Concomitant Analysis of the Epidermal Growth Factor Receptor Family in Esophageal Cancer: Overexpression of Epidermal Growth Factor Receptor mRNA but Not of c-erbB-2and c-erbB-3
✍ Scribed by Helmut Friess; Akira Fukuda; Wen-Hao Tang; Adrian Eichenberger; Neva Furlan; Arthur Zimmermann; Murray Korc; Markus W. Büchler
- Publisher
- Springer
- Year
- 1999
- Tongue
- English
- Weight
- 458 KB
- Volume
- 23
- Category
- Article
- ISSN
- 0364-2313
No coin nor oath required. For personal study only.
📜 SIMILAR VOLUMES
Breast cancer cells are derived from epithelial cells lining the ducts of the breast. One of the fundamental characteristics that distinguish tumour cells from normal cells is that cancer cells grow in an apparently unregulated way. Understanding the mechanisms that regulate the growth and different
Expression of the c-erbB3 protein was determined in transitional cell carcinoma of the bladder by immunohistochemistry. Strong membrane staining was observed in 10 per cent of cases (7/70) and cytoplasmic and membrane overexpression in 20 per cent (14/70). Overexpression of the epidermal growth fact
Background: Receptors belonging to the epidermal growth factor receptor (EGFR) family transfer extracellular signals by homotypic and heterotypic receptor interaction and cross-activation. Cell differentiation, death, and proliferation are regulated via these receptor-tyrosine-kinases. However, the
## Abstract Inhibiting epidermal growth factor‐receptor (ErbB‐1) represents a powerful anticancer strategy. Activation of retinoid pathways is also in development for cancer treatment. Retinoic acid receptor‐β—the tumor suppressor and main retinoid mediator—‐is silenced in many tumors. The ErbB‐1 i