OBJECTIVETo explore the clinical characteristics of ovarian cancer in hereditary breast/ovarian cancer.

METHODSNinety-one cases of hereditary breast/ovarian cancer were analyzed in terms of age, histological features, stage, familial history, survival time and prognostic factors by SPSS statistical software.

RESULTSThe overall median survival time of the patients was 47 months, and the 2-and 5-year survival rates were 71.2% and 33.5%, respectively. The median age at diagnosis of ovarian cancer was 52 years with the majority of patients (60.4%) diagnosed before 55. Among 39 cases with double primary cancers, there are 20 cases (51.3%) with interval no less than 60 months. The most frequent histological types of ovarian cancer is serous adeno-carcinoma (59.3%). Most patients were in stage III or IV (76.9%) with poor differentiation (59.3%).

CONCLUSIONThe age of diagnosis in ovarian cancer in patients with hereditary breast/ovarian cancer is earlier than that of sporadic ones. Most of the cases were advanced with poor differentiation. Stage and differentiation are the prognostic factors. In patients with double primary cancers, the clinical pathological characteristics of ovarian cancer had the main effect on their prognosis. The survival of hereditary ovarian cancer is similar to that of sporadic ones.

Breast Neoplasms ; genetics ; mortality ; pathology ; Cystadenocarcinoma, Serous ; genetics ; mortality ; Family Health ; Female ; Humans ; Middle Aged ; Ovarian Neoplasms ; genetics ; mortality ; pathology ; Prognosis ; Survival Rate

PURPOSE: Lymphatic invasion (LI) is regarded as a predictor of the aggressiveness of ovarian cancer (OC). However, LI is not always the major determinant of long-term patient survival. To establish proper diagnosis and treatment for OC, we analyzed differentially expressed genes (DEGs) for patients with serous epithelial OC, with or without LI, who did or did not survive for 5 years. MATERIALS AND METHODS: Gene expression data from 63 patients with OC and LI, and 35 patients with OC but without LI, were investigated using an Affymetrix Human Genome U133 Array and analyzed using The Cancer Genome Atlas (TCGA) database. Among these 98 patients, 16 survived for 5 years or more. DEGs were identified using the Bioconductor R package, and their functions were analyzed using the DAVID web tool. RESULTS: We found 55 significant DEGs (p<0.01) from the patients with LI and 20 highly significant DEGs (p<0.001) from those without it. Pathway analysis showed that DEGs associated with carbohydrate metabolism or with renal cell carcinoma pathways were enriched in the patients with and without LI, respectively. Using the top five prognostic marker genes, we generated survival scores that could be used to predict the 5-year survival of patients with OC without LI. CONCLUSION: The DEGs identified in this study could be used to elucidate the mechanism of tumor progression and to guide the prognosis and treatment of patients with serous OC but without LI.
Cystadenocarcinoma, Serous/*genetics/*mortality/pathology ; Databases, Genetic ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Microarray Analysis ; Middle Aged ; Ovarian Neoplasms/*genetics/*mortality/pathology ; Prognosis ; Regression Analysis ; Retrospective Studies ; Survival Rate

OBJECTIVETo investigate the therapeutic principles and prognosis of synchronous primary colorectal carcinomas (SCC).

METHODSThe data of 66 SCC patients surgically treated from 1984 to 2003 were retrospectively reviewed.

RESULTSThe synchronous primary colorectal carcinomas were diagnosed and resected simultaneously in 65 patients except one that was misdiagnosed. Thirty patients underwent combined resection, 35 patients segmental resection. Sixty-two patients received radical resection, while three patients had palliative resection due to hepatic metastasis. The overall postoperative 3-, 5-, 10-year survival rates were 70.3%, 60.0%, 40.6%, respectively. In the patients who had simultaneous radical resection, the 3-, 5-, 10-year survival rates were 76.0%, 65.9%, 46.4% respectively.

CONCLUSIONThe extent of resection should be individually determined by the lesion location, extent and distance between the lesions, as well as the patient's general condition. More extensive bowel resection, such as total or subtotal colectomy are suggested for those patients with hereditary nonpolyposis colorectal carcinoma syndrome in order to reduce or avoid the risk of metachronous colorectal carcinoma. The postoperative survival in patients with synchronous primary colorectal carcinoma is similar to those with solitary lesion.

Adult ; Aged ; Colorectal Neoplasms ; mortality ; pathology ; surgery ; Colorectal Neoplasms, Hereditary Nonpolyposis ; genetics ; surgery ; Female ; Humans ; Male ; Middle Aged ; Neoplasms, Multiple Primary ; genetics ; surgery ; Ovarian Neoplasms ; surgery ; Prognosis ; Stomach Neoplasms ; surgery ; Survival Rate

PURPOSE: Ovarian cancer (OC) is the most fatal of gynecological malignancies with a high rate of recurrence. We aimed to evaluate the expression of solute carrier family 6, member 12 (SLC6A12) and methylation of its promoter CpG sites in a xenograft mouse model of metastatic OC, and to investigate the regulatory mechanisms that promote aggressive properties during OC progression. MATERIALS AND METHODS: Expression of SLC6A12 mRNA was determined by reverse-transcription quantitative polymerase chain reaction (RT-qPCR), and DNA methylation status of its promoter CpGs was detected by quantitative methylation-specific PCR. The metastatic potential of SLC6A12 was evaluated by in vitro migration/invasion transwell assays. Gene expression and DNA methylation of SLC6A12 and clinical outcomes were further investigated from publicly available databases from curatedOvarianData and The Cancer Genome Atlas. RESULTS: SLC6A12 expression was 8.1–14.0-fold upregulated and its DNA methylation of promoter CpG sites was 41–62% decreased in tumor metastases. After treatment with DNA methyltransferase inhibitor and/or histone deacetylase inhibitor, the expression of SLC6A12 was profoundly enhanced (~8.0-fold), strongly supporting DNA methylation-dependent epigenetic regulation of SLC6A12. Overexpression of SLC6A12 led to increased migration and invasion of ovarian carcinoma cells in vitro, approximately 2.0-fold and 3.3-fold, respectively. The meta-analysis showed that high expression of SLC6A12 was significantly associated with poor overall survival [hazard ratio (HR)=1.07, p value=0.016] and that low DNA methylation levels of SLC6A12 at specific promoter CpG site negatively affected patient survival. CONCLUSION: Our findings provide novel evidence for the biological and clinical significance of SLC6A12 as a metastasis-promoting gene.
Animals ; Carrier Proteins/genetics/*metabolism ; Cell Line, Tumor ; Cell Migration Assays ; *CpG Islands ; *DNA Methylation ; Disease Progression ; Epigenesis, Genetic ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Mice ; Neoplasm Invasiveness ; Neoplasm Transplantation ; Ovarian Neoplasms/genetics/*metabolism/mortality/pathology ; Polymerase Chain Reaction ; Prognosis ; *Promoter Regions, Genetic ; RNA, Messenger/*metabolism ; Up-Regulation