Further, we showed that the waiting time for onset of breast cancer in G homozygous patients for EGF genotypes (55 years) was significantly lower in comparison to A-allele carriers (59 years) (log-rank test: p = 0.038).
Our results do not support a strong association between common variants in the ESR1 and EGF genes and breast cancer risk, tumour characteristics or survival.
Levels of breast cancer 1 (BRCA1), EGF receptor (EGFR, also known as ERBB1), ERBB4, tubulointerstitial nephritis antigen-like 1 (TINAGL1) and ESR1 protein were examined with immunohistochemical analysis using immunofluorescence methods and confocal laser scanning microscopy.
These findings indicated that plasma EGF levels served as a protective marker against breast cancer in our study and EGFG-1380A variant might be a modifier on it.
Previous studies have shown a correlation between expression of the EGF receptor type III mutation (EGFRvIII) and a more malignant phenotype of various cancers including: non-small-cell lung cancer, glioblastoma multiforme, prostate cancer and breast cancer.
Human epidermal growth factor receptor 2 (HER2 gene) and chromosome 17 polysomy are associated with breast cancer prognosis, chemotherapy and hormone therapy.
The existence of such field within the human breast was inferred from the results on primary breast cancer obtained by PCR-based microsatellite analysis of allelic imbalance (AI) of the EGF receptor gene.
Tumor‑infiltrating lymphocytes were closely associated with histological grade (P=0.03), estrogen receptor status (P=0.006), human epidermal growth factor receptor 2 status (P=0.047) and molecular subtype in breast cancer (P=0.012).
The epidermal growth factor (EFG) family of receptors and their respective ligands play a major role in breast cancer progression and are the targets of new therapeutic approaches.
Here, we found that SQ reversed epidermal growth factor (EGF)-induced motility and invasion in breast cancer cell lines by the in vitro Wound healing and Transwell assay.
Taken together, our results suggest that TA modulates EGF-R/Jak2/STAT1/3 and P38/STAT1/p21<sup>Waf1/Cip1</sup> pathways and induce G1-arrest and intrinsic apoptosis in breast carcinomas.
Here, we show that epidermal growth factor (EGF) stimulation increases the ability of PTPα to activate Src by dephosphorylating Tyr530 in BT-20 and SKBR3 breast cancer cell lines.
We report here that MDA-468, a human breast cancer cell line with a very high number of EGF receptors, is growth-inhibited at EGF concentrations that stimulate most other cells.
Finally, EGFR and RANK combinatorial in vitro analyses revealed a significant upregulation of AKT and ERK signaling after EGF stimulation in cell lines and also an increase of breast cancer cell invasiveness.
The experimental results showed that age, sequence of radiotherapy and surgery, surgical margins of the primary site, human epidermal growth factor, high-dose clinical target volume, and estrogen receptors are relatively more important risk factors associated with SPCs in patients with breast cancer.
AVL-292, which has no effect on EGFR family activation, prevents NRG- and EGF-dependent growth factor-driven resistance to lapatinib in HER2(+) breast cancer cells.
Growth hormone-releasing hormone (GHRH) and epidermal growth factor (EGF) are autocrine/paracrine growth factors in breast cancer and a substantial proportion of TNBC expresses receptors for GHRH and EGF.
To elucidate the relationship between epidermal growth factor (EGF)/transforming growth factor (TGF-alpha) and estradiol-17 beta (E) in cell proliferation, we examined their effects on the breast cancer cell line, CAMA-1.
The spontaneous expression of HLA class I and class II molecules in two human breast carcinoma cell lines (MCF7, T47D) and their modulation during epidermal growth factor treatment are reported.
The early peak of relapse in patients with breast carcinomas that overexpress HER2 oncoprotein and dissemination to the axillary lymph nodes might be related to proliferation of micrometastatic lesions induced by EGF family growth factors released at the time of surgery.
In MCF-7 breast cancer cells Gab2 was markedly tyrosine phosphorylated in response to heregulin and also following EGF, insulin or bFGF administration, indicating that a variety of RTKs implicated in breast cancer development or progression couple to this docking protein.