BRCA1 loss preexisting in small subpopulations of prostate cancer is associated with advanced disease and metastatic spread to lymph nodes and peripheral blood.

Purpose: A preliminary study performed on a small cohort of multifocal prostate cancer (PCa) detected BRCA1 allelic imbalances among circulating tumor cells (CTC). The present analysis was aimed to elucidate the biological and clinical roles of BRCA1 losses in metastatic spread and tumor progression in PCa patients.

Experimental Design: To map molecular progression in PCa outgrowth, we used fluorescence in situ hybridization analysis of primary tumors and lymph node sections, and CTCs from peripheral blood.

The profile of ErbB/Her family genes copy number assessed by real-time PCR in parathyroid adenoma and hyperplasia associated with sporadic primary hyperparathyroidism.

Hyperparathyroidism (pHPT) is a relatively frequent endocrinopathy, however, the molecular mechanisms of its etiology remain poorly understood. This disorder is mainly associated with benign tumours (adenoma) and hyperplasia of the parathyroid, hence, the focus is directed also to genes that are likely to be involved in carcinogenesis. Among such genes are ErbB/Her family genes already used in diagnosis of other tumours (e.

[Housekeeping genes as a reference in quantitative real-time RT-PCR].

The determination of gene expression levels in normal tissue is necessary for the analysis and interpretation of results of gene profiling studies in pathological samples. With the real-time reverse transcription-PCR technique, which enables one to detect the amplification rate during the process, assessment of the amount of gene transcript is fast and accurate. The most important problem in this type of analysis is the variability in the amount of genetic material between samples, caused mostly by changes in the efficiency of mRNA isolation and reverse transcription.

Protoporphyrin IX induces apoptosis in HeLa cells prior to photodynamic treatment.

Photodynamic therapy (PDT) combining treatment with a light-excited compound and laser light induction, via cellular ROS generation, kills cancer cells by damaging organelles and impairing metabolic pathways. As the exact mechanisms underlying cancer cell death due to PDT treatment remain controversial, the influence of photosensitizer itself, protoporphyrin IX (PpIX) on cancer cells was investigated. The concentration-dependent viability of HeLa cells was estimated after PpIX-treatment.

Tumor suppressor Fhit protein interacts with protoporphyrin IX in vitro and enhances the response of HeLa cells to photodynamic therapy.

Fhit, the product of tumor suppressor fragile histidine triad (FHIT) gene, exhibits antitumor activity of still largely unknown cellular background. However, it is believed that Fhit-Ap(3)A or Fhit-AMP complex might act as a second class messenger in cellular signal transduction pathway involved in cell proliferation and apoptosis. We demonstrate here for the first time that the photosensitizer, protoporphyrin IX (which is a natural precursor of heme) binds to Fhit protein and its mutants in the active site in vitro.