A population-based review of the feasibility of platinum-based combination chemotherapy after tyrosine kinase inhibition in EGFR mutation positive non-small cell lung cancer patients with advanced disease

Mariano, Caroline; Bosdet, Ian; Karsan, Aly; Ionescu, Diana N.; Murray, Nevin; Laskin, Janessa; Zhai, Yongliang; Melosky, Barbara; Sun, Sophie; Ho, Cheryl

doi:10.1016/j.lungcan.2013.10.007

Cited by 8 publications

(9 citation statements)

References 29 publications

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“…2 B ), which is similar to the findings in a previous report. 19 It is noteworthy, however, that the EGFR gene copy numbers were quite similar between histological structures within each lesion (see Fig. 2 C ).…”

Section: Discussionmentioning

confidence: 74%

Heterogeneity of EGFR Aberrations and Correlation with Histological Structures: Analyses of Therapy-Naive Isogenic Lung Cancer Lesions with EGFR Mutation

Suda

Murakami

et al. 2016

Journal of Thoracic Oncology

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Introduction EGFR gene somatic mutation is reportedly homogeneous. However, there are few data regarding the heterogeneity of expression of mutant EGFR protein and EGFR gene copy number, especially in extrathoracic lesions. These types of data may enhance our understanding of the biology of EGFR-mutated lung cancer and our understanding of the heterogeneous response patterns to EGFR TKIs. Methods An 81-year-old never-smoking female with lung adenocarcinoma could not receive any systemic therapy because of her poor performance status. After her death, 15 tumor specimens from different sites were obtained by autopsy. Expression of mutant EGFR protein and EGFR gene copy numbers were assessed by immunohistochemical analysis and by silver in situ hybridization, respectively. Heterogeneity in these EGFR aberrations was compared between metastatic sites (distant versus lymph node) or histological structures (micropapillary versus nonmicropapillary). Results All lesions showed positive staining for mutant EGFR protein, except for 40% of the papillary component in one of the pulmonary metastases (weak staining below the 1+ threshold). Expression of mutant-specific EGFR protein, evaluated by H-score, was significantly higher in the micropapillary components than in the nonmicropapillary components (Mann-Whitney U test, p = 0.014). EGFR gene copy number was quite different between lesions but not correlated with histological structure or metastatic form. However, EGFR gene copy numbers were similar between histological structures in each lesion. Conclusion These data indicate that expression of EGFR mutant protein and EGFR gene copy number do not change as a consequence of tumor progression. This also justifies using the biopsy specimens from metastases as a surrogate for primary tumors.

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Section: Discussionmentioning

confidence: 74%

Heterogeneity of EGFR Aberrations and Correlation with Histological Structures: Analyses of Therapy-Naive Isogenic Lung Cancer Lesions with EGFR Mutation

Suda

Murakami

et al. 2016

Journal of Thoracic Oncology

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“…For example, in the NEJ002 trial that compared gefitinib with carboplatin/paclitaxel in the first-line setting, 68 patients (88 %) of the 77 patients who had stopped receiving frontline gefitinib received cytotoxic chemotherapy (Inoue et al 2013). [However, in a population-based study, only 46 % of patients received cytotoxic chemotherapy after EGFR-TKI treatment failure (Mariano et al 2014)]. In the next section, we consider whether the chemosensitivity of lung cancers with EGFR mutation is altered after they acquire resistance to EGFR-TKIs.…”

Section: Treatment Strategy For Lung Cancers With Egfr Mutationsmentioning

confidence: 99%

Role of EGFR mutations in lung cancers: prognosis and tumor chemosensitivity

Suda

Mitsudomi

2015

Arch Toxicol

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Lung cancers with an epidermal growth factor receptor (EGFR) gene mutation account for ~40 % of adenocarcinomas in East Asians and ~15 % of those in Caucasians and African Americans, which makes them one of the most common molecularly defined lung cancer subsets. The discriminative clinical and pathological features of lung cancers with EGFR mutations have been intensively studied, and the predictive role of an EGFR mutation for treatment with EGFR tyrosine kinase inhibitors (EGFR-TKIs) is well established. However, controversial issues remain regarding the clinical and therapeutic implications of EGFR mutations in lung cancers. These include the prognostic impact of the EGFR mutation, its predictive implication for successful treatment with anticancer agents other than EGFR-TKIs, appropriate cytotoxic agents for lung cancers with this mutation, and the chemosensitivity of EGFR-mutation-positive lung cancers after acquisition of resistance to EGFR-TKIs. In this review, we discuss these unanswered but important questions, referring to in vitro studies, basic research, retrospective analyses, and the results of phase III clinical trials.

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“…In recent years, NSCLC has exhibited a rising morbidity rate. Furthermore, the pathogenesis of NSCLC has not been established (17,18). Currently, it is believed that cell cycle control abnormalities are associated with the cancerous transformation of cells; malignant tumors may have a dysregulated cell cycle (17).…”

Section: Discussionmentioning

confidence: 99%

Effect of miR-1244 on cisplatin-treated non-small cell lung cancer via MEF2D expression

Yang

Zhou

et al. 2017

Oncology Reports

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Abstract. The aim of this study was to investigate the function of miR-1244 in cisplatin-treated non-small cell lung cancer (NSCLC). The results of quantitative PCR analysis revealed that the expression levels of miR-1244 in cisplatin-treated A549 and NCI-H522 human lung cancer cell lines were lower than those in untreated A549 and NCI-H522 cells. Similarly, the expression level of miR-1244 in NSCLC tissue samples from cisplatin-treated patients was also lower than that in non-cisplatin-treated NSCLC patients. Notably, the overall survival times of cisplatin-treated NSCLC patients with high miR-1244 expression were superior to those patients with low miR-1244 expression. We found that overexpression of miR-1244 suppressed cell viability and increased LDH toxicity in cisplatin-treated A549 and NCI-H522 cells. Additionally, overexpression of miR-1244 induced the apoptosis of cisplatin-treated A549 and NCI-H522 cells. Furthermore, overexpression of miR-1244 promoted caspase-3 activity and p53 and Bax protein expression, and suppressed myocyte enhancer factor 2D (MEF2D) and cyclin D1 protein expression in cisplatin-treated A549 and NCI-H522 cells. Small interfering RNA (siRNA) targeting MEF2D suppressed the protein expression of MEF2D, and was able to decrease the proliferation, promote caspase-3 activity, p53 and Bax protein expression and inhibit cyclin D1 protein expression in cisplatin-treated A549 and NCI-H522 cells following the overexpression of miR-1244. In summary, we found that miR-1244 affected cisplatin-treated NSCLC via MEF2D expression.

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A population-based review of the feasibility of platinum-based combination chemotherapy after tyrosine kinase inhibition in EGFR mutation positive non-small cell lung cancer patients with advanced disease

Cited by 8 publications

References 29 publications

Heterogeneity of EGFR Aberrations and Correlation with Histological Structures: Analyses of Therapy-Naive Isogenic Lung Cancer Lesions with EGFR Mutation

Heterogeneity of EGFR Aberrations and Correlation with Histological Structures: Analyses of Therapy-Naive Isogenic Lung Cancer Lesions with EGFR Mutation

Role of EGFR mutations in lung cancers: prognosis and tumor chemosensitivity

Effect of miR-1244 on cisplatin-treated non-small cell lung cancer via MEF2D expression

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