The localization of activated TGF-beta1 to the fibroblasts and endothelial cells within JNA tumors suggests that TGF-beta1 may play a role in the stromal cell proliferation and angiogenesis associated with JNA. Additional receptor studies and more quantitative methods of analysis are needed to further define the role of TGF-beta1 in the pathogenesis of JNA.

Computed tomography-guided needle biopsy is a safe and reliable minimally invasive technique for the diagnosis of poorly accessible or deep-seated lesions of the head and neck. Diagnostic needle biopsies allow improved preoperative planning and patient counseling in surgical patients and avoidance of open surgical procedures in patients with benign disease or recurrent malignant neoplasms.

Transforming growth factor beta 1 (TGF-beta1), which is implicated in the pathogenesis of fibrotic diseases such as interstitial fibrosis, may be associated with subglottic stenosis. To study this hypothesis, we measured TGF-beta1 expression sequentially in 28 rats after posterior cricoid injury, using both standard immunohistochemistry and reverse transcriptase-polymerase chain reaction. In addition, an osmotic pump infused TGF-beta1 in 18 rats, normal saline solution in 9 rats, and neutralizing antibodies in 9 rats. Specimens were stained for fibronectin and procollagen at 1, 7, and 21 days and underwent optical density analysis. In the injured airway, TGF-beta1 expression peaked at 1 day and returned to baseline by 21 days. The TGF-beta1 infusion led to an increase in the expression of extracellular matrix proteins relative to controls. In contrast, neutralizing antibodies led to a decrease in extracellular matrix protein expression. These findings suggest that TGF-beta1 may possibly play a role in the pathogenesis of subglottic stenosis.

Loss of expression of TGF-beta RII correlates with tumor grade. The localization of activated TGF-beta1 within neoplastic epithelium, tumor-associated stroma, and endothelium suggests that it might play a role in the stromal proliferation and/or angiogenesis associated with MEC.

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