Human Papilloma Virus (HPV) is becoming a menace worldwide, especially to the developing world, due to its involvement in a variety of malignancies, with cervical cancer being the most important and prevalent. There are many HPV types; HPV 16/18 are the most carcinogenic but few others are also characterized as high-risk (HR). They can cause a variety of low- or high-grade cellular abnormalities, most frequently detected in a routine Pap test. Most infections clear within 2 years, however, a minority persists and potentially could progress to cervical cancer. Molecular tests detecting HPV DNA, RNA or proteins are now being available either commercially or in-house developed. DNA detection is nowadays an established tool for diagnosis and monitoring of HPV-related disease, however, there is lack of a reference method and standardization with reference materials. The various available test formats create confusion on which molecular test to choose and what are its limitations. Therefore, the need for lab accreditation and participation in proficiency testing has to be stressed. Novel HPV biomarkers (RNA, protein etc.) are now intensively examined for their inclusion as adjunct tools. Recently, developed prophylactic vaccines for HPV 16/18 have already proven safe and efficient and raise high expectations for the complete eradication of these types in the future

AIM: To investigate three isoforms of survivin in colorectal adenocarcinomas. METHODS: We used the LightCycler Technology (Roche), along with a common forward primer and reverse primers specific for the splice variants and two common hybridization probes labeled with fluorescein and LightCycler-Red fluorophore (LC-Red 640). Real time quantitative polymerase chain reaction (PCR) was performed on cDNAs from 52 tumor specimens from colorectal cancer patients and 10 unrelated normal colorectal tissues. In the patients group, carcinoembryonic antigen (CEA) and CA19-9 tumor markers were also measured immunochemically. RESULTS: Wild type survivin mRNA isoform was expressed in 48% of the 52 tumor samples, survivin-2b in 38% and survivin-DeltaEpsilonx3 in 29%, while no expression was found in normal tissues. The mRNA expression of wild type survivin presented a significant correlation with the expression of the ratio of survivin-2b, survivin-DeltaEpsilonx3, survivin-2b/wild type survivin and survivin-DeltaEpsilonx3/wild type survivin (P < 0.001). The mRNA expression of wild-survivin and survivin-DeltaEpsilonx3 was related with tumor size and invasion (P = 0.006 and P < 0.005, respectively). A significant difference was found between survivin-2b and morphologic cancer type. Also, the ratio of survivin-DeltaEx3/wild-survivin was significantly associated with prognosis. No association was observed between the three isoforms and grade, metastasis, Dukes stage and gender. The three isoforms were not correlated with CEA and CA19-9. CONCLUSION: Survivin isoforms may play a role in cell apoptosis and their quantification could provide information about clinical management of patients suffering from colorectal cancer

Dilated cardiomyopathy (DCM) is associated with increased inflammatory response reflected among other markers in high-sensitivity C-reactive protein (hsCRP) and soluble interleukin-2 receptor (sIL-2R) levels. We examined prospectively 60 consecutive patients with DCM. Of them, 30 were dyslipidemic (group I) and 30 normolipidemic (group II). Group I patients were randomized to either simvastatin therapy (20 mg/day, group Ia, n = 15) or hypolipidemic diet therapy (group Ib, n = 15). Patients were re-evaluated 6 months later. High-sensitivity C-reactive protein and sIL-2R levels were significantly higher in group I compared with group II patients (19.5 +/- 3.4 vs 3.03 +/- 3.5 mg/L, P = .01, 1137 +/- 441 vs 599 +/- 235 pg/mL, P = .001, respectively). There was a significant correlation between sIL-2R and hsCRP levels in dyslipidemic patients but not in normolipidemic patients. Significant reduction of hsCRP and sIL-2R levels was observed only in group Ia patients. Patients with DCM having dyslipidemia have increased inflammatory response, which is reduced after 6 months of statin therapy