A never-smoking status was related to better survival outcome, whereas EGFR mutation, two or more metastatic sites, and intra-abdominal metastasis were each associated with a poor PFS.
Activation of the ERBB PI3K/Akt pathway was positively correlated with a higher stage (p=0.001), higher grade (p=0.001), histological type II disease (p=0.0003) and metastases (p=0.02).
We report two cases of lung adenocarcinoma with EGFR exon 20 mutations and a presentation of diffuse, tiny, innumerable lung and brain nodules resembling miliary metastases.
Five of them were given gefitinib as neoadjunvant treatment after the EGFR-TKI sensitive mutations were detected in their biopsies of mediastinal lymph nodes metastases.
ErbB-2 amplification with a gene copy number > 1.6 in tumour tissue and erbB-1 deletion with a gene copy number < 0.4 in tumour-surrounding mucosa are of clinical relevance and indicate an early tumour recurrence or metastasis (p < 0.05).
Additionally, EGFR mutation (P = 0.005), good performance status (P < 0.001) and absence of extracranial metastases (P=0.033) correlated with better survival.
Brain metastases from breast and other primary sites, and metastases to multiple organs in the autopsied cases, also contained somatic mutations in EGFR, HRAS, KRAS, NRAS or PIK3CA.
Functional outcomes and survival after surgical stabilization for inoperable non-small-cell lung cancer with spinal metastasis of the thoracic and lumbar spines: a retrospective comparison between epidermal growth factor receptor-tyrosine kinase inhibitor and platinum-based chemotherapy groups.
Six independent prognostic factors including sex (P = 0.008), the presence of visceral metastasis (P = 0.008), the number of metastases in the vertebral body (P = 0.011), Frankel score (P < 0.001), D-dimer (P = 0.002), and sensitive epidermal growth factor receptor mutation (p < 0.001) were identified and entered into the nomogram.
Next to investigate the relationship between EGFR mutations and tumor metastasis, we compared the DNA sequences of the EGFR gene between the primary tumor and the lymph node metastasis in 31 clinical samples.
A combined test using both cell sediment DNA and supernatant ccfDNA samples increases the concordance rate of EGFR mutations between primary tumour and corresponding metastases.
However, features of metastasis to other organs and the independent prognostic influence of metastatic lesions were not elucidated in patients with lung cancer harboring EGFR mutations.
Phase II/III data however, from non-EGFR mutation enriched populations, have demonstrated no benefit in progression free or overall survival with the addition of erlotinib to metastasis directed radiotherapy.
Conclusions Incorporation of EGFR mutation status in advanced NSCLC further differentiates survival curves of M categories in 8th TNM classification and more precisely predicts survival compared to number of metastasis or number of metastatic sites alone.
The impact of EGFR signaling on tumor cell migration was studied in vitro by using 11 primary human adaCP cultures treated with the EGFR ligand EGF and its inhibitor gefitinib.
The rates of bone (32.2 vs 22.8 %, P = 0.007) and brain (16.3 vs 9.4 %, P = 0.008) metastasis were significantly higher in EGFR mutation group than the wild-type group.
The incidence of EGFR gene mutations in the bone metastases was 75%, in the primary adenocarcinoma--12.8%, and in the adenocarcinoma metastases to CNS--14.75%.
Factors such as tumor pathology subtype, concurrent systemic chemotherapy, epidermal growth factor receptor (EGFR) mutation status, use of EGFR tyrosine kinase inhibitors (TKIs), systemic disease status, presence of a metastatic lesion only in delayed MRI, and volume and number of metastases were analyzed.
The discovery of anti-EGFR resistance in the setting of Kirsten rat sarcoma viral oncogene (KRAS) and more recently, neuroblastoma RAS viral oncogene (NRAS) mutations in CRC has changed the focus of therapy for metastatic disease to one based on the molecular characteristics of the tumor.
Patients had advanced NSCLC, oncogenic EGFR mutations in the tumor, and no prior chemotherapy for metastatic disease and were treated with erlotinib or chemotherapy.
Finally, TrkB expression was correlated with metastasis in patient samples, and TrkB was detected more often in tumors that did not have Kras or epidermal growth factor receptor mutations.
No significant differences were observed in the occurrence of EGFR gene mutations in primary tumors compared to metastases (7.9% vs. 11.2%; p=0.092), or in FFPE samples compared to cytological samples (8.9% vs. 8.1%; p=0.813).