Expression of epidermal growth factor receptor on oral squamous cell carcinoma
References (30)
- et al.
A native 170,000 epidermal growth factor receptor kinase complex from shed plasma membrane vesicles
Journal of Biological Chemistry
(1982) - et al.
Similar effects of platelet derived growth factor and epidermal growth factor on the phosphorylation of tyrosine in cellular proteins
Cell
(1982) - et al.
Distribution and number of epidermal growth factor receptors in skin is related to epithelial cell growth
Developmental Biology
(1983) - et al.
Cellular localization of human epidermal growth factor receptor
Cell Biology International Reports
(1984) - et al.
STNMP— A new classification for oral cancer
British Journal of oral Surgery
(1977) Epidermal growth factor-like transforming growth factor. Isolation, chemical characterisation, and potentiation by other transforming factors from feline sarcoma virus-transformed cell
Journal of Biological Chemistry
(1983)- et al.
The epidermal growth factor-induced calcium signal in A431 cells
Journal of Biological Chemistry
(1986) - et al.
Epidermal growth factor receptors in human bladder cancer: comparison of invasive and superficial tumours
The Lancet
(1985) - et al.
Epidermal growth factor induces redistributions of actin and α-actin in human epidermal carcinoma cells
Experimental Cell Research
(1981) - et al.
125I-labelled human epidermal growth factor (HEGF): binding, internalisation and degradation in human fibroblasts
Journal of Cell Biology
(1976)
Epidermal growth factor
Annual Review of Biochemistry
Epidermal growth factor: biology and receptor metabolism
Journal of Cell Science
Control of a cell surface major glycoprotein by epidermal growth factor
Science
Close similarity of epidermal growth factor receptor and v-erb B oncogene protein sequences
Nature
Growth factors from murine sarcoma virus-transformed cells
Cited by (81)
Targeted inactivation of EPS8 using dendrimer-mediated delivery of RNA interference
2019, International Journal of PharmaceuticsCitation Excerpt :Coupled with rapid uptake into cells, this suggests that ligand-conjugated dendrimers likely represent a highly efficient means to deliver therapeutic agents to target cells. Many squamous cell carcinomas express high levels of the EGFR compared to normal keratinocytes (Cardinali et al., 1995; Ozanne et al., 1986; Partridge et al., 1988; Prime et al., 1994), making it an attractive gateway into the cancer cell. However, a major concern with the use of EGF as a targeting ligand is the potential for stimulation of growth-promoting pathways, which would be undesirable in cancer treatment.
Loss of CD151/Tspan24 from the complex with integrin α3β1 in invasive front of the tumour is a negative predictor of disease-free survival in oral squamous cell carcinoma
2013, Oral OncologyCitation Excerpt :Its value, however, as a predictive and prognostic indicator is undermined by the lack of consistency between studies. Indeed, association between EGFR expression, disease stage at presentation, patient survival and response to EGFR-targeted therapies show significant discrepancies between cohorts.2,20,22–26 These analyses were carried out using the quantitative-evaluation of EGFR levels in the malignant lesions treated as uniform entities.
Established and Emerging Concepts in Epidermal Growth Factor Receptor Biology
2007, International Journal of Radiation Oncology Biology PhysicsEpidermal growth factor receptor distribution in pericoronal follicles: relationship with the origin of odontogenic cysts and tumors
2007, Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology and EndodontologyCitation Excerpt :Cells presenting a membrane-only staining pattern seem to respond more quickly to changes in the levels of circulating ligand, whereas cells presenting cytoplasm-only or combined staining, in which all or some of the receptor has been internalized, show a slower, more physiologic response.33 Our findings concerning EGFR distribution in NOM are similar to previous descriptions: presence of EGFR in the epithelial cells of proliferating layers,15,34,35,37,38 decreasing in intensity toward superficial layers.38 The cells in the parabasal and basal layers are in constant proliferation for the maintenance of tissue homeostasis.