Human epididymal secretory protein E4 (HE4, also known as WAP four-disulphide core domain protein 2) is a new promising biomarker for ovarian cancer but its specificity against ovarian endometriotic cysts is only superficially known. We, thus, analysed serum HE4 concentrations together with a tumour marker CA125 in serum samples of women diagnosed with various types of endometriosis, endometrial cancer or ovarian cancer, and in samples from healthy controls. The mean serum concentration of HE4 was significantly higher in serum samples of patients with both endometrial (99.2 pM, P<0.001) and ovarian (1125.4 pM, P<0.001) cancer but not with ovarian endometriomas (46.0 pM) or other types of endometriosis (45.5 pM) as compared with healthy controls (40.5 pM). The serum CA125 concentrations were elevated in patients with ovarian cancer, advanced endometriosis with peritoneal or deep lesions, or ovarian endometriomas, but not in the patients with endometrial cancer. The microarray results revealed that the mRNA expression of the genes encoding HE4 and CA125 reflected the serum protein concentrations. Taken together, measuring both HE4 and CA125 serum concentrations increases the accuracy of ovarian cancer diagnosis and provides valuable information to discriminate ovarian tumours from ovarian endometriotic cysts.

Purpose: Three years of adjuvant imatinib therapy are recommended for patients with GI stromal tumor (GIST) with high-risk features, according to survival findings in the Scandinavian Sarcoma Group XVIII/AIO (Arbeitsgemeinschaft Internistische Onkologie) trial. To investigate whether the survival benefits have persisted, we performed the second planned analysis of the trial. Patients and Methods: Eligible patients had macroscopically completely excised, KIT-positive GIST with a high risk of recurrence, as determined by using the modified National Institutes of Health criteria. After surgery, the patients were randomly assigned to receive imatinib for either 1 or 3 years. The primary objective was recurrence-free survival (RFS), and the secondary objectives included survival. Results: A total of 400 patients were entered onto this open-label study between February 4, 2004, and September 29, 2008. During a median follow-up of 90 months, 171 recurrences and 69 deaths were detected. Patients assigned to the 3-year group had longer RFS than those assigned to the 1- year group; 5-year RFS was 71.1% versus 52.3%, respectively (hazard ratio [HR], 0.60; 95% CI 0.44 to 0.81; P < .001), and survival was 91.9% versus 85.3% (HR, 0.60; 95% CI, 0.37 to 0.97; P = .036). Patients in the 3-year group survived longer in the subset with centrally confirmed GIST and without macroscopic metastases at study entry (93.4% v 86.8%; HR, 0.53; 95% CI, 0.30 to 0.93; P = .024). Similar numbers of cardiac events and second cancers were recorded in the groups. Conclusion: Three years of adjuvant imatinib therapy results in longer survival than 1 year of imatinib. High 5-year survival rates are achievable in patient populations with high-risk GIST.

The survival outcomes of patients with gastrointestinal stromal tumor (GIST) with overt metastases improved greatly after the approval of imatinib.¹ Yet, the median survival time of patients with advanced GIST is still only about 2 to 3 years. Administration of imatinib in the adjuvant setting to patients who have a high risk of recurrence despite macroscopically complete surgery is an attractive strategy for improving survival. Imatinib remains the only approved tyrosine kinase inhibitor (TKI) for adjuvant treatment of GIST.

Gastrointestinal stromal tumor (GIST) is a common type of sarcoma.¹ Most GISTs are local when detected and are treated with surgery. Their malignancy potential varies, with the most important factors associated with prognosis after surgery being tumor mitotic rate and size, site in the gastrointestinal tract, and presence of tumor rupture.²

Capecitabine, an oral prodrug of fluorouracil, is active in the treatment of advanced breast cancer, but it is not considered a standard agent in the adjuvant setting. Capecitabine is converted to fluorouracil after its ingestion in the liver and in malignant tumors that contain thymidine phosphorylase, potentially leading to high intratumoral concentrations of fluorouracil.¹ In preclinical models, some standard agents used in the treatment of breast cancer, such as paclitaxel, docetaxel, and cyclophosphamide, increase cancer thymidine phosphorylase concentration, suggesting that concomitant administration of these agents with capecitabine could lead to improved efficacy over capecitabine alone.^2,3 Indeed, data from a few randomized trials carried out in the treatment of advanced breast cancer suggest that this may be the case.^4-6