We conclude that NSCLC in contrast to SCLC expresses high levels of EGF receptors which may be used to facilitate the differential diagnosis in some cases of lung cancer.
Collectively, our in vivo and in vitro findings support that TWIST1 collaborates with the EGF pathway in promoting EMT in EGFR mutated lung adenocarcinoma and that large series of EGFR mutated lung cancer patients are needed to further define the prognostic role of TWIST1 reactivation in this subgroup.
We created a proof-of-principle database [DNA-mutation Inventory to Refine and Enhance Cancer Treatment (DIRECT)], starting with lung cancer-associated EGF receptor (EGFR) mutations, to provide a resource for clinicians to prioritize treatment decisions based on a patient's tumor mutations at the point of care.
Results of multiple clinical trials suggest that EGF receptor (EGFR) tyrosine kinase inhibitors (TKI) exhibit negative effects on platinum-based chemotherapy in patients with lung cancer with wild-type (WT) EGFR, but the underlying molecular mechanisms are still uncertain.
Potential ligand-binding sites within the epidermal growth factor (EGF)-like repeats of Notch1 have been identified, but the ligand-binding domains in Notch3, which is implicated in lung cancer, are not known.
Epidermal growth factor (EGF)/DNA complexes targeted to cancer cells overexpressing the EGF receptor resulted in efficient transduction of several lung cancer cell lines in vitro.
Smoking patients with lung cancer with EBs were significantly younger (63.6 versus 67.7 years, p = 0.0179) and had tumors with a lower frequency of epidermal growth factor gene (EGFR) mutations (3.8% versus 24.2%, p = 0.0184) compared with those without EBs.
The authors have previously shown that DAB(389)EGF is selectively toxic to EGFR-overexpressing cells, including human brain tumour and lung carcinoma cell lines.
Lung cancer is one of the leading cause of cancer death worldwide, the most common histological type of lung cancer is non-small cell lung cancer (NSCLC), whose occurrence and development is closely related to the mutation and amplification of epidermal growth factor receptors (EGFR).
Patients with advanced or metastatic forms of lung cancer with an activating mutation in <i>epidermal growth factor receptor</i> (<i>EGFR</i>) are given tyrosine kinase inhibitors (TKIs) targeted therapies that are more efficient than chemotherapy.
To establish and develop a reliable and simple Real-time PCR assay with high resolution melting (Real-time PCR-HRM) method for detection epidermal growth factor (EGFR) and BIM mutation of lung cancer and looking for effective targeted drugs to control lung cancer.
A test to predict outcome after treatment with an epidermal growth factor rector/tyrosine kinase inhibitor and a screening blood test for lung cancer are being investigated for use in proteomic profiling.
Examples of these molecularly targeted biomarker therapies are: tyrosine kinase inhibitors in chronic myeloid leukemia and gastrointestinal tumors; anaplastic lymphoma kinase (ALK) inhibitors in lung cancer with EML4-ALk fusion; HER2/neu blockage in HER2/neu-positive breast cancer; and epidermal growth factor receptors (EGFR) inhibition in EGFR-mutated lung cancer.