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RISS 인기검색어
- 검색키워드
- 저자 : Yan Hon (검색결과 4 건)
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Perforated Early Gastric Cancer: Uncommon and Easily Missed a Case Report and Review of Literature
Raymond Hon Giat Lim,Asim Shabbir,Clifton Ming Tay,Benjamin Wong,Choon Seng Chong,Koji Kono,Jimmy Bok Yan So 대한위암학회 2013 Journal of gastric cancer Vol.13 No.1
Gastric carcinoma rarely presents as a perforation, but when it does, is perceived as advanced disease. The majority of such perforations are Stage III/IV disease. A T1 gastric carcinoma has never been reported to perforate spontaneously in English literature. We present a 56 year-old Chinese male who presented with a perforated gastric ulcer. Intra-operatively, there was no suspicion of malignancy. At operation, an open omental patch repair was performed. Post-operative endoscopy revealed a macroscopic Type 0~III tumour and from the ulcer edge biopsy was reported as adenocarcinoma. Subsequently, the patient underwent open subtotal gastrectomy and formal D2 lymphadenectomy. The final histopathology report confirms T1b N0 disease. The occurrence of a perforated early gastric cancer reemphasises the need for vigilance, including intra-operative frozen section and/or biopsy, as well as routine post-operative endoscopy for all patients.
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Perforated Early Gastric Cancer: Uncommon and Easily Missed a Case Report and Review of Literature
Lim, Raymond Hon Giat,Tay, Clifton Ming,Wong, Benjamin,Chong, Choon Seng,Kono, Koji,So, Jimmy Bok Yan,Shabbir, Asim The Korean Gastric Cancer Association 2013 Journal of gastric cancer Vol.13 No.1
Gastric carcinoma rarely presents as a perforation, but when it does, is perceived as advanced disease. The majority of such perforations are Stage III/IV disease. A T1 gastric carcinoma has never been reported to perforate spontaneously in English literature. We present a 56 year-old Chinese male who presented with a perforated gastric ulcer. Intra-operatively, there was no suspicion of malignancy. At operation, an open omental patch repair was performed. Post-operative endoscopy revealed a macroscopic Type 0~III tumour and from the ulcer edge biopsy was reported as adenocarcinoma. Subsequently, the patient underwent open subtotal gastrectomy and formal D2 lymphadenectomy. The final histopathology report confirms T1b N0 disease. The occurrence of a perforated early gastric cancer reemphasises the need for vigilance, including intra-operative frozen section and/or biopsy, as well as routine post-operative endoscopy for all patients.
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Yun-Wei Li,Yan-Ming Li,Yan Hon,Qi-Lin Wan,Rui-Li He,Zhi-Zhong Wang,Cui-Hua Zhao 대한심장학회 2017 Korean Circulation Journal Vol.47 No.2
Background and Objectives: Ischemic post-conditioning (PostC) has been demonstrated as a novel strategy to harness nature’s protection against myocardial ischemia-reperfusion (I/R). Hypercholesterolemia (HC) has been reported to block the effect of PostC on the heart. Angiotensin II type-1 (AT1) modulators have shown benefits in myocardial ischemia. The present study investigates the effect of a novel inhibitor of AT1, azilsartan in PostC of the heart of normocholesterolemic (NC) and HC rats. Materials and Methods: HC was induced by the administration of high-fat diet to the animals for eight weeks. Isolated Langendorff’s perfused NC and HC rat hearts were exposed to global ischemia for 30 min and reperfusion for 120 min. I/R-injury had been assessed by cardiac hemodynamic parameters, myocardial infarct size, release of tumor necrosis factor-alpha troponin I, lactate dehydrogenase, creatine kinase, nitrite in coronary effluent, thiobarbituric acid reactive species, a reduced form of glutathione, superoxide anion, and left ventricle collagen content in normal and HC rat hearts. Results: Azilsartan post-treatment and six episodes of PostC (10 sec each) afforded cardioprotection against I/R-injury in normal rat hearts. PostC protection against I/R-injury was abolished in HC rat hearts. Azilsartan prevented the HC-mediated impairment of the beneficial effects of PostC in I/R-induced myocardial injury, which was inhibited by L-N5-(1-Iminoethyl)ornithinehydrochloride, a potent inhibitor of endothelial nitric oxide synthase (eNOS). Conclusion: Azilsartan treatment has attenuated the HC-induced impairment of beneficial effects of PostC in I/R-injury of rat hearts, by specifically modulating eNOS. Azilsartan may be explored further in I/R-myocardial injury, both in NC and HC conditions, with or without PostC.
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Deng, Niantao,Goh, Liang Kee,Wang, Hannah,Das, Kakoli,Tao, Jiong,Tan, Iain Beehuat,Zhang, Shenli,Lee, Minghui,Wu, Jeanie,Lim, Kiat Hon,Lei, Zhengdeng,Goh, Glenn,Lim, Qing-Yan,Tan, Angie Lay-Keng,Sin P BMJ Group 2012 Gut Vol.61 No.5
<P><B>Objective</B></P><P>Gastric cancer is a major gastrointestinal malignancy for which targeted therapies are emerging as treatment options. This study sought to identify the most prevalent molecular targets in gastric cancer and to elucidate systematic patterns of exclusivity and co-occurrence among these targets, through comprehensive genomic analysis of a large panel of gastric cancers.</P><P><B>Design</B></P><P>Using high-resolution single nucleotide polymorphism arrays, copy number alterations were profiled in a panel of 233 gastric cancers (193 primary tumours, 40 cell lines) and 98 primary matched gastric non-malignant samples. For selected alterations, their impact on gene expression and clinical outcome were evaluated.</P><P><B>Results</B></P><P>22 recurrent focal alterations (13 amplifications and nine deletions) were identified. These included both known targets (<I>FGFR2</I>, <I>ERBB2</I>) and also novel genes in gastric cancer (<I>KLF5</I>, <I>GATA6</I>). Receptor tyrosine kinase (RTK)/RAS alterations were found to be frequent in gastric cancer. This study also demonstrates, for the first time, that these alterations occur in a mutually exclusive fashion, with <I>KRAS</I> gene amplifications highlighting a clinically relevant but previously underappreciated gastric cancer subgroup. <I>FGFR2</I>-amplified gastric cancers were also shown to be sensitive to dovitinib, an orally bioavailable FGFR/VEGFR targeting agent, potentially representing a subtype-specific therapy for <I>FGFR2</I>-amplified gastric cancers.</P><P><B>Conclusion</B></P><P>The study demonstrates the existence of five distinct gastric cancer patient subgroups, defined by the signature genomic alterations <I>FGFR2</I> (9% of tumours), <I>KRAS</I> (9%), <I>EGFR</I> (8%), <I>ERBB2</I> (7%) and <I>MET</I> (4%). Collectively, these subgroups suggest that at least 37% of gastric cancer patients may be potentially treatable by RTK/RAS directed therapies.</P>
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