유리피판을 이용한 하인두-식도 재건 치험례

봉정표,정윤규,이훈범,김주봉,이재화,나동균,김석원 大韓成形外科學會 1997 Archives of Plastic Surgery Vol.24 No.6

Hypopharyngo-esophageal cancer is usually found at late stage. Its main treatment is surgical intervention and it often requires radical resection. Reconstruction of the hypopharyngo-esophageal defect after the resection of carcinomas of the hypopharynx and the cervical esophagus has traditionally been carried out with deltopectoral or musculocutaneous flap. Another approach is to reconstruct the defect with the colon or stomach. Recent advances in microvascular surgical techniques have resulted in one stage reconstruction with free flap. Both jejunal free flap and radial forearm free flap is a good alternative for the reconstruction of hypopharyngo-esophageal defect. Six cases of the radial forearm flap and nine cases of the jejunal flap were used to reconstructed the hypopharyngo-esophageal defect in 15 patients. In jejunal free flap, upper margin was reconstructed with end to side anastomosis and lower margin with end to end anastomosis. In radial forearm free flap, we used trapezoid shaped flap and tubed by complete or partial tubing according to the condition of the defects. Stricture and fistula are troublesome complications. The complications were peritonitis(n=1) and fistula(n=1). We concluded that both forearm and jejunal free flap is a useful alternative in reconstruction of hypopharynx and cervical esophagus.

혈행화된 두개골 피판을 이용한 안와저 및 안와하연의 재건술 치험례

정윤규,이훈범,김석원,봉정표,김균태,김주봉 大韓成形外科學會 1998 Archives of Plastic Surgery Vol.25 No.5

A number of methods have been introduced for support the orbital floor following a maxillectomy without orbital exenteration or severe facial trauma. These methods including skin graft and muscular sling provided the unsatisfactory results, like as diplopia, orbital ptosis, enophthalmos and severe facial deformity. Therefore the bone and soft tissue reconstructions using microvascular free flaps were performed recently by many surgeons, but long time operation, donor site morbidity, postoperative large scar, and ptosis of the flap were pointed out as disadvantages of free flap reconstruction. Vascularized calvarial bone flap, a modified method of free calvarial bone graft, was adequate for reconstruction of the orbital floor and the infraorbital rim as a horizontal buttress, especially in case of poor vascular bed and postradiated state. The authors introduced the vascularized calvarial bone flap for the orbital floor and the infraorbital rim reconstruction in 3 cases of maxillectomy, and could be obtained satisfactory results aesthetically and functionally.

자기-광전이 형식을 유도하는 두 가지 다체사영연산자 방법의 비교

최상돈,이현정,석적영,조상규,강남룡 慶北大擧校 師範大學 科學敎育硏究所 2000 科學敎育硏究誌 Vol.24 No.-

We consider a magneto-optical transition theory based on the many-body projection technique. And we use two kinds of projectors ; projection-isolation operators and projection operators. The second method turns out to be more convenient than the first method.

띠간 자기광학 전이에서 두 다체 사영방법의 비교

최상돈,김영미,이연주,석적영,조상규 慶北大擧校 師範大學 科學敎育硏究所 2000 科學敎育硏究誌 Vol.24 No.-

If we apply a circularly polarized light to semiconductors, in the external static magnetic field, then the electrons absorb the light at the resonance frequency, resulting in the interband-transition from valence band to conduction band. The linewidth is affected by various mechanisms. Here we will compare the isolated operator method and the single operator method.

Mutational analysis of the <i>CASP6</i> gene in colorectal and gastric carcinomas

LEE, JONG WOO,KIM, MEE RAN,SOUNG, YOUNG HWA,NAM, SUK WOO,KIM, SANG HO,LEE, JUNG YOUNG,YOO, NAM JIN,LEE, SUG HYUNG Blackwell Publishing Ltd 2006 APMIS Vol.114 No.9

<P>Failure of apoptosis is one of the hallmarks of cancer. As an execution-phase caspase, caspase-6 plays a crucial role during apoptosis. To explore the possibility that the genetic alterations of <I>CASP</I>, which encodes caspase-6, might be involved in the development of human cancers, we analyzed the entire coding region and all splice sites of the human <I>CASP6</I> gene for the detection of somatic mutations in 100 colorectal carcinomas and 50 gastric carcinomas. Overall, we detected three somatic mutations of the <I>CASP6</I> gene, including two missense mutations and one splice-site mutation. The mutations were observed in two of the 100 colorectal carcinomas (2.0%) and one of the 50 gastric carcinomas (2.0%). Of note, one colorectal carcinoma with the <I>CASP6</I> mutation harbored <I>CASP3</I> and <I>CASP8</I> gene mutations as well. We also analyzed caspase-6 expression by immunohistochemistry, and found that caspase-6 was expressed in 60% of the gastric cancers and 90% of the colorectal cancers. This is the first report on <I>CASP6</I> gene mutations in human cancers, and these data indicate that the <I>CASP6</I> gene is occasionally mutated in gastric and colorectal carcinomas. Also, the data suggest the possibility that deficiency of caspase-6 expression might contribute to the pathogenesis of gastric cancers.</P>

Genomic structures of dysplastic nodule and concurrent hepatocellular carcinoma

Lee, Minho,Kim, Kyung,Kim, Shinn Young,Jung, Seung-Hyun,Yoon, Jonghwan,Kim, Min Sung,Park, Hyeon-Chun,Jung, Eun Sun,Chung, Yeun-Jun,Lee, Sug Hyung Elsevier 2018 Human pathology Vol.81 No.-

<P><B>Summary</B></P> <P>Although high-grade dysplastic nodule (HGDN) is a preneoplastic lesion that precedes hepatocellular carcinoma (HCC), the genomic structures of HGDN in conjunction with HCC remain elusive. The objective of this study was to identify genomic alterations of HGDN and its difference from HCC that may drive HGDN progression to HCC. We analyzed 16 regions of paired HGDN and HCC from 6 patients using whole-exome sequencing to find somatic mutation and copy number alteration (CNA) profiles of HGDN and HCC. The numbers of mutations, driver mutations, and CNAs of HGDNs were not significantly different from those of HCCs. We identified that the CNA gain of 1q25.3-1q42.13 was predominant in the HCCs compared with that in the HGDNs. Two cases (one nodule-in-nodule case and another case with closely attached HCC and HGDN) showed several overlapped driver mutations (<I>CTNNB1</I> and <I>CEBPA</I>) and CNAs (losses of <I>CDKN2A</I>, <I>RB1</I>, and <I>TP53</I>) between HGDNs and HCCs, suggesting their roles in the early HCC development. The other 4 cases with spatially separated HCCs and HGDNs showed few overlapped alterations between the paired HCCs and HGDNs. Mutations in <I>ERBB2</I> and <I>CCND1</I>, and CNAs (gains of <I>CTNNB1</I>, <I>MET</I>, and <I>SMO</I> and losses of <I>PTEN</I>, <I>TP53</I>, and <I>SETD2</I>) were identified as “HCC predominant,” suggesting their roles in the progression of HGDN to HCC. Our data show that HCCs are direct descendants of HGDNs in some cases, but there is no direct evidence of such relationship in spatially separated cases. Genomic features of HGDN identified in this study provide a useful resource for dissecting clues for the genetic diagnosis of HGDN and HCC.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Using WES, we identified genomic structures of HGDN in conjunction with HCC. </LI> <LI> Mutations of 2 genes and CNAs of 6 genes were identified as “HCC specific.” </LI> <LI> Copy number gain of 1q25.3-1q42.13 might play a crucial role in HGDN progression to HCC. </LI> </UL> </P>

PIK3CA gene is frequently mutated in breast carcinomas and hepatocellular carcinomas

Lee, Jong Woo,Soung, Young Hwa,Kim, Su Young,Lee, Hae Woo,Park, Won Sang,Nam, Suk Woo,Kim, Sang Ho,Lee, Jung Young,Yoo, Nam Jin,Lee, Sug Hyung Nature Publishing Group 2005 Oncogene Vol.24 No.8

A recent report revealed that phosphoinositide-3-kinase, catalytic, alpha (PIK3CA) gene is somatically mutated in several types of human cancer, suggesting the mutated PIK3CA gene as an oncogene in human cancers. However, because the previous report focused the mutational search primarily on colon cancers, the data on PIK3CA mutations in other types of human cancers have been largely unknown. Here, we performed mutational analysis of the PIK3CA gene by polymerase chain reaction-single-strand conformation polymorphism assay in 668 cases of common human cancers, including hepatocellular carcinomas, acute leukemias, gastric carcinomas, breast carcinomas, and non-small-cell lung cancers. We detected PIK3CA somatic mutations in 26 of 73 hepatocellular carcinomas (35.6%), 25 of 93 breast carcinomas (26.9%), 12 of 185 gastric carcinomas (6.5%), one of 88 acute leukemias (1.1%), and three of 229 non-small-cell lung cancers (1.3%). Some of the PIK3CA mutations were detected in the early lesions of breast cancer carcinoma, hepatocellular carcinoma, and gastric carcinomas, suggesting that PIK3CA mutation may occur independent of stage of the tumors. The high incidence and wide distribution of PIK3CA gene mutation in the common human cancers suggest that alterations of lipid kinase pathway by PIK3CA mutations contribute to the development of human cancers.Oncogene (2005) 24, 1477–1480. doi:10.1038/sj.onc.1208304 Published online 20 December 2004

Mutational analysis of proapoptotic death associated protein 3 ( DAP3 ) P-loop domain in common human carcinomas

Lee, Jong Woo,Soung, Young Hwa,Kim, Su Young,Nam, Suk Woo,Park, Won Sang,Lee, Jung Young,Yoo, Nam Jin,Lee, Sug Hyung Taylor Francis 2006 Acta oncologica Vol.45 No.4

Clinicopathological features of diabetic and nondiabetic renal diseases in type 2 diabetic patients with nephrotic-range proteinuria

Lee, Yu Ho,Kim, Ki-Pyo,Kim, Yang Gyun,Moon, Ju-Young,Jung, Su Woong,Park, Eunji,Kim, Jin Sug,Jeong, Kyung-Hwan,Lee, Tae Won,Ihm, Chun-Gyoo,Jo, Young-Il,Choi, Hoon-Young,Park, Hyeong-Cheon,Lee, So-Youn Williams & Wilkins Co 2017 Medicine Vol.96 No.36

<▼1><P>Supplemental Digital Content is available in the text</P></▼1><▼2><P><B>Abstract</B></P><P>Heavy proteinuria with or without features of nephrotic syndrome is associated with many primary and systemic diseases. For diabetic patients, distinguishing nondiabetic renal disease (NDRD) from diabetic nephropathy (DN) is important in choosing treatment modalities and determining renal prognosis. However, clinical relevance of heavy proteinuria is inconsistent with clinical DN assessments. This study investigated the clinicopathological features and renal outcomes of DN and NDRD in type 2 diabetic patients with nephrotic-range proteinuria.</P><P>We enrolled 220 cases of type 2 diabetic patients who underwent renal biopsy. They were grouped according to the presence of nephritic-range proteinuria and pathological features. Baseline characteristics, laboratory findings, types of pathological diagnosis, and renal outcomes were analyzed in patients with heavy proteinuria.</P><P>Upon kidney biopsy, 129 patients (58.6%) showed nephritic-range proteinuria. Patients with heavy proteinuria (an average urine protein-to-creatinine ratio of 10,008 ± 7307 mg/gCr) showed lower serum albumin levels and higher total cholesterol levels, but did not show any difference in age, duration of diabetes, renal function, or the presence of retinopathy compared with those with mild-to-moderate proteinuria (an average urine protein-to-creatinine ratio of 1581 ± 979 mg/gCr). Renal biopsy revealed that the prevalence of NDRD was 37.2% in patients with heavy proteinuria, which was significantly lower than that in patients with mild-to-moderate proteinuria (63.7%). The most common pathological types of NDRD were membranous nephropathy (41.7%), IgA nephropathy (14.6%), and minimal change disease (10.4%). NDRD patients showed lower prevalence of diabetic retinopathy and better kidney function irrespective of proteinuria. Immunosuppressive treatment was administered more frequently in patients with heavy proteinuria (56.3%) compared with patients with mild-to-moderate proteinuria (20%) because of the pathological differences according to the amount of proteinuria. Renal outcomes were significantly worse in patients with DN than in patients with NDRD.</P><P>DN patients with heavy proteinuria exhibited different prevalence of NDRD and worse prognosis. Renal biopsy in type 2 diabetic patients should be more extensively considered to accurately diagnose NDRD, guide further management, and predict renal outcomes, especially in patients with nephrotic-range proteinuria.</P></▼2>

Clonal Structures of Regionally Synchronous Gastric Adenomas and Carcinomas

Jung, Seung-Hyun,Kim, Shin Young,An, Chang Hyeok,Lee, Sung Hak,Jung, Eun Sun,Park, Hyeon-Chun,Kim, Min Sung,Chung, Yeun-Jun,Lee, Sug Hyung American Association for Cancer Research 2018 Clinical Cancer Research Vol.24 No.19

<P><B>Purpose:</B> Gastric adenoma (GA) is a premalignant lesion that precedes intestinal-type gastric carcinoma (GC). However, genetic progression mechanisms from GA to GC have not been clarified.</P><P><B>Experimental Design:</B> We performed whole-exome sequencing–based mutational analyses for 15 synchronous pairs of attached GAs and GCs.</P><P><B>Results:</B> There was no significant difference in the number of driver mutations or copy-number alterations between GAs and GCs. Well-known mutations of <I>TP53, APC, RNF43,</I> and <I>RPL22</I> were recurrently detected in synchronous GA/GC pairs. In addition, we discovered novel <I>KDM6A, PREX2, FAT1, KMT2C, GLI3,</I> and <I>RPL22</I> mutations and hypermutation in GAs, but did not identify recurrent drivers for GA-to-GC progression. Clonal structure analyses revealed that most GA/GC pairs exhibit parallel evolution with early divergence rather than stepwise evolution during GA-to-GC progression. Of note, three cases were identified as clonally nonrelated GA/GC pairs despite the lack of histologic differences. We found differences in dominant mutational signatures 1, 6, 15, and 17 in GA/GC trunks, GA branches, and GC branches. Compared with our previous work on synchronous colon adenoma/carcinoma genome structures, where most drivers were in the trunk with parallel evolution, synchronous GA/GC genomes showed a different model of parallel evolution, with many drivers in the branches.</P><P><B>Conclusions:</B> The preferred sequence of mutational events during GA-to-GC progression might be more context-dependent than colon adenoma progression. Our results show that nonclonal synchronous GA/GC is common and that GA genomes have already acquired distinct genomic alterations, suggesting caution in the diagnosis of synchronous GA and GC, especially in residual or recurrent cases. <I>Clin Cancer Res; 24(19); 4715–25. ©2018 AACR</I>.</P>