Expression of TGFβ type-II receptor in association with markers of proliferation and apoptosis in premalignant lung lesions
✍ Scribed by Teresita Muñoz-Antonia; Carlos Muro-Cacho; Swati Sharma; Alan Cantor; Gerold Bepler
- Publisher
- John Wiley and Sons
- Year
- 2007
- Tongue
- English
- Weight
- 806 KB
- Volume
- 110
- Category
- Article
- ISSN
- 0008-543X
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
BACKGROUND.
Analysis of the early molecular abnormalities that play an oncogenic role in the progression of pulmonary neoplasia may lead to the identification of useful markers for early detection and prognosis. In normal squamous epithelium, transforming growth factor β (TGFβ) regulates cell growth and differentiation via specific membranous receptors and intracellular signaling molecules (Smads). The authors previously observed that, in head and neck squamous cell carcinoma, the expression of the TGFβ type II receptor (TβR‐II) decreases as tumors become less differentiated and more biologically aggressive.
METHODS.
In this pilot study of 48 premalignant bronchoepithelial lesions, the authors evaluated the expression of TβR‐II and 2 proliferation markers (Ki‐67 and MCM2), and the amount of early DNA fragmentation as evidence of apoptosis.
RESULTS.
The authors observed that the progression of premalignant lesions toward carcinoma in situ is accompanied by a decrease in TBR II expression and apoptosis and an increase in the expression of Ki‐67 and MCM2.
CONCLUSIONS.
These results suggested that the TGFβ pathway may be impaired early in the neoplastic process and that a combination of selected markers can provide a useful profile to detect preneoplastic changes in individuals at high risk for developing pulmonary carcinoma. Cancer 2007. © 2007 American Cancer Society.
📜 SIMILAR VOLUMES
To clarify the role of transforming growth factor-b (TGF-b) and its receptors in hepatocyte growth, we studied the expression of TGF-b1 and its receptors and the sensitivity to growth inhibition by TGF-b1 protein in rat hepatocytes derived from resting and regenerating livers. In hepatocytes derived
Transforming growth factor-b (TGF-b1) is a potent negative regulator of cell growth that transduces signals through interactions with type I and II receptors. Abnormal expression and mutational alterations of these receptors have been observed in several human malignancies. In this study, we investi
Transforming growth factor-1 (TGF-1) inhibits cell growth in susceptible cells by interacting with a family of protein kinases that control cell cycle progression. In the present study, we investigated the effects of TGF-1 on cyclin D1 expression and activity in COLO-357 human pancreatic cancer c
To understand the molecular mechanisms whereby normal human salivary gland cells become malignant and escape growthinhibitory control by transforming growth factor (TGF)-PI, we examined the effect of TGF-P I on the proliferation and expression of TGF-P receptors in cells and the expression of TGF-P