Laparoscopic adenomyomectomy combined with levonorgestrel-releasing intrauterine system is effective for long-term management of adenomyosis.

BACKGROUD: Laparoscopic adenomyomectomy combined with intraoperative placement of levonorgestrel-releasing intrauterine device (LNG-IUS) is a novel conservative surgical procedure for adenomyosis. Our study aimed to compare the efficacy of surgery with or without intraoperative placement of LNG-IUS treatment in adenomyosis. METHODS: We retrospectively reviewed the medical records of adenomyosis patients who received laparoscopic adenomyomectomy from January 2014 to April 2020, finally including 70 patients undergoing surgery-LNG-IUS as group A and 69 patients undegoing surgery only as group B. Risk factors for three-year relapse were analyzed using Cox's multivariate proportional hazard analysis. RESULTS: Visual analog scale and Mansfield-Voda-Jorgensen Menstrual Bleeding Scale scores of group A at 3, 6, 12, 24, and 36 months were significantly lower than those of group B at the corresponding points (P < .001 for both scales). Individuals in both groups showed statistically significant symptom relief. The recurrence rate in group A was significantly lower than that in group B at 36 months after the surgery (2.94% vs. 32.84%, P < .001). A cox proportional hazard model showed that relapse was significantly associated with coexisting ovarian endometriosis (adjusted hazard ratio [aHR], 2.94; 95% confidence interval [CI], 1.33-7.02, P = .015). Patients who received surgery-LNG-IUS had a lower risk of recurrence than those with surgery-alone (aHR, 0.07; 95% CI, 0.016-0.31, P < .001). CONCLUSIONS: Conservative surgery with intraoperative placement of LNG-IUS is effective and well-accepted for long-term therapy with a lower recurrence rate for adenomyosis. Coexistent ovarian endometriosis is a major factor for adenomyosis relapse.

Risk Factors for Symptomatic Recurrence after Laparoscopic Adenomyomectomy: A 3-Year Follow-up.

STUDY OBJECTIVE: To identify the clinical risk factors for symptomatic recurrence of adenomyosis after laparoscopic adenomyomectomy with a three-year follow-up. DESIGN: Retrospective study. SETTING: University-affiliated hospital. PATIENTS: A total of 149 patients were included in this study, including 52 patients with symptomatic recurrence and 97 without recurrence. INTERVENTION: Laparoscopic adenomyomectomy was performed first. MEASUREMENTS AND MAIN RESULTS: General clinical data, including preoperative, intraoperative, and postoperative indices, symptomatic recurrence, and follow-up information, were collected. Comparison of women with and without symptomatic recurrence revealed significant differences for age at surgery (p = .026), presence of concomitant ovarian endometrioma (p <.001), and prescription of postoperative hormonal suppression (yes/no) (p <.0001). A Cox proportional hazard model indicated that concomitant ovarian endometrioma was a significant risk factor for recurrence (hazard ratio [HR], 2.06; 95% confidence interval [CI], 1.10-3.85, p = .001). Patients who received postoperative hormonal suppression had a lower risk of recurrence than those without hormonal suppression (HR, 0.30; 95% CI, 0.16-0.55, p <.0001). Those aged ≥40 years also had a lower risk of symptomatic recurrence than those <40 years (HR, 0.46; 95% CI, 0.24-0.88, p = .03). CONCLUSIONS: Concomitant ovarian endometrioma is a risk factor for symptomatic recurrence of adenomyosis after laparoscopic adenomyomectomy. Postoperative hormonal suppression and older age at surgery (≥40 years) are protective factors.

ANP32B-mediated repression of p53 contributes to maintenance of normal and CML stem cells.

Proper regulation of p53 signaling is critical for the maintenance of hematopoietic stem cells (HSCs) and leukemic stem cells (LSCs). The hematopoietic cell-specific mechanisms regulating p53 activity remain largely unknown. Here, we demonstrate that conditional deletion of acidic leucine-rich nuclear phosphoprotein 32B (ANP32B) in hematopoietic cells impairs repopulation capacity and postinjury regeneration of HSCs. Mechanistically, ANP32B forms a repressive complex with p53 and thus inhibits the transcriptional activity of p53 in hematopoietic cells, and p53 deletion rescues the functional defect in Anp32b-deficient HSCs. Of great interest, ANP32B is highly expressed in leukemic cells from patients with chronic myelogenous leukemia (CML). Anp32b deletion enhances p53 transcriptional activity to impair LSC function in a murine CML model and exhibits synergistic therapeutic effects with tyrosine kinase inhibitors in inhibiting CML propagation. In summary, our findings provide a novel strategy to enhance p53 activity in LSCs by inhibiting ANP32B and identify ANP32B as a potential therapeutic target in treating CML.

Small interfering RNA-mediated knockdown of Twist attenuates the aggressive phenotypes of human endometrial carcinoma Ishikawa cells.

The present study aimed to determine the effect of Twist downregulation on the proliferation, apoptosis and migration of human endometrial carcinoma Ishikawa cells. Endogenous expression of the Twist transcription factor was knocked down by delivery of Twist-targeting small interfering RNA (siRNA). Changes in the expression of epithelial-mesenchymal transition biomarkers, namely epithelial (E)-cadherin, neural (N)-cadherin and Twist, were determined by western blot analysis. Cell cycle distribution and apoptosis were evaluated by flow cytometry. Cell proliferation and migration were analyzed using cell-counting and wound-healing assays, respectively. Transfection with Twist siRNA led to a significant reduction in the expression of Twist and N-cadherin (P<0.05), while significantly increasing the expression of E-cadherin, relative to negative control transfectants (all P<0.05). Proliferation was also significantly decreased in Ishikawa cells transfected with Twist siRNA (P<0.05), which was accompanied by an increased rate of apoptosis and cell cycle arrest at S-phase. In addition, Twist downregulation led to a significant reduction in cell migration (P<0.05). These data suggest that Twist serves a role in the regulation of cell proliferation and migration in Ishikawa cells and may represent a potential target for the treatment of human endometrial carcinoma.