However, many questions remain unanswered and future issues in the development of EGFR inhibitors will include the identification of biological predictors of response, combination with other therapies and also their use in earlier stages of cancer.
Pathological analyses indicate that a significant large population of human ductal cancers may utilize the EGFR-GEP100-Arf6-AMAP1 pathway for their malignancy.
Mutations of EGFR were identified in 2 (40%) of 5; these mutations have been previously reported in cancer but did not affect classic activation hotspot sites.
These results have significant implications for the use of such tools in personalizing the approach to cancers treated with EGFR-directed targeted therapies.
<b>Purpose:</b> This study evaluates the cytotoxicity of AuNPs coated with polyallylamine (AuNPs-PAA) and conjugated or not to the epidermal growth factor receptor (EGFR)-targeting antibody Cetuximab (AuNPs-PAA-Ctxb) in normal human kidney (HK-2), liver (THLE-2) and microvascular endothelial (TIME) cells, and compares it with two cancer cell lines that are EGFR-overexpressing (A431) or EGFR-negative (MDA-MB-453).
The current diagnostic test measures the overall EGFR mutation status of the cancer tissue, and may ignore the presence of non-mutated, gefitinib-unresponsive cancer cells.
Since epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors, including gefitinib (GEF) have been reported to induce the apoptosis of several cancer cell lines, in the present study, we examined whether the cytotoxic effects of GEF are further enhanced under amino acid starvation (AAS) culture conditions.
We show that EGFR deletion/inhibition results in reduced tumor formation in H2-<i>c-fos</i>LTR mice by directly inhibiting the proliferation of cancer-initiating osteoblastic cells by a mechanism involving RSK2/CREB-dependent c-Fos expression.
The therapeutic role of EGFR inhibitors in thyroid malignancies is still controversial even though the full activation of EGF signaling has recently been proposed as involved in the dedifferentiation of human thyroid cancers.
Despite the latest advancements in cancer diagnostics and therapeutics against EGFR, the survival rates of patients with advanced head and neck cancer remain disappointing due to anti-EGFR resistance.
Dysregulation of the epidermal growth factor receptor (EGFR) signaling pathway is associated with the development and progression of malignancy, and EGFR-targeted therapies offer the promise of better treatment for many types of solid tumors, including non-small cell lung cancer.
We apply s-RT-MELT in the screening of p53 and EGFR mutations in cell lines and clinical samples and demonstrate its advantages for rapid, multiplexed mutation scanning in cancer and for genetic variation screening in biology and medicine.
Bcl-2 and Bax genes are probably involved in the reduction of malignancy of glioblastoma cell caused by the introduction of EGFR-antisense into these tumor cells.