Targeted therapies for the treatment of non-small-cell lung cancer: Monoclonal antibodies and biological inhibitors

Silva, Ana P. S.; Coelho, Priscila V.; Anazetti, Maristella; Simioni, Patricia Ucelli

doi:10.1080/21645515.2016.1249551

Cited by 43 publications

(47 citation statements)

References 133 publications

(75 reference statements)

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“…Chemotherapy is a common method for treating NSCLC, but it has limited survival benefits and considerable adverse effects, including alopecia, dyspnea, and neutropenia. Thus, molecular targeted therapies with high specificity are urgently needed …”

Section: Introductionmentioning

confidence: 99%

The efficacy and safety of ALK inhibitors in the treatment of ALK-positive non-small cell lung cancer: A network meta-analysis

et al. 2018

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PurposeThe current study was carried out to compare the effectiveness and safety of different ALK inhibitors in treating ALK+ NSCLC.MethodsProgression‐free survival (PFS), disease control rate (DCR), overall response rate (ORR), and intracranial ORR and DCR have been aggregated to appraise the effectiveness of each ALKi. The discontinuation rate due to adverse events (AEs) was pooled to evaluate their safety. Bayesian network meta‐analyses were used to compare the ORR, DCR, PFS, and discontinuation rate of patients treated with alectinib, ceritinib, crizotinib, and chemotherapy.ResultsCompared with chemotherapy, ALK inhibitors significantly prolonged PFS [hazard ratio (HR) and 95% confidence interval (CI): alectinib, 0.50 (0.43‐0.58); ceritinib, 0.75 (0.69‐0.83); crizotinib, 0.71 (0.66‐0.76)]. The ORRs were significantly higher for ALK inhibitors than for chemotherapy [odds ratio (OR) and corresponding 95% CI: alectinib, 11.69 (4.29‐36.56); ceritinib, 7.85 (3.44‐19.27); crizotinib, 6.04 (3.33‐11.71)]. The discontinuation rates were lower for ALK inhibitors than for chemotherapy [OR and corresponding 95% CI: alectinib, 0.42 (0.12‐1.36); ceritinib, 0.52 (0.20‐1.35); crizotinib, 0.70 (0.30‐1.62)].Conclusions ALK+ NSCLC patients treated with ALKi tend to have longer PFS than those treated with chemotherapy. ALKi‐naïve patients tended to response better than their ALKi‐pretreated counterparts. Alectinib appeared to be preferable for treating brain metastases due to its high intracranial efficacy. Patients treated with alectinib or ceritinib tended to have higher ORR and DCR than patients with similar baselines treated with crizotinib or chemotherapy. No significant differences in discontinuation rate were found for alectinib, ceritinib, crizotinib, and chemotherapy.

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Section: Introductionmentioning

confidence: 99%

The efficacy and safety of ALK inhibitors in the treatment of ALK-positive non-small cell lung cancer: A network meta-analysis

et al. 2018

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“…NSCLC includes different histological types, in which the main ones are large cell carcinoma, squamous cell carcinoma and adenocarcinoma, the latter being responsible for most cases of NSCLC, and the most common type of lung carcinoma in women and nonsmokers. 4,8,[15][16][17][18] Oncogenes and tumor suppressor genes (TSGs) that are overexpressed or containing modifications are the most common molecular alterations involved in lung carcinomas. Some of the most activated oncogenes in NSCLC include epidermal growth factor receptor (EGRF) and KRAS, while the most common tumor suppressor genes include TP53, p16, and TSG of chromosome 3p.…”

Section: Non-small-cell Lung Cancermentioning

confidence: 99%

“…These interactions between receptors and ligands are also active forms of control of autoimmune responses by the inhibition of the activation of cytotoxic T lymphocytes. [6][7][8] Experimental studies have shown that increased expression of PD-L1 results in unfavorable responses in patients with certain types of tumors, and this expression affects the T lymphocyte response, resulting in the exhaustion or even apoptosis of this population. 9 Therefore, the interaction of PD-L1 with the PD-1 receptor promotes an escape of the tumor cells because of the blockade of the T lymphocyte response.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of PD-1 protein by the CRISPR-Cas9 method as antitumor therapy of non-small cell lung cancers

Biggi¹,

Simioni²

2019

Rev. Fac. Ciênc. Méd. Sorocaba

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Lung carcinoma is the second most common type of tumor in the world. Among them, 85% of the cases are of non-small cell lung cancer (NSCLC). It is known that, in general, NSCLC tumor cells proliferate due to a reduction in the cytotoxic T lymphocyte response. In the immune response to tumors, the interaction of the programmed death ligand 1 (PD-L1), expressed in tumor cells and the programmed cell death protein 1 (PD-1), expressed in cytotoxic T lymphocytes, promotes suppression of the immune response, leading to inhibition of the activation of cytotoxic T lymphocytes. Despite the biological therapies that have proven effective for the treatment of lung tumors, studies seek a genetic treatment option, such as the CRISPR/Cas9 method. This review aims to provide an update of the CRISPR-Cas9 method and its application as a therapeutic tool in NSCLC to deactivate the gene encoding the PD-1 protein. The genetic alteration of PD-1 protein by CRISPR-Cas9 can affect the interaction between receptor and ligand, allowing cytotoxic T lymphocytes to recognize and exert an antitumor response to NSCLC tumors.

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“…The lung carcinoma also known as adenocarcinoma occurs due to gene mutation in EGFR and anaplastic lymphoma kinase. The treatment possibly involves targeting HER2, MAP kinase, KRAS, RAS, B-RAF, C-RAF and reactive oxygen species (ROS1) gene for effective therapy in lung carcinoma [31].…”

Section: Lung Cancermentioning

confidence: 99%

Epidermal growth factor receptor based active targeting: a paradigm shift towards advance tumor therapy

Akhter

Madhav

Ahmad

2018

Artificial Cells, Nanomedicine, and Biotechnology

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The epidermal growth factor receptor (EGFR) is a cell surface receptor belonging to erythroblastic leukemia viral oncogene homologue (ErbB) family of tyrosine kinase. It plays critical role in the regulation of cell proliferation, survival and differentiation. The EGFR receptor is crucial in a variety of tumor development due to unlikely triggered by receptor overexpression, chromosomal mutation and or ligand-dependent receptor dimerization. The EGFR inhibition established a major therapeutic target in cancer therapy. The signal transduction pathway of EGFR is directly involved in tumor pathogenesis and progression. The combinatorial approach with EGFR inhibitors bring novel therapeutic regime with proved clinical efficacy. This critique briefly addressed EGFR receptor characteristics, worldwide report on various cancers and EGFR based potential targeting modalities in skin, breast, ovary, brain, lungs, pancreas, gastric and colorectal tumors and molecular pathways involved in EGFR targeting.

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Targeted therapies for the treatment of non-small-cell lung cancer: Monoclonal antibodies and biological inhibitors

Cited by 43 publications

References 133 publications

The efficacy and safety of ALK inhibitors in the treatment of ALK-positive non-small cell lung cancer: A network meta-analysis

The efficacy and safety of ALK inhibitors in the treatment of ALK-positive non-small cell lung cancer: A network meta-analysis

Inhibition of PD-1 protein by the CRISPR-Cas9 method as antitumor therapy of non-small cell lung cancers

Epidermal growth factor receptor based active targeting: a paradigm shift towards advance tumor therapy

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