The aim of this study was to analyze and compare the hormonal (estrogen receptor (ER) and progesterone receptor (PR)) and human epidermal growth factor (HER2) status among women with carcinoma breast belonging to two different age groups and classify them in molecular subtypes (luminal A, luminal B, triple negative, and HER2).
Human Epidermal Growth Factor 2-positive Breast Cancer with Mammographic Microcalcification: Relationship to Pathologic Complete Response after Neoadjuvant Chemotherapy.
In addition, the results indicated that USP18 may promote the epidermal growth factor (EGF)-mediated EGF receptor (EGFR)/AKT/S‑phase kinase-associated protein 2 (Skp2) pathway by upregulating EGFR and Skp2 in a AKT/forkhead box O3-dependent manner in breast cancer.
Triple‑negative breast cancer (TNBC) is a type of breast cancer that is characterized by the lack of expression of estrogen and progesterone receptors, and epidermal growth factor receptor 2.
Since TQ has been reported to up-regulate several growth factors such as vascular endothelial growth factor (VEGF), EGF and PTEN expression, the present review article discusses the targeting potential of TQ for therapeutic intervention against such types of breast cancer.
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.
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 results showed a significant association between overexpression of CD133 and estrogen receptor status (OR 0.35, 95% CI 0.18-0.70), progesterone receptor status (OR 0.56, 95% CI 0.43-0.74), human epidermal growth factor-2 status (OR 1.81, 95% CI 1.33-2.45), lymph node metastasis (OR 1.98, 95% CI 1.34-2.92), and tumor histological grade (OR 1.79, 95% CI 1.26-2.54) in breast cancer.
Combined vaccination with EGF and VEGF from shuffling showed better immunotherapy on EGF-EGFR signaling-dependent epithelial tumors such as breast cancer than the single-agent EGF vaccination.
This study investigated the effect of N-linked glycosylation on the binding of Herceptin to HER2 protein in breast cancer and on the sensitivity of cancer cells to the chemotherapeutic agent doxorubicin (DXR) and growth factors (EGF and IGF-1).
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.
In human epidermal growth factor 2-positive breast cancer (HER2<sup>+</sup>BC), neoadjuvant chemotherapy and anti-HER2-targeted therapy (nCT) achieves a complete pathologic response (pCR) in 40-67% of patients.
In order to extend and validate our studies, we investigated the migratory capability and the level of potential epidermal growth factor receptor (EGFr) targets in a breast cancer cell line after EGF modulation.
Human aspartyl (asparaginyl) β-hydroxylase (HAAH) is a highly conserved enzyme that hydroxylates epidermal growth factor-like domains in transformation-associated proteins and is overexpressed in a variety of cancers, including breast cancer.
These patients may benefit from adjuvant chemotherapy, particularly those with luminal A and luminal B/human epidermal growth factor-2-negative endocrine-responsive breast cancer.
Core needle biopsy specimens of primary breast cancer were collected at Okayama University Hospital from hormone receptor-positive and human epidermal growth factor 2-negative patients that subsequently received two weeks of neoadjuvant hormone therapy.
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.
Through these selective, regulated interactions Lamellipodin mediates directional sensing of epidermal growth factor (EGF) gradients and invasive 3D migration of breast cancer cells.
Expression of the oncogenic transcription factor MYC is disproportionately elevated in triple-negative breast cancer (TNBC), as compared to estrogen receptor-, progesterone receptor- or human epidermal growth factor 2 receptor-positive (RP) breast cancer.
These studies indicate a role for paracrine EGF via EGFR independent of estrogen and prolactin in the transcriptional activation of PRLR gene expression and its contribution to high levels of PRLRs in breast cancer.