Clinical features of abdominal actinomycosis: a 15-year experience of a single institute.

This study was designed to evaluate the clinical features of abdominal actinomycosis and to assess its therapeutic outcome. We reviewed patients with abdominal actinomycosis in Seoul St. Mary hospital, between January 1994 and January 2010. Twenty-three patients (5 male and 18 female, mean age, 47.8 yr; range, 6-75 yr), with abdominal actinomycosis were included. Emergency surgery was performed in 50% due to symptoms of peritonitis. The common presentation on preoperative computerized tomography was a mass with abscess, mimicking malignancy. The mean tumor size was 7.0 cm (range, 2.5-10.5). In all patients, actinomycotic masses were surgically removed. Mean duration of hospital stay was 17.8 days (range, 5-49). Long term oral antibiotic treatment (mean 4.2 months; range, 0.5-7.0 months) were administered to all patients. All patients were free of recurrence after a median follow up of 30.0 months (mean 35.5 ± 14.8 months, range, 10.0-70.0 months); recurrence was not seen in any patient. In conclusion, abdominal actinomycosis should be included as a differential diagnosis when an unusual abdominal mass or abscess presents on abdominal CT. Assertive removal of necrotic tissue with surgical drainage and long term antibiotic treatment provide a good prognosis in patients with actinomycosis.

The combination effect of sodium butyrate and 5-Aza-2'-deoxycytidine on radiosensitivity in RKO colorectal cancer and MCF-7 breast cancer cell lines.

BACKGROUND: The overall level of chromatin compaction is an important mechanism of radiosensitivity, and modification of DNA methylation and histone deacetylation may increase radiosensitivity by altering chromatin compaction. In this study, we investigated the effect of a demethylating agent, a histone deacetylase(HDAC) inhibitor, and the two agents combined on radiosensitivity in human colon and breast cancer cell lines. METHODS: In this study, we used RKO colorectal cancer cell line and MCF-7 breast cancer cell lines and normal colon cell lines. On each of the cell lines, we used three different agents: the HDAC inhibitor sodium butyrate(SB), the demethylating agent 5-Aza-2'-deoxycytidine(5-aza-DC), and radiation. We then estimated the percentage of the cell survival using the XTT method and experimented to determine if there was an augmentation in the therapeutic effect by using different combinations of the two or three of the treatment methods. RESULTS: After treatment of each cell lines with 5-aza-DC, SB and 6 grays of radiation, we observed that the survival fraction was lower after the treatment with 5-aza-DC or SB than with radiation alone in RKO and MCF-7 cell lines(p < 0.001). The survival fraction was lowest when the two agents, 5-aza-DC and SB were combined with radiation in both RKO and MCF-cell lines. CONCLUSION: In conclusion, 5-aza-DC and SB can enhance radiosensitivity in both MCF-7 and RKO cell lines. The combination effect of a demethylating agent and an HDAC inhibitor is more effective than that of single agent treatment in both breast and colon cancer cell lines.

HCCR-1-interacting molecule "deleted in polyposis 1" plays a tumor-suppressor role in colon carcinogenesis.

BACKGROUND & AIMS: Human cervical cancer oncogene (HCCR-1) has appeared to act as a negative regulator of p53 and contributes to tumorigenesis of various organs including the colon. We identified the HCCR-1 binding protein deleted in polyposis 1 (DP1) and accessed the role of HCCR-1 and DP1 in colon tumorigenesis. METHODS: Yeast 2-hybrid was used to identify HCCR-1 interacting proteins. Various molecular biological approaches were used to examine the expression profile of HCCR-1 and DP1, subcellular localization, epitope mapping, the biological role of DP1, and the serum HCCR-1 level. Loss of heterozygosity frequency around DP1 also was examined. RESULTS: We identified that HCCR-1 interacted with DP1. These 2 proteins colocalized in mitochondria but the expression of HCCR-1 showed negative correlation with that of DP1 in colorectal cancer (CRC). DP1 played a tumor-suppressor role in colon tumorigenesis (ie, DP1-transfected RKO cells showed growth inhibition, apoptosis, decreased telomerase activity, and up-regulation of p53). These phenomena were reversed when HCCR-1 was overexpressed. Loss of heterozygosity around the DP1 gene was observed frequently (50%) in CRCs. We examined the use of serum HCCR-1 in CRC patients. The sensitivity of HCCR-1 (76.0%) for detecting CRC was proven to be much higher than that of CA19-9 (32.0%). CONCLUSIONS: DP1 plays a tumor-suppressor role in CRC. DP1 and HCCR-1 are supposed to regulate each other negatively by interaction, but further study is required to get better insight into the biological significance of the interaction.