The aim of our analysis was to compare the cost-effectiveness of high-dose intensity-modulated radiation therapy (IMRT) and hypofractionated intensity-modulated radiation therapy (HF-IMRT) versus conventional dose three-dimensional radiation therapy (3DCRT) for the treatment of localised prostate cancer. A Markov model was constructed to calculate the incremental quality-adjusted life years and costs. Transition probabilities, adverse events and utilities were derived from relevant systematic reviews. Microcosting in a large university hospital was applied to calculate cost vectors. The expected mean lifetime cost of patients undergoing 3DCRT, IMRT and HF-IMRT were 7,160 euros, 6,831 euros and 6,019 euros respectively. The expected quality-adjusted life years (QALYs) were 5.753 for 3DCRT, 5.956 for IMRT and 5.957 for HF-IMRT. Compared to 3DCRT, both IMRT and HF-IMRT resulted in more health gains at a lower cost. It can be concluded that high-dose IMRT is not only cost-effective compared to the conventional dose 3DCRT but, when used with a hypofractionation scheme, it has great cost-saving potential for the public payer and may improve access to radiation therapy for patients.

Numerous studies investigated the localization of pituitary adenylate cyclase-activating polypeptide (PACAP) and its receptors in different tumors and described the effects of analogs on tumor growth to show its potential role in oncogenesis. Recently, our research group has found significantly lower levels of PACAP27-like immunorreactivity (LI) and PACAP38-LI in different human samples of primary small cell lung cancer and colon cancer compared to normal healthy tissues. There are only few human studies showing the presence of PACAP and its receptors in urogenital tumors; therefore, the aim of the present study was to compare PACAP-LI in different healthy and pathological human samples from urogenital organs (kidney, urinary bladder, prostate, testis) with radioimmunoassay (RIA) method. Similar to our earlier observations, the PACAP27-LI was significantly lower compared to PACAP38-LI in all samples. We did not find significant alterations in PACAP-LI between healthy and tumoral samples from the urinary bladder and testis. On the other hand, we found significantly lower PACAP38-LI level in kidney tumors compared with healthy tissue samples, and we showed higher PACAP27-LI in prostatic cancer compared to samples from benign prostatic hyperplasia. These data indicate that PACAP levels of different tissue samples are altered under pathological conditions suggesting a potential role of PACAP in the development of different urogenital tumors.

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Background/Aim: In spite of early detection, appoximately 15% of the small renal cell carcinomas (RCC) will develop metastasis within 5 years follow-up. The aim of this study was to identify new biomarkers to estimate the postoperative relapse of the most common conventional RCC. Patients and Methods: Tissue multi arrays of conventional RCC without metastasis at the time of operation from a cohort of 634 patients were analysed by immunohistochemistry for expression of the chitinase 3-like protein 2 (CHI3L2). Cancer specific survival of patients was estimated with Kaplan-Meier analysis, univariate and multivariate Cox regression models. Results: Kaplan-Meier analysis estimated a shorter cancer-free survival for patients with CHI3L2 positive tumors. In multivariate analysis, the CHI3L2 positivity associated with a 3.5 times higher risk for tumor relapse (p<0.001). Conclusion: Expression of CHI3L2 in tumor cells of conventional RCC define a group of patients at high risk for postoperative progression.

Background/Aim: The association of Wilms' tumor (WT), papillary renal cell tumor (PRCT) and mucinous tubular and spindle cell carcinoma (MTSCC) with embryonal rests has already been documented, but the cellular origin of metanephric adenoma (MA) is not yet known. The aim of this study was to understand their developmental evolution and find diagnostic markers. Materials and Methods: CD57, KRT7, AMACR, SCEL, WT1 and CDH17 expression was analysed by immunohistochemistry in the four types of tumors and the associated pre-neoplastic lesions. Results: Immunohistochemistry was able to differentiate WT, MA, MTSCC and PRCT. A phenotypic correlation between MA and perilobar nephrogenic rest associated with WT was identified. Conclusion: Perilobar nephrogenic rest and MA arise from differentiation arrested cells of the proximal domain of the S-shape body. We propose that WT1, MA, MTSCC and PRCT derive from different forms of maturation arrested embryonal rests. Metanephric adenoma (MA) is an epithelial tumor of the kidney composed of small, uniform, embryonal-looking cells, which are frequently seen in nephrogenic rests (NR) associated with Wilms tumor (WT) (1). Initially it was suggested that MA derives from persistent blastemal cells (2). Following the first description several concepts were published regarding its possible origin. It has been proposed, that the more active malignant WT matures with time into an inactive benign MA (3). Because MA may display a papillary growth pattern and sometimes psammoma bodies, which are characteristic for papillary renal cell tumor (PRCT), it was considered to be a solid variant of PRCT (4). PRCT is composed by solid, tubular and papillary structures and display the whole spectrum of epithelial differentiation, from small blastema-like cells towards more differentiated epithelial cells. Another kidney tumor, mucinous tubular and spindle cell carcinoma (MTSCC) may also contain small cells growing in solid or papillary formations (5, 6). Because of the latter growth pattern, it was proposed that MTSCC is a variant of PRCT (7). The association of WT, MTSCC and PRCT with NR and pre-neoplastic lesion (PNL) has already been documented, but the origin of MA is not yet known (6, 8, 9). WT, MTSCC and PRCT arise from not fully differentiated cells that may explain their heterogeneous morphology and overlapping phenotype, the latter leading in some cases to differential diagnostic problem. Although the genetic analysis can identify WT, MA, MTSCC and PRCT unequivocally, it does not give information about their cellular origin (5, 6, 10-12). Several antibodies have been proposed to identify WT, MA, MTSCC and PRCT, even those with an overlapping phenotype. It was reported that solid growing PRCT, a mimicry of MA, is positive for KRT7 and AMACR, epithelial predominant WT for WT1 and MA for WT1 and CD57 antibodies (13-15). Recently, CDH17 has been added to this panel as an MA-specific marker (16). The aim of this study was to establish the marker profile of diagnostic importance for the abovementio...