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Monday, July 11, 2016

Clinical Efficacy of Ovarian Cancer Screening - open access



open access

Introduction

Various trials of ovarian cancer screening programs have been reported worldwide. One of these reports was an examination of a screening program for prostate, lung, colorectal and ovarian cancer (PLCO) in the United States of America (USA) that was performed using a randomized controlled trial [1, 2] and the largest study for ovarian cancer screening with survival data. The screening strategy involved annual screening with transvaginal sonography (TVS) and CA125 level measurements (CA125 cut-off of ≧35. Both methods were performed for three years. CA125 levels were measured at years four and five. After that, follow-up was performed for more than five years). The authors' conclusion was that simultaneous screening with measurement of the CA 125 level and TVS did not reduce ovarian cancer mortality compared with the standard care.
To investigate the validity of ovarian cancer screening, we verified the analyses of previous reports. For our analysis, we selected reports throughout the world in which large-scale investigations were performed in population of more than 30,000. We herein discuss whether ovarian cancer screening is globally effective....

Conclusion

In summary, annual screening with the use of CA125/TVS can detect the precursors of type I ovarian carcinoma, such as cystic tumors, and identify patients who should be closely observed. Thus annual screening may be useful for detecting type I ovarian carcinoma at an earlier stage. Furthermore, annual screening may improve the prognoses or induce the down staging (from stage IV to stage III) of cases of type II ovarian carcinoma, which would further increase its efficacy in Asia, and also make it effective in Europe and the USA, just as the UKCTOCS showed a significant mortality reduction in the UK.
 

Two types of ovarian cancer

New histopathological, molecular and genetic studies have recently provided a better model for ovarian carcinogenesis, including two broad categories, designated as type I, in which precursor lesions in the ovaries have clearly been described, and type II, in which such lesions have not been clearly described and tumors may develop de novo from the tubal and/or ovarian surface epithelium [14]. Type I carcinomas are, in general, slow-growing, indolent neoplasms, and include low-grade serous (rare tumors), mucinous, endometrioid, clear cell and transitional cell cancers. As we previously reported, Type I carcinomas often develop from benign ovarian cysts, and those detected within one year (mean: 7.1 ± 2.8 months) after the visit for follow-up of ovarian cysts were mostly stage I diseases (17/19; 89%) [15]. In contrast, type II carcinomas are high-grade clinically aggressive neoplasms, and include a majority of high-grade serous cancers, which are often found at an advanced stage and are highly genetically unstable. The majority of type II carcinomas, but not type II carcinomas, have TP53 mutations, and almost half of the cases involve hypermethylation, or a dysfunction of the breast cancer gene (BRCA 1/2). These biological aspects are evidence of the aggressive nature of type II carcinoma.

 Figure 2 
Comparison of the rates of different histological subtypes of ovarian cancer in Europe, the USA and Asia.



  Figure 3 
Comparison of the rates of type I and type II ovarian carcinomas among different races. Type II cancer was significantly more common in Europe and the USA than in Asia (p<0.001). Conversely, type I was relatively common in Asia. There were unidentified cancers in addition to type I and type II cancers.

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