Objective To investigate the MRI manifestations of alveolar soft part sarcoma(ASPS)and to improve the diagnostic accuracy of ASPS.Methods The clinical and MRI data of 9 patients with ASPS confirmed by surgical pathology were analyzed ret-rospectively,and the MRI features were summarized and analyzed.Results Four cases were located in the thigh,three cases in the pelvis,one case in the calf,and one case under the chin.Seven cases were spindle shaped,one case was irregular,and one case was quasi-circular.All nine cases had clear boundaries.Seven cases of ASPS had lung metastases,and two of these also had brain metasta-ses.On T1WI,three cases showed isointense signals,and six cases showed slightly hyperintense signals.On T2WI,seven cases showed mixed hyperintense signals and two cases showed homogeneous hyperintense signals.On diffusion weighted imaging(DWI),six cases showed mixed hyperintense signals,one case showed homogeneous hyperintense signals,and one case showed isointense sig-nal;the average apparent diffusion coefficient(ADC)value was(1.14±0.10)×10-3 mm2/s.Six cases showed inhomogeneous obvious enhancement,and one case showed homogeneous enhancement;three cases showed relatively obvious enhancement in small strip-like fat suppression(FS)-T2WI hyperintense areas of ASPS.All nine cases of ASPS showed"flow void vessels sign",with seven cases showed"flow void vessels"both intratumor and peritumor,while the other two cases showed"flow void vessels"only peritumor.Six cases of ASPS showed cystic changes and necrosis.Three cases showed"pseudocapsule".Two cases showed T2WI hypointense septa-tion.Conclusion Hyperintense signals on T1WI,"flow void vessels sign"on T2WI,and inhomogeneous obvious enhancement in ASPS are helpful for diagnosis,with final confirmation relying on pathology.

Objective To investigate the MRI manifestations of alveolar soft part sarcoma(ASPS)and to improve the diagnostic accuracy of ASPS.Methods The clinical and MRI data of 9 patients with ASPS confirmed by surgical pathology were analyzed ret-rospectively,and the MRI features were summarized and analyzed.Results Four cases were located in the thigh,three cases in the pelvis,one case in the calf,and one case under the chin.Seven cases were spindle shaped,one case was irregular,and one case was quasi-circular.All nine cases had clear boundaries.Seven cases of ASPS had lung metastases,and two of these also had brain metasta-ses.On T1WI,three cases showed isointense signals,and six cases showed slightly hyperintense signals.On T2WI,seven cases showed mixed hyperintense signals and two cases showed homogeneous hyperintense signals.On diffusion weighted imaging(DWI),six cases showed mixed hyperintense signals,one case showed homogeneous hyperintense signals,and one case showed isointense sig-nal;the average apparent diffusion coefficient(ADC)value was(1.14±0.10)×10-3 mm2/s.Six cases showed inhomogeneous obvious enhancement,and one case showed homogeneous enhancement;three cases showed relatively obvious enhancement in small strip-like fat suppression(FS)-T2WI hyperintense areas of ASPS.All nine cases of ASPS showed"flow void vessels sign",with seven cases showed"flow void vessels"both intratumor and peritumor,while the other two cases showed"flow void vessels"only peritumor.Six cases of ASPS showed cystic changes and necrosis.Three cases showed"pseudocapsule".Two cases showed T2WI hypointense septa-tion.Conclusion Hyperintense signals on T1WI,"flow void vessels sign"on T2WI,and inhomogeneous obvious enhancement in ASPS are helpful for diagnosis,with final confirmation relying on pathology.

Objective: Resistance to chemotherapy drugs makes ovarian cancer (OC) difficult to treat and ultimately kills patients. Long non-coding RNAs are closely related to carboplatin resistance in OC. In present study, we explored the role of lncRNA X-inactive specific transcript (XIST) on carboplatin resistance in OC. Methods: Cell viability, proliferation, and apoptosis were assessed through 2,5-diphenyl-2H-tetrazolium bromide, colony formation, and flow cytometry assays, respectively. Microtubule-associated protein 1A/1B-light chain 3 expression was evaluated by immunofluorescence assay to analyze the cell autophagy. The interaction of XIST/miR-506-3p or miR-506-3p/forkhead box protein P1 (FOXP1) was analyzed using RNA immunoprecipitation (RIP) and dual-luciferases reporter assays. The function of XIST/miR-506-3p/FOXP1 axis in vivo was further confirmed by tumor xenograft study and immunohistochemistry. Results: The expression of XIST and FOXP1 increased while miR-506-3p decreased in OC and carboplatin resistance cells. XIST silencing repressed the proliferative and autophagic capacities of carboplatin resistance cells while promoted the apoptosis. XIST overexpression led to the opposite results. XIST targeted miR-506-3p and downregulated its expression. MiR-506-3p inhibition facilitated the proliferative and autophagic capacities while suppressed the apoptosis of cells, XIST knockdown reversed these effects. MiR-506-3p bound to FOXP1. XIST knockdown or miR-506-3p overexpression reversed the increase of cell proliferative and autophagic abilities and the decrease of apoptosis rate induced by FOXP1 overexpression. XIST affected autophagy and carboplatin resistance in vivo via regulating the miR-506-3p/FOXP1 axis. Conclusion XIST knockdown inhibited autophagy and carboplatin resistance of OC through FOXP1/protein kinase B (AKT)/mammalian target of rapamycin pathway by targeting miR-506-3p.