hCG beta expression by cervical squamous carcinoma--in vivo histological association with tumour invasion and apoptosis.

Aims: To investigate the correlation of beta-subunit of human chorionic gonadotrophin (hCG beta) expression by cervical carcinomas with measures of tumour apoptosis.

Methods And Results: Eighty-nine cervical carcinoma patients' samples were subject to hCG beta immunohistochemistry and scored with respect to intensity of immunopositivity and percentage of positive cells. Apoptosis was evaluated by three independent parameters: morphological characteristics [haematoxylin and eosin (H&E)], terminal deoxynucleotidyl transferase biotin-dUTP nick end labelling (TUNEL) and poly (ADP-ribose) polymerase (PARP) immunopositivity.

Detection of TMPRSS2:ERG fusion gene in circulating prostate cancer cells.

Aim: To investigate the existence of TMPRSS2:ERG fusion gene in circulating tumor cells (CTC) from prostate cancer patients and its potential in monitoring tumor metastasis.

Methods: We analyzed the frequency of TMPRSS2:ERG and TMPRSS2:ETV1 transcripts in 27 prostate cancer biopsies from prostatectomies, and TMPRSS2:ERG transcripts in CTC isolated from 15 patients with advanced androgen independent disease using reverse transcription polymerase chain reaction (RT-PCR). Fluorescence in situ hybridization (FISH) was applied to analyze the genomic truncation of ERG, which is the result of TMPRSS2:ERG fusion in 10 of the 15 CTC samples.

Hedgehog signalling in androgen independent prostate cancer.

Objectives: Androgen-deprivation therapy effectively shrinks hormone-naïve prostate cancer, both in the prostate and at sites of distant metastasis. However prolonged androgen deprivation generally results in relapse and androgen-independent tumour growth, which is inevitably fatal. The molecular events that enable prostate cancer cells to proliferate in reduced androgen conditions are poorly understood.

Identification of a recurrent t(4;6) chromosomal translocation in prostate cancer.

Purpose: We developed and describe a practical method by which primary prostate cancer specimens can be screened for recurrent chromosomal translocations, which is a potential source of fusion genes, as well as a process by which identified translocations can be mapped to define the genes involved.

Materials And Methods: A series of 7 prostate cancer cell lines and 25 transiently established primary cell cultures, which were sourced from tissue harvested at 16 radical prostatectomies and 9 channel transurethral prostate resections, were screened for chromosomal translocations using multiplex-fluorescence in situ hybridization technology. A series of fluorescence in situ hybridization based breakpoint mapping experiments were performed to identify candidate genes involved in regions associated with recurrent translocation.

Striate palmoplantar keratoderma arising from desmoplakin and desmoglein 1 mutations is associated with contrasting perturbations of desmosomes and the keratin filament network.

Background: Several hereditary human diseases are now known to be caused by distinct mutations in genes encoding various desmosome components. Although the effects of some of these mutant genes have been analysed by targeted disruption experiments in mouse models, little is known about the cell and tissue changes in affected human patients.

Objectives: To investigate the effects of heterozygous nonsense mutations in desmoplakin (Dp) and desmoglein (Dsg) 1 which cause the autosomal dominant disorder striate palmoplantar keratoderma (SPPK), focusing on changes in desmosome structure and composition and the associated keratin intermediate filament (KIF) network in palm skin, and in cultured keratinocytes generated from the same site.