Interobserver agreement in prostate cancer detection using multiparametric MRI.

PURPOSE: The purpose of this prospective observational study was to evaluate the diagnostic performance of multiparametric (mp) magnetic resonance imaging (MRI) for prostate cancer detection and to assess the interobserver variability, using the Prostate Imaging Reporting and Data Systems (PI-RADS). METHODS: 50 patients (mean age 68.42±6.58 years) with suspected prostate cancer fulfilling the inclusion criteria and without any exclusion criteria were enrolled. All patients were examined with mp-MRI protocol, as per European Society of Urogenital Radiology (ESUR) guidelines, before systematic transrectal ultrasound (TRUS)-guided biopsy. All examinations were read by three independent radiologists with 3-year experience in prostate MRI. Sensitivity (Se), specificity (Sp), positive predictive value (PPV) and negative predictive value (NPV) were calculated. Interobserver agreement was evaluated using Kappa Cohen coefficient of agreement. RESULTS: mp-MRI and histopathological results of TRUSguided biopsy showed a very good agreement in prostate cancer detection. The overall Se, Sp, PPV and NPV ranged between 93.3-96.7%, 55.0-80.0%, 76.3-87.9% and 88.2-94.1%, respectively. The Kappa Cohen coefficient of interobserver agreement was 0.643 between Readers 1 and 2, 0.664 between Readers 1 and Reader 3 and 0.568 between Readers 2 and 3. CONCLUSIONS: Our results showed a high Se for the detection of prostate cancer with mp-MRI and a high NPV to rule out prostate malignancy. PI-RADS version 2 provides an adequate standardization of mp-MRI, allowing a good level of interobserver agreement.

A phase II single institution single arm prospective study with paclitaxel, ifosfamide and cisplatin (TIP) as first-line chemotherapy in high-risk germ cell tumor patients with more than ten years follow-up and retrospective correlation with ERCC1, Topoisomerase 1, 2A, p53 and HER-2 expression.

PURPOSE: One half of high-risk germ cell tumor (HRGCT) patients relapse after standard chemotherapy. This phase II study evaluated prospectively the toxicity and efficacy in first-line of the paclitaxel-ifosfamide-cisplatin combination (TIP) in HRGCT patients and tried to identify biomarkers that may allow patient-tailored treatments. METHODS: Between October 1997- September 2000, 28 chemo-naive HRGCT patients were enrolled. Patients received 4 cycles of TIP (paclitaxel 175 mg/m(2) day 1/; ifosfamide 1.2 g/m(2)/day, days 1-5; Mesna 1.2 g/m(2)/day, days 1-5; and cisplatin 20 mg/m(2)/day, days 1-5 every 3 weeks). A non-randomized comparison was made between HRGCT patients treated in the same period with first-line TIP and bleomycin-etoposide-cisplatin (BEP) (28 patients vs 20). In 17 HRGCT patients treated between 1998-2006, ERCC1, Topoisomerase 1 and 2A, p53 and HER-2 expression was retrospectively analysed by immunohistochemistry (IHC) (7 patients with TIP, 10 with BEP), and correlations were made with response to chemotherapy and survival. RESULTS: With a median follow-up of 72 months [range 48+...89+], 5-year disease free survival (DFS) was 55%, with 95% CI 36-72, and the overall survival (OS) was 63%, with 95% CI 44-78. In June 2015, with a median follow-up of 196.47 months (range 177.30-209.27) (>15 years), 12 [%?] patients were alive and disease-free, and 16 [%?] had died (12 specific causes). There was no significant correlation between the expression of ERCC1, Topoisomerase 1 and 2A, HER-2 and p53 and response to treatment. CONCLUSION: Long-term follow-up showed no difference in OS between TIP vs BEP as first-line therapy. Both regimens had mild toxicity.

Hepatocellular carcinoma: insights in the biological treatment beyond sorafenib.

UNLABELLED: Hepatocellular carcinoma has an increasing incidence and an impressive mortality. At present, the only authorized systemic treatment is the multi-kinase inhibitor sorafenib. A multitude of clinical trials are aimed at improving outcomes, both in firstY- and in second-line therapy. In this multitude of clinical trials, the purpose of our article was to familiarize physicians with the mechanisms of action of new biological therapies and to offer an algorithm for optimal trial selection for each patient, based on clinical and biological indicators. The available data were structured as follows: antiangiogenic therapy, c -MET inhibitors, combinations of chemotherapy with sorafenib, immune response modulators, cellular metabolism modulators, mTOR inhibitors, other multi-kinase inhibitors. CONCLUSION: Treatment of advanced hepatocellular carcinoma remains a challenge for oncologists. Choosing the "right" trial may be the only chance of prolonging patient survival and improve his/her clinical status.