Differential expression and cross-talk of peroxisome proliferator-activated receptor γ and retinoid-X receptor α in urothelial carcinomas of the bladder.

Purpose: the peroxisome proliferator-activated receptor γ (PPARγ), known to play a key role in homeostatic biological pathways, is also implicated in the process of carcinogenesis. Ligands for PPARγ and its heterodimeric partner, retinoid-X receptor (RXR), have exhibited anticancer effects both in vitro and in vivo. Unexpectedly, some studies suggested that PPARγ ligands may stimulate cancer formation.

Coordinated increased expression of Cyclooxygenase2 and nuclear factor κB is a steady feature of urinary bladder carcinogenesis.

Objectives: The inescapable relationship between chronic inflammation and carcinogenesis has long been established. Our objective was to investigate COX-2 and NF-κB immunohistochemical expression in a large series of normal epithelium and bladder carcinomas.

Methods: Immunohistochemical methodology was performed on formalin-fixed, paraffin-embedded sections from urinary bladder carcinomas of 140 patients (94 males and 46 females with bladder carcinomas).

Expression of the regulatory cell cycle proteins p21, p27, p14, p16, p53, mdm2, and cyclin E in bone marrow biopsies with acute myeloid leukemia. Correlation with patients' survival.

Cell cycle control is a crucial event in normal hematopoiesis, and abnormalities of regulatory cell cycle genes have been found to contribute to the development of many hematologic malignancies. The present study investigates the immunohistochemical expression of seven essential cell cycle proteins (p21, p27, p14, p16, p53, mdm2, and cyclin E) in paraffin-embedded sections from 42 bone marrow biopsies obtained from an equal number of patients with newly diagnosed acute myeloid leukemia (AML). This study revealed (i) a high frequency of p53+/mdm2-/p21-phenotype, which is probably a result of p53 gene mutation and/or inhibition of mdm2 action by p14(ARF); (ii) expression of p27+/cyclinE-phenotype in most cases, suggesting that p27 may act as a potent cyclin-dependent kinase inhibitor; (iii) expression of p16 only in very few cases; and (iv) no relationship between the expression of any of the above proteins and survival as well as histologic subtype.