Targeted therapies and immunotherapy in non-small-cell lung cancer

Cortinovis, Diego; Abbate, Maria Ida; Bidoli, Paolo; Capici, Serena; Canova, Stefania

doi:10.3332/ecancer.2016.648

Cited by 36 publications

(27 citation statements)

References 132 publications

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“…16 Despite that there still remains a challenge to identify predictive markers for selecting patients who are more likely to benefit from immunotherapies, the employment of immune check-point inhibitors and combinations of different immunotherapy modalities will undoubtedly bring new hope in treating lung cancer, especially those of nononcogene addiction or high mutational load types. 115…”

Section: Lung Cancer Treatment and Molecular Targetsmentioning

confidence: 99%

Current status of research and treatment for non-small cell lung cancer in never-smoking females

Saito

Espinoza-Mercado

Liu

et al. 2017

Cancer Biology & Therapy

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Lung cancer is the leading cause of cancer-related deaths worldwide with over 1 million deaths each year. The overall prognosis of lung cancer patients remains unsatisfactory, with a 5-year overall survival rate of less than 15%. Although most lung cancers are a result of smoking, approximately 25% of lung cancer cases worldwide are not attributable to tobacco use. Notably, more than half of the lung cancer cases in women occur in non-smokers. Among non-small-cell lung cancer (NSCLC) cases, cigarette-smokers have a greater association with squamous cell carcinoma than adenocarcinoma, which is more common in non-smokers. These findings imply that specific molecular and pathological features may associate with lung adenocarcinoma arising in non-smoker female patients. Over the past decade, whole genome sequencing and other '-omics' technologies led to the discovery of pathogenic mutations that drive tumor cell formation. These technological developments may enable tailored patient treatments throughout the course of their disease, potentially leading to improved patient outcomes. Some clinical and laboratory studies have shown success outcomes using epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) tyrosine kinase inhibitors (TKI) in patients with EGFR mutations and ALK rearrangements, respectively. In fact, these 2 mutations are predominantly present in female non-smokers with adenocarcinoma. Immunotherapy has also recently emerged as a major therapeutic modality in NSCLC. In this review, we summarize the current understanding of NSCLC biology and new therapeutic molecular targets, focusing on the pathogenesis of non-smoker female NSCLC patients.

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Section: Lung Cancer Treatment and Molecular Targetsmentioning

confidence: 99%

Current status of research and treatment for non-small cell lung cancer in never-smoking females

Saito

Espinoza-Mercado

Liu

et al. 2017

Cancer Biology & Therapy

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“…Table 3. Potential new targeted therapies for NSCLC (42,43). The numbers of pathways and drugs being tested is very impressive and the clinical responses can be dramatic in some patients.…”

Section: Future Directionsmentioning

confidence: 99%

First-line therapy for non-small cell lung cancer including targeted therapy: A brief review

Robbins¹,

Pulmonary²,

Kummet³

2018

Southwest J Pulm Crit Care

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Operative removal of non-small cell lung cancer remains the mainstay of therapy. When this is not possible, cytotoxic chemotherapy and/or radiotherapy can be given but are marginally effective in prolonging overall survival. However, with a better understanding of the pathobiology of the lung cancer cells, new targeted therapies have been developed which may produce dramatic responses in selected patients. This brief review will emphasize these newer therapies in this rapidly evolving field.

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“…Further, substantial evidence indicates that numerous cytokines related to cell proliferation play key roles in pathways that promote tumor cell proliferation and suppress their apoptosis [14,15], thereby signi cantly affecting patient prognosis. Bene ted from the results above, some corresponding inhibitors like MEK inhibitors (trimetazidine) [16,17], MET-TKIs (tepotinib and cabozantinib) [18,19], PI3K inhibitor [20], and STAT3 and Src inhibitors [21,22] have been developed widely applied in clinical and showing good clinical effects. Some newly discovered cytokines, including YES (pp62c-yes) [23], YES/YES-associated protein 1 [24], and NF-1 [25], can increase the sensitivity of NSCLC cells to EGFR-TKIs by activating the AKT or MAPK pathway, showing great research bene ts.…”

Section: Introductionmentioning

confidence: 95%

FGL1 Regulates Acquired Resistance to Gefitinib by Inhibiting Apoptosis in Non-small Cell Lung Cancer

Sun

Gao

Liu

et al. 2020

Preprint

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Background: This study investigated the role of fibrinogen-like protein 1 (FGL1) in regulating gefitinib resistance of PC9/GR non-small cell lung cancer (NSCLC). Methods: The effect of different concentrations of gefitinib on cell proliferation were evaluated using the CCK-8 assay. FGL1 expression in the normal human bronchial epithelial cell line Beas-2B, as well as four lung tumor cell lines, H1975, A549, PC9, and PC9/GR, was investigated by using western blotting and qRT-PCR. FGL1 was knocked down using small interfering RNA to evaluate the effects of FGL1 on PC9 and PC9/GR. The correlation between FGL1 expression and gefitinib resistance was determined in vitro via CCK-8 and colony formation assays, and flow cytometry and in vivo via flow cytometry and immunohistochemistry. Results: FGL1 expression was significantly upregulated in non-small cell lung cancer cells with EGFR mutation and higher in the gefitinib-resistant NSCLC cell line PC9/GR than in the gefitinib-sensitive NSCLC cell line PC9. Further, FGL1 expression in PC9 and PC9/GR cells increased in response to gefitinib treatment in a dose-dependent manner. Knockdown of FGL1 suppressed cell viability, reduced the gefitinib IC50 value, and enhanced apoptosis in PC9 and PC9/GR cells upon gefitinib treatment. Mouse xenograft experiments showed that FGL1 knockdown in PC9/GR tumor cells enhanced the inhibitory and apoptosis-inducing actions of gefitinib. The potential mechanism of gefitinib in inducing apoptosis of PC9/GR cells involves inhibition of PARP1 and caspase 3 expression via suppression of FGL1.Conclusions: FGL1 confers gefitinib resistance in the NSCLC cell line PC9/GR by regulating the PARP1/caspase 3 pathway. Hence, FGL1 is a potential therapeutic target to improve the treatment response of NSCLC patients with acquired resistance to gefitinib.

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Targeted therapies and immunotherapy in non-small-cell lung cancer

Cited by 36 publications

References 132 publications

Current status of research and treatment for non-small cell lung cancer in never-smoking females

Current status of research and treatment for non-small cell lung cancer in never-smoking females

First-line therapy for non-small cell lung cancer including targeted therapy: A brief review

FGL1 Regulates Acquired Resistance to Gefitinib by Inhibiting Apoptosis in Non-small Cell Lung Cancer

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