Evans 증후군 1례

장성익,이의재,황성수,이경일,이원익,이준성 최신의학사 1990 最新醫學 Vol.33 No.1

Sister Chromatid Exchange(SCE)의 意義

張性翼,朱剛 慶北大學校 醫科大學 1982 慶北醫大誌 Vol.23 No.1

사람의 임파구를 배양하여 BudR 10㎍/㎖와 Hoechst 33258 50㎍/㎖로 처리하여 Giemsa 염색한 결과 전염색체에서 SCE가 나타났다. Sister chromatid exchange (SCE) events which previously have been detected by autoradiography can now be detected by BudR with Hoechst 33258 technique. SCE has been proved to the highly sensitive index of the interaction of carginogens with chromosomes, and abnormalities related to SCE formation occurred in a number of hereditary diseases known or suspected to involve a defect in DNA repair. Blood leukocytes were cultured according to conventional methods. BudR (10㎍/㎖) was added to culture medium 3 hours before colchicine treatment. The lymphocytes incorporated with BudR were stained in Hoechst 33258 and followed Giemsa stain. The result obtained is that SCE seems to be found out on all the chromosomal numbers including sex chromosome.

Significance of Cancer Cytogenetics

장성익 啓明大學校 醫科大學 1989 계명의대학술지 Vol.8 No.2

마우스 부신피질의 Cell Cycle과 Cell Displacement

장성익,주강 대한해부학회 1976 Anatomy & Cell Biology Vol.9 No.1

퍼지 프로세서의 추론부에 관한 연구 ( A Study on the Inference Block of the Fuzzy Processor )

장성익,정재경,김원찬,이충웅 대한전자공학회 1991 대한전자공학회 학술대회 Vol.1991 No.11

암의 세포유전학

장성익 啓明大學校 醫科大學 1991 계명의대학술지 Vol.10 No.1

Now, cancer is a disease of gene which can be classified to somatic cell genetic diseases. Cancer might be resulted from a relative genetic insufficiency to tolerate carcinogen exposure in major oncoderm. The balance between exogenous stimulus(carcinogen exposure) and constitutional responce(capacity to resist or repair mutational damage) is altered in favor of the DNA- damaging tendency, and cancer develops. It has been found that the cancer-relevant genes were located on the specific regions of chromosomes. Specific chromosome abnormalities were discovered in leukemia and malignant lymphoma. However, most of solid tumours were not still investigated in specific karyotypes for the specific cancers. Oncogenes are corelated to sites of translocations on the chromosome and antioncogenes are corelated to locus of deletions on the chromosome in cancer cells. Aneuploidy is a phenomenon of cancer progressing which is revealed on the secondary change of mitosis. Recently multistep oncogenesis theory which is concerned with oncogenes, antioncogenes and genomes of the chromosomes has been attractive point of view in explanstion of cancer developing. To understand this hypothesis investigators should approach to cytogenetics. Cancer cytogenetics, even still obscure, may be applied to clinical diagnosis or prediction of prognosis from the patient. I believe that analysis of karyotypes can predict the cancer susceptability from normal state of individuals in the future.

위암의 세포유전학적 분석

김홍태,장성익 啓明大學校 醫科大學 1993 계명의대학술지 Vol.12 No.4

To investigate the common specific chromosomal abnormalities of the stomach cancer in Korea, cytogenetic analysis was performed on four primary and one case of lymph node metastatic gastric carcinomas. Hypodiploidy or diploidy were found, however the nonclonal metaphases revealed random loss or gain of one or several different chromosomes in primary cases. In the metastatic case variable numerical and structural chromosomal abnormalities were found. Nonrandom numerical abnormalities were monosomy on chromosome 7 and 18, and loss of Y chromosme, however hyperdiploidy pattern were found in metastatic case. The nonrandom clone in metastatic case had following structural abnormalities del(1)(q41), dup(1q), 3q+,del(5)(p14), 14p+, 15p+. The common specific chromosomal abnormalities were not found especially in primary cases. In summary, it is presumed that chromosome changes are different by individuals in gastric cancer. So it suggests that mechanism of oncogenesis may be related by personal.

Human Herpes Virus 6(HHV-6)의 변형유전자의 특성과 위치

최동호,이인환,김홍태,최인장,장성익 啓明大學校 醫科大學 1994 계명의대학술지 Vol.13 No.2

HIV-1 virus와 동반적 감염을 일으키고 AIDS의 진행에 관여하며 다른 AIDS와 관련된 종양형성에 관여할 것으로 의심되는 HHV-6 변형유전자의 위치 및 특성을 알기위하여 변형유전자를 포함한다고 의심되는 DNA분절(Sal 1-L)을 Xbal, BamH1, Hind Ⅲ, Nhel, BstX1의 효소를 절단하여 6가지의 subclone을 얻고 이것을 NIH3T3 세포, CV-1 세포, HUVE 세포에 도입하여 focal assay, anchorage independency test, nude mice에서 tumorigenicity를 조사하고 HIV-LTR과의 상호관계를 조사한 결과를 요약하면 HHV-6의 Sal 1-L의 subclone인 Sal 1-L-SH(1.0kb)를 NIH 3T3, CV-1 및 HUVE에 transfrection하였을 경우 NIH 3T3 및 CV-1 세포배양에서 focus 형성을 보았으며 이것을 cylinder를 이용한 focus cloning을 하고 hygromycin으로 plasmid DNA가 transfection만 된 세포들을 모아(selection) soft agar assay 및 cell aggregation으로 anchorage independency를 확인하였다. Nude mice에 접종하여 종양 형성을 관찰하였으며 이 종양 세포에서 DNA를 추출하여 Southern blot hybridization으로 insert DNA(Sal 1-L-SH)에 기인한 종양임을 알았다. 이로써 HHV-6의 Sal 1-L-SH fragment내에 변형유전자가 포함되어 있음이 확인되었다. 그러나 사람의 혈관내피세포(HUVE)에서는 focus등의 형태학적 변화가 보이지 않았으며 또 HIV-TAT 및 HIV-LTR 등과의 복합적 세포내 도입에서도 세포변형은 얻을수가 없어 Kaposi씨 육종이 혈관 내피세포에서 기인하지 않거나 이 종양셩성에 HHV-6 외의 다른 인자가 관여할 것으로 생각된다. 한편 HIV-LTR CAT과 Sal 1-L-SH 유전자를 같이 transfection하여 CAT assay를 하였을 경우 HIV-LTR의 표현 즉 acetylation이 15배나 항진되어 HHV-6의 Sal 1-L-SH fragment AIDS의 진행을 transactivation으로 촉진시킬 것으로 짐작된다. 더욱이 DNA sequence에 의해 이 유전자가 3개의 ORF를 가지고 있으며 이중 ORF-1에 해당하는 283aa의 polypeptide가 transactivation을 유발시키는 중심단백질로 추정된다. 이에 따라 이 단백질에 대한 항체로 종양의 HHV-6 관련유무를 판단할 수 있을것으로 생각되며 이 단백질을 직접 세포내 도입하여 세포의 변형 등을 추구하여야 할 것으로 생각된다. HHV-6 was isolated in 1986 from patients suffering from lymphoproliferative disorders and AIDS. The antibodies directed against HHV-6 indicate a previous viral infection in 80~90% of the general population. HHV-6 isolates have been divided into two distinct subgroups(subgroup A and B) based on restriction enzyme profiles, prevalence in the population, and their in vitro ability to grow in cultured cells. Subgroup A strain(strains GS and U1102) is correlated with lymphoproliferative disorders. HHV-6 has also been associated with human several malignanicies. The association between HHV-6 and human cancer might be strengthened if other fragments representing different regions of the genome with demonstrated transforming potential were also used for these analyses. These associations have led to the analysis of genomic HHV-6 DNA and cloned restriction fragments(Sal 1-L-SB, -SH, -BN, -BS, -HS, -NS) for their ability to transform cells in vitro. A 4.1-kb Sall-L fragment which exhibited transforming activity was identified. This fragment was retained in focal and tumor-derived cell lines. In addition, the Sal 1-L fragment was shown to transactivate the HIV-1 LTR. Initial experiments have co-localized both the transforming and transactivation activities to a 1.9kb Sall-L-SH fragment and implicate a 283-aa ORF as the functional element. Moreover, the identification of a transforming and transactivation region in HHV-6 has strengthened the association of HHV-6 as a co-factor in AIDS and AIDS-related malignancies.

위암의 세포유전학적 분석

정용욱,장성익 啓明大學校 醫科大學 1994 계명의대학술지 Vol.13 No.4

In order to find out the specific chromosomal abnormalities of the gastric adenocarcinoma in Korea, author investigated one primary and two cell lines of gastric cancer with G-banding technique. All tumor cells had clonal chromosomal abnormalities : total 101 numerical and 25 structural karyotypic abnomalies were identified. The most prominent and recurring numerical abnonormalities were trisomy 1, 2, 3, 6, 9, 10, 16, X and tetrasomy 1, 7, 9, 18, 20, 21 and recurrent structural abnormalities were del(1) (q32 →qter), del(1)(p34 →qter), del(3)(p25 →qter), der(4)(4 : 1)(q32 : qter), del(10)(p13 →pter) del(X)(p22). The above results of wide variety of karyotyping in stomach cancer cells indicate that these are general due to secondary changes rather than primary changes specific to stomach cancer cells and also the break at bands 1p34, 2p24, 3p25, 4p14, 5q34, 6p11, 8q24, 11p15, 11q23 give rise to the deletion of cellular oncogenes fgr, src-2, N-myc, rafl, raf2, fms, K-rasl, myc, abl, H-ras1.

B형 간염 virus 양성 간암과 음성 간암의 세표유전학적 차이

김홍태,백상헌,장성익 啓明大學校 醫科大學 1993 계명의대학술지 Vol.12 No.4

To a better understanding for molecular mechanism of oncogenesis in hepatoma, primary hepatocellular carcinoma and hepatoma cell lines(Hep 3B, PLC/PRF/5, Hep G2) were subjected to detailed cytogenetic analysis with G-banding method after cell cultures. No cloned chromosomal abnormalities were found in the primary hepatoma(below 10%). On the other hand, all hepatoma cell lines were cloned, the specific chromosomal abnormalities in Hep 3B were del(1p21), del(6q14) and t(1 : 11) (p11 : q13). Gen of AMYLA, CGA, SEA and HSTFl were located on 1p21 and 6q14 respectively. SEA and HSTFl were located on 11q13. Regions of chromosome abnormalities in PLC / PRF / 5 were the same found in Hep 3B. Besides, del(1q32) and del(1p32) were also cloned. Gene of CRl and MYCLl were located on 1q32 and 1p32 respectively. The characteristic findings of chromosome abnormalities in Hep G2 were del(1p31) and del (1q22). And GSTl and DAF were located on these regions each other. Del(6q11) and del(1p22) were also found in Hep G2. From the above results, it is presumed that HBV may integrate to AMYlA gene or near this gene and leads to ioss of functions to this gene. And impaired regulation of CGA occurs in next step. SEA, HSTFl and MYCLl oncogenes may act as a progressing factor of tumourgenesis in HBsAg(+) hepatoma, Some factors like chemical agents may cause functional loss of GSTl and DAF at first and functional loss of cell regulation of CGA occurs in next step. SKI oncogene may promote the progression of carinogenesis in this cell line. Whether any causative agents are involed in carcinogenesis of hepatoma, fuctional loss of CGA gene is the most important factor in tumour-genesis in hepatoma.