Estrogen receptor β and 17β-hydroxysteroid dehydrogenase type 6, a growth regulatory pathway that is lost in prostate cancer.

Estrogen receptor β (ERβ) is activated in the prostate by 5α-androstane-3β,17β-diol (3β-Adiol) where it exerts antiproliferative activity. The proliferative action of the androgen receptor is activated by 5α-dihydrotestosterone (DHT). Thus, prostate growth is governed by the balance between androgen receptor and ERβ activation.

Birt-Hogg-Dubé renal tumors are genetically distinct from other renal neoplasias and are associated with up-regulation of mitochondrial gene expression.

Background: Germline mutations in the folliculin (FLCN) gene are associated with the development of Birt-Hogg-Dubé syndrome (BHDS), a disease characterized by papular skin lesions, a high occurrence of spontaneous pneumothorax, and the development of renal neoplasias. The majority of renal tumors that arise in BHDS-affected individuals are histologically similar to sporadic chromophobe renal cell carcinoma (RCC) and sporadic renal oncocytoma. However, most sporadic tumors lack FLCN mutations and the extent to which the BHDS-derived renal tumors share genetic defects associated with the sporadic tumors has not been well studied.

Molecular cytogenetic characterization shows higher genetic homogeneity in conventional renal cell carcinoma compared to other kidney cancers.

In this study seven primary kidney tumors out of 13 were cytogenetically characterized by comparative genomic hybridization (CGH) on the surgical specimens as well as by spectral karyotyping (SKY) analysis after short-term culturing. In two of the seven cases only a normal karyotype was identified. Non-clonal aberrations were observed in four of the seven cases.

Loss of 14q31-q32.2 in renal cell carcinoma is associated with high malignancy grade and poor survival.

The present study was undertaken to further approach the importance of 14q deletions in renal cell carcinoma (RCC) development. The initial screening using 2 RFLP markers from distal 14q identified loss of heterozygosity (LOH) in 17 of 45 informative cases (38%). In addition, in 37 patients with primary RCCs, it was shown that cases with LOH at D14S1 had significantly shorter survival as compared to cases with-out LOH (p<0.

Gene expression profiling identifies clinically relevant subtypes of prostate cancer.

Prostate cancer, a leading cause of cancer death, displays a broad range of clinical behavior from relatively indolent to aggressive metastatic disease. To explore potential molecular variation underlying this clinical heterogeneity, we profiled gene expression in 62 primary prostate tumors, as well as 41 normal prostate specimens and nine lymph node metastases, using cDNA microarrays containing approximately 26,000 genes. Unsupervised hierarchical clustering readily distinguished tumors from normal samples, and further identified three subclasses of prostate tumors based on distinct patterns of gene expression.