Estrogen receptors inhibit Smad3 transcriptional activity through Ap-1 transcription factors.

Breast tumorigenesis and breast cancer progression involves the deregulation or hyperactivation of intracellular signaling proteins that leads to uncontrolled cellular proliferation, invasion and metastasis. For example, the expression and cellular responses to estogen receptor (ER) and transforming growth factor beta (TGFbeta) signaling pathways change during breast tumorigenesis and breast cancer progression. While the expression and activity of ER and TGFbeta maybe significant in the development of breast cancer, alterations in the cross-talk between these pathways may be equally important.

Phospho-serine-118 estrogen receptor-alpha detection in human breast tumors in vivo.

Purpose: To determine whether estrogen receptor (ER)-alpha specifically phosphorylated at Ser(118) is detectable in multiple human breast cancer biopsy samples. To gain insight into possible roles for P-Ser(118)-ERalpha in human breast cancer in vivo.

Experimental Design: A specific antibody for P-Ser(118)-ERalpha was validated for immunohistochemistry (IHC), and Western blot analysis confirmed IHC results.

New insights into estrogen receptor function in human breast cancer.

An important new concept associated with estrogen receptor (ER) function in breast cancer is that ER status/ phenotype is multifaceted. In particular, the two full-length, ligand binding ERs (ER-alpha and ER-beta) and possibly multiple variant isoforms of ER must be considered. In addition, cross-talk factors that can influence ER activity in a ligand independent fashion and factors downstream of the ER, including coactivators and corepressors, clearly have important roles in ER function.

Identification of leptin receptors in lung and isolated fetal type II cells.

Leptin is a cytokine involved in regulation of the satiety response. Receptors for this protein have been identified in brain as well as many other peripheral tissues. Some of the highest levels of receptor concentration occur in the lung.

Activated mitogen-activated protein kinase expression during human breast tumorigenesis and breast cancer progression.

Purpose: The purpose of this study is to address the hypothesis that activatedmitogen-activated protein kinase (MAPK; extracellular signal-regulated kinases 1 and 2) has a role in breast tumorigenesis, breast cancer progression, and the development of tamoxifen resistance.

Experimental Design: H-score analysis and a specific antibody for the immunohistochemical detection of activated MAPK in formalin-fixed, paraffin-embedded tissue sections were used to compare expression in: (a) human breast tumors and their matched adjacent normal breast tissue; (b) primary human breast tumors and their matched lymph node metastases; and (c) primary breast tumors from patients who later proved to be sensitive or resistant to tamoxifen treatment.

Results: Active MAPK expression was detected in 48% of primary human breast tumors and was significantly increased in tumors compared with adjacent normal breast (Wilcoxon test, P = 0.

Tetrahydrocannabinol (THC) alters synthesis and release of surfactant-related material in isolated fetal rabbit type II cells.

Over the years, there has been a great deal of interest in the biological consequences of marijuana use. While evidence indicates that cannabinoids may have therapeutic uses in alleviating certain disease discomfort, there is little recent information on potential health risks, particularly related to the developing fetus. The present study was undertaken to determine the effects of delta 9-tetrahydrocannabinol (THC), the major psychoactive component in marijuana on fetal lung development specifically related to surfactant production.

Analysis of pulmonary surfactant by Fourier-transform infrared spectroscopy following exposure to Stachybotrys chartarum (atra) spores.

Lung cells are among the first tissues of the body to be exposed to air-borne environmental contaminants. Consequently the function of these cells may be altered before other cells are affected. As gas exchange takes place in the lungs, changes in cellular function may have serious implications for the processes of oxygen uptake and carbon dioxide elimination.