The goal of ovarian cancer screening is to detect disease when confined to the ovary (stage I) and thereby prolong survival. We believe this is an elusive goal because most ovarian cancer, at its earliest recognizable stage, is probably not confined to the ovary. We propose a new model of ovarian carcinogenesis based on clinical, pathological, and molecular genetic studies that may enable more targeted screening and therapeutic intervention to be developed. The model divides ovarian cancer into two groups designated Type I and Type II. Type I tumors are slow growing, generally confined to the ovary at diagnosis and develop from well established precursor lesions so-called "borderline" tumors. Type I tumors include low-grade micropapillary serous carcinoma, mucinous, endometrioid, and clear cell carcinomas. They are genetically stable and are characterized by mutations in a number of different genes including KRAS, BRAF, PTEN, and beta-catenin. Type II tumors are rapidly growing, highly aggressive neoplasms that lack well defined precursor lesions; most are advanced stage at, or soon after, their inception. These include high-grade serous carcinoma, malignant mixed mesodermal tumors (carcinosarcomas) and undifferentiated carcinomas. The Type II tumors are characterized by mutation of TP53 and a high level of genetic instability. Screening tests that focus on stage I disease may detect low-grade Type I neoplasms while missing the more aggressive Type II tumors which account for most ovarian cancers. A more rational approach to early detection of "ovarian cancer" should focus on low volume rather than low stage of disease.In the United States, the incidence of ovarian cancer ranks eighth among cancers (excluding skin cancer) in women, but fifth in terms of age-adjusted mortality (http://www.cancer.org/docroot/home/index.asp). The high mortality rate is generally attributed to its occult development resulting in advanced, widespread disease occurring in approximately 75% of women at diagnosis. However, in about 25% of women disease is confined to the ovary (stage I) and 5 year survival is over 90% compared to 30% for women with advanced disease 1 . This observation suggests that diagnosing ovarian cancer when confined to the ovary may improve survival. Accordingly, there has been a concerted effort to develop screening methods for the early detection of stage I ovarian cancer.

Background The diagnostic performance of CT for pancreatic cancer is interpreter-dependent, and approximately 40% of tumours smaller than 2 cm evade detection. Convolutional neural networks (CNNs) have shown promise in image analysis, but the networks' potential for pancreatic cancer detection and diagnosis is unclear. We aimed to investigate whether CNN could distinguish individuals with and without pancreatic cancer on CT, compared with radiologist interpretation. MethodsIn this retrospective, diagnostic study, contrast-enhanced CT images of 370 patients with pancreatic cancer and 320 controls from a Taiwanese centre were manually labelled and randomly divided for training and validation (295 patients with pancreatic cancer and 256 controls) and testing (75 patients with pancreatic cancer and 64 controls; local test set 1). Images were preprocessed into patches, and a CNN was trained to classify patches as cancerous or non-cancerous. Individuals were classified as with or without pancreatic cancer on the basis of the proportion of patches diagnosed as cancerous by the CNN, using a cutoff determined using the training and validation set. The CNN was further tested with another local test set (101 patients with pancreatic cancers and 88 controls; local test set 2) and a US dataset (281 pancreatic cancers and 82 controls). Radiologist reports of pancreatic cancer images in the local test sets were retrieved for comparison.

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Hepatitis B virus (HBV) infection is a global health issue. Universal infantile hepatitis B (HB) vaccination is very efficacious. However, HBV infections among those immunized subjects have been reported. The long-term efficacy of postnatal passive-active HB vaccination in high-risk subjects is not well explored. A total of 8,733 senior high school students who were born after July 1987 were assayed for hepatitis B surface antigen (HBsAg) and antibodies to HBsAg (anti-HBs). The overall HBsAg and anti-HBs-positive rates were 1.9% and 48.3%, respectively. The HBsAg-positive rate was 15% in HB immunoglobulin (HBIG) recipients (adjusted odds ratio [OR]: 15.63; 95% confidence interval [CI]: 10.99-22.22). Among students who did not receive HBIG, there was a significantly negative association between HB vaccination dosage and HBsAg-positive rate (P for trend 5 0.011). Adjusted ORs for those who received 4, 3, and 1 to 2 doses were 1.00, 1.52 (95% CI: 0.91-2.53), and 2.85 (95% CI: 1.39-5.81), respectively. Among HBIG recipients, the HBsAgpositive rate was significantly higher in subjects with maternal hepatitis B e antigen (HBeAg) positivity and who received HBIG off-schedule. A booster dose of HB vaccination was administered to 1974 HBsAg-and anti-HBs-negative subjects. Prebooster and a postbooster blood samples were drawn for anti-HBs quantification. The proportions of postbooster anti-HBs titer <10 mIU/mL was 27.9%. Subjects with prebooster anti-HBs titers of 1.0-9.9 mIU/mL had significantly higher postbooster anti-HBs titers than those with prebooster anti-HBs titers of <1.0 mIU/mL (P < 0.0001). Conclusion: Having maternal HBeAg positivity is the most important determinant for HBsAg positivity in adolescents who received postnatal passive-active HB vaccination 15 years before. A significant proportion of complete vaccinees may have lost their immunological memories against HBsAg. (HEPATOLOGY 2013;57:38-45) H epatitis B virus (HBV) infection is a global issue, affecting two billion people in the world, with 360 million chronic carriers of hepatitis B surface antigen (HBsAg).1 The sequalae of chronic HBV infection, including hepatic failure, liver cirrhosis, and hepatocellular carcinoma, shorten lives and impose great economic burdens on society.Taiwan has been an endemic area of HBV infection, with an HBV infection rate of 95% and a 15%-20% HBsAg carrier rate in the general population.2 Vertical transmission is the main cause of persistent HBV infection in Taiwan 3 ; fortunately, it can be blocked by passive-active vaccination after birth. [4][5][6] To control HBV infection, a hepatitis B (HB) vaccination program was launched in Taiwan in 1984, starting with newborns of highly infectious mothers, and expanded to all newborns in 1986. 7The remarkable effectiveness of universal infantile HB vaccination program (UIHBVP) is well documented. [8][9][10][11][12] In Taiwan, the HBV infection and carrier rates of children born after the program has declined dramatically. [10][11][12] The incidence of infantile fulminant he...

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