at the time of diagnosis. The majority of patients had adenocarcinoma, and adenocarcinoma and Asians are the dominant groups treated with targeted therapy, whereas the patient mix and carcinoma type differ between Asian and non-Asian countries.…”

Section: Discussionmentioning

confidence: 99%

Efficacy of epidermal growth factor receptor tyrosine kinase inhibitor in the treatment of patients with nonsmall cell lung cancer

Li,

Luo

et al. 2023

Medicine

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This study aimed to examine the effectiveness of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) in treating patients with nonsmall cell lung cancer (NSCLC), and the association between clinical characteristics and effectiveness. This retrospective study included 140 patients with NSCLC admitted to our hospital between July 2020 and July 2022. The patients were categorized into 2 groups according to the treatment that they received: a comparison group (67 patients) and a research group (73 patients). The comparison group received conventional chemotherapy, and the research group received conventional chemotherapy and EGFR-TKI-targeted therapy. The immune and tumor marker levels, clinical response, and relationship between clinical characteristics and response to therapy were compared between the 2 groups before and after treatment. After treatment, the levels of neuron-specific enolase and carcinoembryonic antigen (CEA) and CD8+ count were significantly lower, and forced vital capacity, forced expiratory volume in 1 second, and CD4+ count were significantly higher in the research group than in the comparison group. After treatment, the clinical effectiveness in the 2 groups significantly improved, and the disease control rate in the research group was significantly higher than that in the comparison group (89% vs 69%, P = .014). The bivariate analysis revealed that smoking history, ECOG Performance Status score, and CEA level were significantly associated with clinical effectiveness. Conventional chemotherapy combined with EGFR-TKI-targeted therapy is effective in patients with NSCLC and has a clinically significant effect on improving patients’ immune function and lung function.

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“…EGFR-TKIs are the preferred choice for EGFR-mutant NSCLC [30,31], but whether these patients could beneft from ICIs treatment remains unknown. Recently, clinicians and researchers focused on the precision and individualized ICIs treatment for these patients [32][33][34].…”

Section: Discussionmentioning

confidence: 99%

YAP1 as a Novel Negative Biomarker of Immune Checkpoint Inhibitors for EGFR-Mutant Non-Small-Cell Lung Cancer

Chen

Fang

et al. 2023

Canadian Respiratory Journal

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Background. Immune checkpoint inhibitors (ICIs) have become a standard care in non-small-cell lung cancer (NSCLC). However, its application to epidermal growth factor receptor (EGFR)-mutant NSCLC patients is confronted with drug resistance. This study aimed to clarify the potential role of Yes1-associated transcriptional regulator (YAP1) in ICIs treatment for EGFR-mutant NSCLC population. Methods. All the clinical data of NSCLC were downloaded from Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) for GSE11969 and GSE72094. Based on YAP1 expression, all the NSCLC patients including the EGFR-mutant and EGFR-wildtype (WT) patients were divided into two groups, YAP1_High and YAP1_Low. Using cBioPortal, genetic alterations were analyzed for identification of immunogenicity in EGFR-mutant NSCLC. MR analysis was used to analyze the hub gene of EGFR. The infiltration of immune cells and the expression of the identified tumor-associated antigens were identified with TIMER. By graph learning-based dimensionality reduction analysis, the immune landscape was visualized. Moreover, survival analysis was performed to verify the predictive value of YAP1 in ICIs treatment for EGFR-mutant NSCLC population using Ren’s research data (NCT03513666). Results. YAP1 was a poor prognostic factor of EGFR-mutant NSCLC population rather than lung adenocarcinoma (LUAD) patients. MR analysis revealed that the EGFR gene regulated YAP1 expression. YAP1 was identified as a hub gene closely associated with immunosuppressive microenvironment and poor prognosis in EGFR-mutant NSCLC population in TCGA LUAD. Tumors with YAP1_High showed an immune-“cold” and immunosuppressive phenotype, whereas those with YAP1_Low demonstrated an immune-“hot” and immunoactive phenotype. More importantly, it was verified that YAP1_High subpopulation had a significantly shorter progression-free survival (PFS) and overall survival (OS) after ICIs treatment in EGFR-mutant NSCLC patients in the clinical trial. Conclusions. YAP1 mediates immunosuppressive microenvironment and poor prognosis in EGFR-mutant NSCLC population. YAP1 is a novel negative biomarker of ICIs treatment in EGFR-mutant NSCLC population. Clinical Trials. This trial is registered with NCT03513666.

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Classification and regression tree for estimating predictive markers to detect T790M mutations after acquired resistance to first line EGFR-TKI: HOPE-002

Cited by 4 publications

References 28 publications

What enlightenment has the development of lung cancer bone metastasis brought in the last 22 years

What enlightenment has the development of lung cancer bone metastasis brought in the last 22 years

Efficacy of epidermal growth factor receptor tyrosine kinase inhibitor in the treatment of patients with nonsmall cell lung cancer

YAP1 as a Novel Negative Biomarker of Immune Checkpoint Inhibitors for EGFR-Mutant Non-Small-Cell Lung Cancer

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