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OBJECTIVE: The purpose of this study was to evaluate postoperative prognosis and progression in patients who received laparoscopic-assisted adenomyomectomy using the double flap method. METHODS: The pelvic cavity was explored by the conventional laparoscopic method, and drainage was achieved through a 5-mm trocar. After a small incision in the abdomen, the uterus was incised from the fundus to the upper cervical margin until exposing the endometrial cavity. Adenomyotic tissue was removed using a scalpel, scissors, or monopolar electrical bovie. The endometrial cavity was repaired with interrupted sutures using 2-0 vicryl. One side of the serosal flap was used to cover the endometrial side of the uterus. The second serosal flap covered the first flap after removal of the serosal surface of the first flap. RESULTS: From January 2008 to March 2012, there were 11 cases of laparoscopic-assisted adenomyomectomy at Chungnam National University Hospital. Nine cases were analyzed, excluding two cases with less than one year of follow-up. The average patient age was 37.0 years and average follow-up duration was 32.8 months. All patients showed improvement in dysmenorrhea (P < 0.001) and hypermenorrhea (P = 0.001) after surgery and were evaluated by visual analogue scale score. However, symptoms of adenomyosis were aggravated in three patients. Adenomyosis was progressed in the side opposite the site of operation. One patient required a total laparoscopic hysterectomy 27 months after surgery. CONCLUSION: Laparoscopic-assisted adenomyomectomy using the double flap method is effective for uterine reduction and relief of dysmenorrhea and hypermenorrhea. Conservative management and careful follow-up are needed because adenomyosis can recur or progress in some patients.

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There have been some reports of coincidental presentation of breast carcinoma and phyllodes tumor in the same breast. Most of the cases were carcinoma that arose from a phyllodes tumor with a histologically identified transitional area, and they behaved less aggressively than the usually encountered carcinoma. Collision tumors are rare clinical entities in which two histologically distinct tumor types show involvement at the same site. The occurrence of these tumors in the breast is extremely rare. Here, we report a case of 45-year-old woman who had both invasive ductal carcinoma as the finding of inflammatory carcinoma and a malignant phyllodes tumor in the same breast. There was no evidence of a transitional area between the phyllodes tumor and the invasive ductal carcinoma. To our knowledge, this is the first report of a collision tumor of inflammatory breast carcinoma coincident with a malignant phyllodes tumor in same breast.

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To discover the molecular mechanism of N-Myc downstream-regulated gene 2 (NDRG2), a newly found differentiation-related tumor suppressor, the relationships between NDRG2 and E-cadherin were investigated in tumor cells and tissues. Positive correlations between the expression of E-cadherin and NDRG2 were shown in several colon cancer cell lines as well as in colon cancer tissues. According to the transcription assays using a reporter plasmid containing E-cadherin promoter region (-368~+51), NDRG2 introduction into colon cancer cell lines induced upregulation of E-cadherin promoter activity and its transcription. On the contrary, inhibition of NDRG2 expression by siRNA treatment caused the decrease of E-cadherin transcription. Snail, a zinc-finger transcriptional repressor, was shown to be a mediator of NDRG2-regulated E-cadherin expression. The enhancement of glycogen synthase kinase 3ß (GSK-3ß) activity by NDRG2 overexpression caused proteasomal degradation of Snail transcription factor followed by transcriptional de-repression of E-cadherin. We also found that NDRG2 could mediate cell density-regulated E-cadherin expression. The increase of NDRG2 expression with cell density preceded E-cadherin expression, and the regulation of Snail activity by GSK-3ß was also related to this process.

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CTHRC1 has been known as a regulator of collagen expression and cell migration. The aim of this research was to clarify the clinicopathologic significance of CTHRC1 expression in human breast cancer. 22 cases of breast cancer tissues, randomly selected from clinically diagnosed patients, showed a significant increase of CTHRC1 mRNA expression compared to the normal tissue from the same patients using RT-PCR and real-time PCR. Additionally we investigated breast cancers from 189 patients by immunohistochemistry (IHC). A high level of CTHRC1 expression was observed in 111 (58.7 %) out of 189 breast cancer patients and the expression was significantly correlated with histologic grade (P = 0.026), nodal status (P < 0.001), and TNM pathologic stage (P = 0.002). High CTHRC1 expression was associated with a shorter recurrence free survival (P = 0.008). Taken together, the results showed that CTHRC1 over-expression was significantly associated with clinicopathological factors of poor prognosis in invasive ductal carcinoma. CTHRC1 could be used as a supplementary prognostic biomarker and a potential therapeutic target in breast cancer.

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