ARCaP uniquely models the molecular basis of prostate cancer bone and adrenal metastases and epithelial to mesenchymal transition.

Purpose:A computational toolkit (spektr 3.0) has been developed to calculate x-ray spectra based on the tungsten anode spectral model using interpolating cubic splines (TASMICS) algorithm, updating previous work based on the tungsten anode spectral model using interpolating polynomials (TASMIP) spectral model. The toolkit includes a matlab (The Mathworks, Natick, MA) function library and improved user interface (UI) along with an optimization algorithm to match calculated beam quality with measurements.Methods:The spektr code generates x-ray spectra (photons/mm2/mAs at 100 cm from the source) using TASMICS as default (with TASMIP as an option) in 1 keV energy bins over beam energies 20–150 kV, extensible to 640 kV using the TASMICS spectra. An optimization tool was implemented to compute the added filtration (Al and W) that provides a best match between calculated and measured x-ray tube output (mGy/mAs or mR/mAs) for individual x-ray tubes that may differ from that assumed in TASMICS or TASMIP and to account for factors such as anode angle.Results:The median percent difference in photon counts for a TASMICS and TASMIP spectrum was 4.15% for tube potentials in the range 30–140 kV with the largest percentage difference arising in the low and high energy bins due to measurement errors in the empirically based TASMIP model and inaccurate polynomial fitting. The optimization tool reported a close agreement between measured and calculated spectra with a Pearson coefficient of 0.98.Conclusions:The computational toolkit, spektr, has been updated to version 3.0, validated against measurements and existing models, and made available as open source code. Video tutorials for the spektr function library, UI, and optimization tool are available.

We report a previously unrecognized prostate-specific protein, PrLZ (prostate leucine zipper), a new member of the Tumor Protein D52 (TPD52) family. The gene for PrLZ was localized at chromosome 8q21.1, a locus most frequently amplified in human prostate cancer. Multiple tissue analyses demonstrated PrLZ predominantly in the prostate gland. Although its expression was enhanced by androgens in androgen receptor-expressing cells, PrLZ was detected in all of the human prostate cancer cell lines, regardless of androgen receptor status. Monoclonal anti-PrLZ antibodies were produced and intense immunohistochemical staining of PrLZ was observed in prostate epithelial cells in intraepithelial neoplasia and prostate cancer, whereas lower-level staining was detected in normal and benign epithelial components of the prostate gland. As the only prostate-specific gene identified in the most frequently amplified genomic region in prostate cancer, PrLZ may be the link between chromosome 8q amplification and malignant transformation of the prostate epithelia.

Epithelial-mesenchymal transition (EMT) in cancer describes

The x-ray spectra calculated by the proposed model agreed with the measured spectra over a wide range of count rates and spectral shapes. The SRE model predicted the distorted, recorded spectra with low count rates over various types and thicknesses of attenuators. The study also validated the hypothesis that the complex spectral distortions in a PCD can be adequately modeled by cascading the count-rate independent SRE and the count-rate dependent PPE.