Previous case reports and research have suggested an association between EGFR gene mutation and miliary patterned lung metastases in non-small cell lung cancer.
In multivariate analysis, lobulated margins (odds ratio, 4.815; 95% confidence interval [CI]: 1.789, 12.961; P = .002), N2 or N3 lymph node involvement (odds ratio, 2.445; 95% CI: 1.005, 5.950; P = .049), and lymphangitic lung metastasis (odds ratio, 8.485; 95% CI: 2.238, 32.170; P = .002) were more common in patients with ALK rearrangement than in those with EGFR mutation.
Here, we show the upregulated expression of EGFR ligand epiregulin in a subset of SACC cells correlates with lung metastasis and unfavorable outcome in patients with SACC.
The effects of IGF-IR and/or EGFR targeting by intraperitoneal administration of the monospecific IGF-IR antibody R1507 or the EGFR antibody Cetuximab or the bispecific IGF-IR/EGFR antibody XGFR* on primary tumor growth and pulmonary metastasis were investigated in an intratibial human xenograft osteosarcoma mouse model.
Physician should recognize this subgroup of patients with lung cancer when facing a picture of miliary pulmonary metastases in chest x-ray or computed tomography scan in patients with a history of never smoking and consider upfront therapy with EGFR tyrosine kinase inhibitors.
Epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) are used as a first line therapy for metastatic lung cancer harboring somatic EGFR mutation.
Chromogenic in situ hybridization to detect EGFR gene copy number in cell blocks from fine-needle aspirates of non small cell lung carcinomas and lung metastases from colo-rectal cancer.
The role of stereotactic body radiation therapy (SBRT) in patients with metastatic lung cancer harboring epidermal growth factor receptor (EGFR) mutations is not defined.
These data suggest that the miR-338-3p/EYA2 axis contributes to EGFR-mediated tumor growth and lung metastasis and that miR-338-3p activation or EYA2 inhibition or combination therapy targeting EGFR/miR-338-3p/EYA2 axis may be a promising way to treat patients with metastatic cancer.
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).
An integrin beta4-EGFR unit promotes hepatocellular carcinoma lung metastases by enhancing anchorage independence through activation of FAK-AKT pathway.
In this paper, we evaluate the co-expression of EGFR and NeuGcGM3 ganglioside in tumors from 92 patients and in two spontaneous lung metastasis models of mice (Lewis lung carcinoma (3LL-D122) in C57BL/6 and mammary carcinoma (4T1) in BALB/c).
The prognosis of patients with advanced NSCLC harboring EGFR mutations with miliary pulmonary metastasis demonstrated significantly worse outcomes compared to those without miliary pulmonary metastasis.
Oncogenic L858R mutation of human epidermal growth factor receptor (EGFR) confers constitutive activation to the kinase and is frequently observed in the pathological process of metastatic lung cancer.
In advanced stages, patients with ALK-rearranged NSCLC, compared with EGFR-mutant NSCLC, were more likely to have lymphadenopathy (OR, 3.47; P < .001), pericardial metastasis (OR, 2.18; P = .04), pleural metastasis (OR, 2.07; P = .004), and lymphangitic carcinomatosis (OR, 3.41; P = .02), but less likely to have lung metastasis (OR, 0.52; P = .003).
Although the association of multiple pulmonary metastases, and particularly miliary metastases, with response to gefitinib treatment in patients with nonsmall cell lung cancer has been reported, the association of miliary pulmonary metastases with epidermal growth factor receptor gene (EGFR) mutations remains unclear.
One patient with exon 19 deletion having high EGFR protein (2+) expression developed lung metastasis, whereas the other 2 patients with exon 19 deletion had low EGFR protein (1+) expression and remained disease free during the study period.
We describe the case of a woman with metastatic lung cancer adenocarcinoma with mutated EGFR with an initial response to gefitinib and radiation therapy, who progressed after 18 months due to the development of a resistance mechanism.