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( Satoshi Ono ),( Mitsuhiro Fujishiro ),( Osamu Goto ),( Shinya Kodashima ),( Masao Omata ) The Editorial Office of Gut and Liver 2008 Gut and Liver Vol.2 No.3
A 72-year-old female with a colonic laterally spreading tumor (LST) was referred to our department. A total colonoscopy revealed a large nongranular LST, 30 mm in diameter, in the ascending colon. Detailed examination with chromoendoscopy confirmed that the lesion was an intramucosal tumor, and endoscopic submucosal dissection (ESD) was performed. After a circumferential incision around the lifted lesion with a submucosal fluid cushion, diffuse adipose tissue was observed in the submucosal layer beneath the lesion. The endoscopic view was blurred when dissecting the submucosal layer due to fat adhering to the lens. Since this made it difficult to continue the procedures, we infused water into the lumen and kept the endoscope tip immersed in the collected water. The resulting improved view made it possible to complete all procedures without withdrawing the endoscope to wipe the lens. The lesion was successfully resected en bloc without complications. The pathological examination indicated the curative resection of a tubulovillous adenoma. We propose that a submerged ESD could also be an effective procedure for colonic neoplasms with submucosal fat by avoiding blurring of the endoscopic view. (Gut and Liver 2008;2:209-212)
Ikuko Sakamoto,Yosuke Hirotsu,Kenji Amemiya,Takahiro Nozaki,Hitoshi Mochizuki,Masao Omata 대한부인종양학회 2023 Journal of Gynecologic Oncology Vol.34 No.1
Objective: Elucidation of clonal origin of synchronous endometrial and ovarian cancers (SEOs). Methods: We reviewed 852 patients who diagnosed endometrial and/or ovarian cancer. Forty-five (5.3%) patients were diagnosed as SEOs. We evaluated blood and tissue samples from 17 patients. We analyzed the clonal origins of 41 samples from 17 patients by gene sequencing, mismatch microsatellite instability (MSI) polymerase chain reaction assay and immunohistochemical (IHC) staining of 4 repair genes. Results: Sixteen of 17 patients had at least 2 or more trunk mutations shared between endometrial and ovarian cancer suggesting the identical clonal origins. The shared trunk mutation are frequently found in endometrial cancer of the uterus, suggesting the uterine primary. Four out of 17 (24%) SEOs had mismatch repair (MMR) protein deficiency and MSI-high (MSI-H) states. One case was an endometrial carcinoma with local loss of MSH6 protein expression by IHC staining, and the result of MSI analysis using the whole formalin-fixed, paraffin-embedded specimen was microsatellite stable. In contrast, ovarian tissue was deficient MMR and MSI-H in the whole specimen. This indicated that MMR protein deficiency could occur during the progression of disease. Conclusion: Most SEOs are likely to be a single tumor with metastasis instead of double primaries, and their origin could be endometrium. In addition, SEOs have a high frequency of MMR gene abnormalities. These findings not only can support the notion of uterine primary, but also can help to expect the benefit for patients with SEOs by immuno-oncology treatment.
Cheng, Ann-Lii,Kang, Yoon-Koo,Lin, Deng-Yn,Park, Joong-Won,Kudo, Masatoshi,Qin, Shukui,Chung, Hyun-Cheol,Song, Xiangqun,Xu, Jianming,Poggi, Guido,Omata, Masao,Pitman Lowenthal, Susan,Lanzalone, Silvan American Society for Clinical Oncology 2013 Journal of clinical oncology Vol.31 No.32
<P><B>Purpose</B></P><P>Open-label, phase III trial evaluating whether sunitinib was superior or equivalent to sorafenib in hepatocellular cancer.</P><P><B>Patients and Methods</B></P><P>Patients were stratified and randomly assigned to receive sunitinib 37.5 mg once per day or sorafenib 400 mg twice per day. Primary end point was overall survival (OS).</P><P><B>Results</B></P><P>Early trial termination occurred for futility and safety reasons. A total of 1,074 patients were randomly assigned to the study (sunitinib arm, n = 530; sorafenib arm, n = 544). For sunitinib and sorafenib, respectively, median OS was 7.9 versus 10.2 months (hazard ratio [HR], 1.30; one-sided <I>P</I> = .9990; two-sided <I>P</I> = .0014); median progression-free survival (PFS; 3.6 <I>v</I> 3.0 months; HR, 1.13; one-sided <I>P</I> = .8785; two-sided <I>P</I> = .2286) and time to progression (TTP; 4.1 <I>v</I> 3.8 months; HR, 1.13; one-sided <I>P</I> = .8312; two-sided <I>P</I> = .3082) were comparable. Median OS was similar among Asian (7.7 <I>v</I> 8.8 months; HR, 1.21; one-sided <I>P</I> = .9829) and hepatitis B–infected patients (7.6 <I>v</I> 8.0 months; HR, 1.10; one-sided <I>P</I> = .8286), but was shorter with sunitinib in hepatitis C–infected patients (9.2 <I>v</I> 17.6 months; HR, 1.52; one-sided <I>P</I> = .9835). Sunitinib was associated with more frequent and severe adverse events (AEs) than sorafenib. Common grade 3/4 AEs were thrombocytopenia (29.7%) and neutropenia (25.7%) for sunitinib; hand-foot syndrome (21.2%) for sorafenib. Discontinuations owing to AEs were similar (sunitinib, 13.3%; sorafenib, 12.7%).</P><P><B>Conclusion</B></P><P>OS with sunitinib was not superior or equivalent but was significantly inferior to sorafenib. OS was comparable in Asian and hepatitis B–infected patients. OS was superior in hepatitis C–infected patients who received sorafenib. Sunitinib-treated patients reported more frequent and severe toxicity.</P>