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TP53 variants in p53 signatures and the clonality of STICs in RRSO samples
Tomoko Akahane,Kenta Masuda,Akira Hirasawa,Yusuke Kobayashi,Arisa Ueki,Miho Kawaida,Kumiko Misu,Kohei Nakamura,Shimpei Nagai,Tatsuyuki Chiyoda,Wataru Yamagami,Shigenori Hayashi,Fumio Kataoka,Kouji Ban 대한부인종양학회 2022 Journal of Gynecologic Oncology Vol.33 No.4
Objective: Precursor lesions may be identified in fallopian tube tissue after risk-reducing salpingo-oophorectomy (RRSO) in patients with pathogenic variants of . Serous tubal intraepithelial carcinoma (STIC) is considered a precursor of high-grade serous carcinoma, whereas the significance of the p53 signature remains unclear. In this study, we investigated the relationship between the p53 signature and the risk of ovarian cancer. Methods: We analyzed the clinicopathological findings and conducted DNA sequencing for variants of p53 signatures and STIC lesions isolated using laser capture microdissectionin 13 patients with pathogenic variants of who underwent RRSO and 17 control patients with the benign gynecologic disease. Results: pathogenic variants were detected significantly higher in RRSO group than control (p<0.001). No difference in the frequency of p53 signatures were observed between groups (53.8% vs 29.4%; p=0.17). sequencing and next-generation sequencing analysis in a patient with STIC and occult cancer revealed 2 mutations causing different p53 staining for STICs and another mutation shared between STIC and occult cancer. Conclusion: The sequence analysis for revealed 2 types of p53 signatures, one with a risk of progression to STIC and ovarian cancer with pathological variants in and the other with a low risk of progression without pathological variants in as seen in control.
Wataru Yamagami,Nobuyuki Susumu,Takeshi Makabe,Kensuke Sakai,Hiroyuki Nomura,Fumio Kataoka,Akira Hirasawa,Kouji Banno,Daisuke Aoki 대한부인종양학회 2018 Journal of Gynecologic Oncology Vol.29 No.2
Objective: Reports on the repeated administration of medroxyprogesterone acetate (MPA) for intrauterine recurrence after fertility-preserving therapy for atypical endometrial hyperplasia (AEH) and early grade 1 endometrioid carcinoma (G1) are lacking. We aimed to clarify the outcomes of repeated MPA therapy in cases of intrauterine recurrence after fertility-preserving therapy with MPA against AEH/early G1. Methods: Patients with AEH or stage IA well-differentiated endometrioid carcinoma without myometrial invasion who underwent first-line MPA therapy for primary lesions or intrauterine recurrence were divided into initial treatment and repeated treatment groups (162 and 82 patients, respectively). Oral MPA administration (400−600 mg/day) was continued until pathological tumor disappearance. Data regarding clinicopathological factors, adverse events, and outcomes following the initial and repeated hormonal treatments were extracted from medical records and analyzed. Results: Complete response rates in the initial and repeated treatment groups were 98.5% and 96.4%, respectively, among patients with AEH, and were 90.7% and 98.1%, respectively, among patients with G1. In the initial treatment group, 5-year recurrence-free survival (RFS) rates were 53.7% and 33.2% among patients with AEH and G1, respectively. In the repeated treatment group, RFS rates were 14.0% and 11.2% among patients with AEH and G1, respectively. Among patients with AEH, the pregnancy rate tended to be lower in the repeated treatment group than in the initial treatment group (11.1% vs. 29.2%; p=0.107), while no significant group difference was observed among patients with G1 (20.8% vs. 22.7%). Conclusion: Repeated treatment is sufficiently effective for intrauterine recurrence after hormonal therapy for AEH/early G1.