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5. Functional categories of TP53 mutation in colorectal cancer: results of an International Collaborative Study

Author

Iacopetta, B., Russo, A., Bazan, V., Dardanoni, G., Gebbia, N., Soussi, T., Kerr, D., Elsaleh, H., Soong, R., Kandioler, D., Janschek, E., Kappel, S., Lung, M., Leung, C.-S.S., Ko, J.M., Yuen, S., Ho, J., Leung, S.Y., Crapez, E., Duffour, J., Ychou, M., Leahy, D.T., O'Donoghue, D.P., Agnese, V., Cascio, S., Di Fede, G., Chieco-Bianchi, L., Bertorelle, R., Belluco, C., Giaretti, W., Castagnola, P., Ricevuto, E., Ficorella, C., Bosari, S., Arizzi, C.D., Miyaki, M., Onda, M., Kampman, E., Diergaarde, B., Royds, J., Lothe, R.A., Diep, C.B., Meling, G.I., Ostrowski, J., Trzeciak, L., Guzińska-Ustymowicz, K., Zalewski, B., Capellá, G.M., Moreno, V., Peinado, M.A., Lönnroth, C., Lundholm, K., Sun, X.F., Jansson, A., Bouzourene, H., Hsieh, L.-L., Tang, R., Smith, D.R., Allen-Mersh, T.G., Khan, Z.A.J., Shorthouse, A.J., Silverman, M.L., Kato, S., and Ishioka, C.

Published
2006
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8. Abstracts

Author

Rosen, L., Reed, J., Ufberg, D., Thorburn, H., Carter, K., Goldberg, J., Finlay, I. G., Church, J. M., Hill, G. L., Carter, F. M., Cohen, Z., McLeod, R. S., Bauer, J. J., Sher, M. E., Gelernt, I. M., Crim, R. W., Fazio, V. W., Lavery, I. C., Williams, J. G., Nemer, F. D., Rothenberger, D. A., Goldberg, S. M., Hyman, N. H., Tuckson, W. B., Deutsch, A. A., Gregoire, R., Cullen, J., Johnson, G. P., Wolff, B. G., Koltun, W., Schoetz, Jr., D. J., Roberts, P. L., Murray, J. J., Coller, J. A., Veidenheimer, M. C., Keighley, M. R. B., Hosie, K., Sakaguchi, M., Tudor, R., Kmiot, W., Ambroze, Jr., W. L., Dozois, R. R., Pemberton, J. H., Kelly, K. A., Wiltz, O., Hashmi, H., Fucini, C., Thayer, M. L., Madoff, R. D., Jacobs, D. M., Bubrick, M. P., Galandiuk, S., Tsao, J., Ilstrup, D. M., Duthie, G. S., Bartolo, D. C. C., Miller, R., Pinho, M., Kunin, J. D., Fleshman, J. W., Kodner, I. J., Fry, R. D., Wexner, S. D., Jagelman, D. G., Corredor, C., Salanga, V., Scholefield, J. H., Whatrup, C., Talbot, I. C., Northover, J. M. A., Sonnex, C., Safavi, A., Gottesman, L., Dailey, T., Moenning, S., Nightengale, S., Simonton, T., Huber, P., Odom, C., Kaplan, E., Strong, S. A., Milsom, J. W., Taylor, C. W., Cho, C. C., Stewart, W. R. C., Hartmann, R. F., Khanduja, K. S., Aguilar, P. S., Rahman, S. M., Arnold, M. W., Caushaj, P., Viratyosin, S., French, T., Madoff, R., Karamjit, S., Meesig, D. M., Macleod, C. A. H., Balcos, E. G., Buls, J. G., Nelson, H., Donohue, J. H., McKean, D. J., Leu, S. Y., Wang, S. R., Hsu, H., Ramanujam, P. S., Alberts, D. S., Clark, L., Ritenbaugh, C., Rowley, S., Kane, N., Jones, C., Davies, A., Baker, P., Neoptolemos, J. P., Devereux, D. F., Robertson, F. M., Spain, D. A., Cance, W. G., Cohen, A. M., Sigurdson, E. R., Enker, W. E., Konishi, F., Yasuda, Y., Ochiai, S., Kanazawa, K., Davis, M., Medina, V., Miller, D., Fielding, L. P., Prats, I., Berman, M., West, B., Savoca, P. E., Ballantyne, G. H., Flannery, J. T., Modlin, I. M., Tsukada, K., Jagelman, D. A., McGannon, E. M., Schroeder, T., Sakamoto, G. D., MacKeigan, J. M., Opelka, F., Timmcke, A., Gathright, J. B., Hicks, T., Ray, J., McKee, C. C., Ragland, J. J., Myers, J. O., Christie, J. P., Marrazzo, III, J., Flemming, F. X., Longo, W. E., Pollard, C. W., Nivatvongs, S., Rojanasakul, A., Jetmore, A. B., Baker, J., Wiltz, O. H., McKee, R. F., Lauder, J., Poon, F., Aitchison, M., Fleshman, James W., Dreznik, Zeev, Kodner, Ira J., Fry, Robert D., Kerner, B. A., Labow, S., Hoexter, B., Moseson, M., Cheape, J. D., Bowinkelman, K., Dziki, A. J., Malthaner, R. A., Harmon, J. W., Saini, N., Duncan, M. D., Fernicola, M. T., Fischer, B. A., Hakki, F. Z., Trad, K. S., Ugarte, R., Senagore, A. J., Mazier, W. P., Kilbride, M., Herrera, L., Goumas, W., Petrelli, N., Bailey, H. R., Huval, W. V., Max, E., Smith, K. W., Marks, G., Mohiuddin, M., Basile, M., Eitan, A., Wolff, B., Dozois, R., Devine, R., Beart, R., Kelly, A., Unti, J. A., Orsay, C. P., Pearl, R. K., Nelson, R. L., Duarte, B., Prasad, M. L., Abcarian, H., Senagore, A., Milson, J. W., Strong, S., Walshaw, R. K., Chaudry, I. H., Hojo, K., Sugihara, K., Katunuma, K., Vernava, A., Beart, R. W., Stewart, J., Diament, R. H., Salter, M., Brennan, T. G., Sheikh, F., Khubchandani, I. T., Miyajima, N., Uematsu, Y., Kodaira, S., Teramoto, T., Orrom, W. J., Duthie, G., Corne, H., Blatchford, G. J., Perry, R. E., Christensen, M. A., Thorson, A. G., Dreznik, Zeev, Wong, W. D., Jensen, L. L., Lee, K. H., Yoon, Choong, Joo, H. Z., Levien, D. H., Gibbons, S., Begos, D., Byrne, D. W., Gordon, P. H., Bégin, L. R., Mitmaker, B., Saclarides, T., Bhattacharyya, A., Britton, C., Stone, J. M., Lowry, A. C., Moran, M., Launer, D. P., McReynolds, D. G., Eastman, A. B., Peck, J. J., Rozycki, G. S., Ramanujam, Paravasthu S., Bellapravalu, Sharad, Venkatesh, Kurakurachi S., Griffin, Kathleen M., Vernava, A. M., Beckman, R., Andrus, C., Johnson, F., Herrmann, V., Kaminski, D. L., Wetter, L. A., Dinneen, M., Levitt, M., Motson, R. W., Rohrer, D. A., Bapna, M. S., Rotstein, L. E., Radhakrishnan, Jayant, Shrader, Charisse, Ravo, B., Frattaroli, F. M., Reggio, D., Litchy, W. J., Hanson, R. B., Morgado, Pedro J., Alfaro, Rodrigo, Alfonzo, Rafael, Vachon, D. A., Oliver, G. C., Eisenstat, T. E., Salvati, E. P., Rubin, R. J., Clay, R. P., Kumar, Sanath, Guillem, J. G., Levy, M. F., Hsieh, L. L., Johnson, M. D., Forde, K. A., Weinstein, I. B., Bilchik, A. J., Fleming, F. X., Pernikoff, B. J., Goldenring, J. R., Fozard, J. B., Lowndes, R. H., Young, H. L., Sackier, J., Leite, J. F. M. S., Fausto-Pontes, Martins, M. I., Kmiot, W. A., Youngs, D. J., Harding, L. K., Hesselwood, S. R., Smith, N., Hartley, M. G., Hudson, M. J., Hill, M. J., Gent, A. E., Grace, R. H., Swarbrick, E. T., Hellier, M. D., Procaccino, J. A., Oakley, J. R., Flanagan, Jr., R. A., Lapos, L., Riether, R. D., Stasik, J. J., Trostle, D. R., Sheets, J. A., Ferrara, A., Armstrong, D. N., Bjorck, S., McMillen, M. A., Nicholson, J. D., Halleran, D. R., Trivisonno, D. P., Ziegler, J. A., Lott, J., Saleeby, R., Sullivan, T., and Nelson, R.

Published
1990
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9. Prognostic significance of EGFR and Her-2 in oral cavity cancer in betel quid prevalent area cancer prognosis

Author

Chen, I-H, Chang, J T, Liao, C-T, Wang, H-M, Hsieh, L-L, and Cheng, A-J

Subjects
Adult, Male, Plants, Medicinal, Receptor, ErbB-2, EGFR, Her-2, Molecular and Cellular Pathology, Taiwan, betel quid, oral cancer, Middle Aged, Prognosis, ErbB Receptors, Surveys and Questionnaires, Biomarkers, Tumor, Carcinoma, Squamous Cell, Prevalence, Humans, Female, Mouth Neoplasms, Areca, Aged
Abstract

Although several studies have found overexpression of epidermal growth factor receptor (EGFR) proteins EGFR and Her-2 in head and neck cancers, the clinical relevance of the finding varies. We examined the expression and clinical association of these molecules with oral squamous cell carcinoma in an area where betel chewing is prevalent. EGFR and Her-2 proteins were measured in 59 paired (grossly normal and cancer) tissues by an enzyme immunoassy method. The cutoff value for gene overexpression was defined as the level of mean expression in normal tissue plus two s.d. A total of 59% of the patients consumed alcohol, 90% smoked tobacco, and 90% chewed betel quid. Of the patients assayed, 34 (58%) and 24 (41%) had EGFR and Her-2 overexpression, with average 3.5- and 1.5-fold elevations. EGFR overexpression has been shown to be statistically associated with T stage, N stage, overall TMN stage, primary tumour depth, lymph node extra-capsular spread, and poor survival. Her-2 overexpression, however, did not demonstrate a similar association with clinicopathological parameters or therapeutic outcome. On multivariant analysis, EGFR overexpression (P=0.041) and N stage (P=0.024) were the only independent factors for overall survival. These results indicate that the molecular targeting therapy to EGFR may be a treatment for oral cavity cancer in the betel quid-chewing prevalent area.

Published
2003

10. Metabolic gene polymorphism frequencies in control populations

Author

Garte, S., Gaspari, L., Alexandrie, A. K., Ambrosone, C., Autrup, H., Autrup, J. L., Baranova, H., Bathum, L., Benhamou, S., Boffetta, P., Bouchardy, C., Breskvar, K., Brockmoller, J., Cascorbi, I., Clapper, M. L., Coutelle, C., Daly, A., Omo, M., Dolzan, V., Dresler, C. M., Fryer, A., Haugen, A., Hein, D. W., Hildesheim, A., Hirvonen, A., Hsieh, L. L., Ingelman-Sundberg, M., Kalina, I., Kang, D., Kihara, M., Kiyohara, C., Kremers, P., Lazarus, P., Le Marchand, L., Lechner, M. C., Lieshout, E. M., Stephanie London, Manni, J. J., Maugard, C. M., Morita, S., Nazar-Stewart, V., Noda, K., Oda, Y., Parl, F. F., Pastorelli, R., Persson, I., Peters, W. H., Rannug, A., Rebbeck, T., Risch, A., Roelandt, L., Romkes, M., Ryberg, D., Salagovic, J., Schoket, B., Seidegard, J., Shields, P. G., Sim, E., Sinnet, D., Strange, R. C., Stucker, I., Sugimura, H., To-Figueras, J., Vineis, P., Yu, M. C., and Taioli, E.

Subjects
Polymorphism, Genetic, Metabole aspecten van maag-, darm- en leveraandoeningen, Cytochrome P-450 Enzyme System, Databases, Factual, Gene Frequency, Genetic Linkage, Neoplasms, Black People, Humans, Metabolic aspects of gastrointestinal diseases, Genetic Predisposition to Disease, White People
Abstract

Item does not contain fulltext Using the International Project on Genetic Susceptibility to Environmental Carcinogens (GSEC) database containing information on over 15,000 control (noncancer) subjects, the allele and genotype frequencies for many of the more commonly studied metabolic genes (CYP1A1, CYP2E1, CYP2D6, GSTM1, GSTT1, NAT2, GSTP, and EPHX) in the human population were determined. Major and significant differences in these frequencies were observed between Caucasians (n = 12,525), Asians (n = 2,136), and Africans and African Americans (n = 996), and some, but much less, heterogeneity was observed within Caucasian populations from different countries. No differences in allele frequencies were seen by age, sex, or type of controls (hospital patients versus population controls). No examples of linkage disequilibrium between the different loci were detected based on comparison of observed and expected frequencies for combinations of specific alleles.

Published
2001

24. p53 polymorphisms associated with mutations in and loss of heterozygosity of the p53 gene in male oral squamous cell carcinomas in Taiwan.

Author

Hsieh, L.-L., Huang, T.-H., Chen, I.-H., Liao, C.-T., Wang, H.-M., Lai, C.-H., Liou, S.-H., Chang, J. T.-C., and Cheng, A.-J.

Subjects
*GENETIC mutation, *GENETICS, *SQUAMOUS cell carcinoma, *CANCER invasiveness, *CANCER patients
Abstract

The present study was designed to examine whether different p53 haplotypes of exon 4-intron 3-intron 6 affect the frequency of mutations and loss of heterozygosity (LOH) of the p53 gene in male oral squamous cell carcinomas (OSCCs) in Taiwan. We found that individuals without two Pro-W-G alleles had significantly higher frequency of p53 mutations than those with two Pro-W-G alleles (odds ratio (OR)=1.98; 95%confidence interval (CI), 1.10-3.56). Out of the 172 p53 gene exon 4 informative male OSCCs, 72 (41.9%) showed LOH. Among these 72 OSCCs with LOH, the frequency of Pro allele loss was 73.6%(53/72). It is notable that alcohol drinking increased the frequency of Arg allele loss (OR=10.56; 95%CI, 1.23-234.94) in OSCCs from patients who both smoked cigarettes and chewed areca quid (AQ). The frequency of LOH of p53 was not different between p53-mutated OSCCs and p53-normal OSCCs. Thus, the present study revealed that (a) the Arg allele is associated with p53 mutations, (b) the Pro allele is preferentially lost in OSCCs associated with cigarette smoking and AQ chewing, while the frequency of Arg allele loss is increased with alcohol drinking, and (c) haploinsufficiency of p53 is in itself likely to contribute to tumour progression in Taiwanese OSCCs.British Journal of Cancer (2005) 92, 30-35. doi:10.1038/sj.bjc.6602271 www.bjcancer.com Published online 7 December 2004 [ABSTRACT FROM AUTHOR]

Published
2005
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25. Association between Genetic Polymorphism of Tumor Necrosis Factor-α and Risk of Oral Submucous Fibrosis, a Pre-Cancerous condition of Oral Cancer.

Author

Chiu, C.-J., Chiang, C.-P., Chang, M.-L., Chen, H.-M., Hahn, L.-J., Hsieh, L.-L., Kuo, Y.-S., and Chen, C.-J.

Subjects
PRECANCEROUS conditions, FIBROSIS, ORAL cancer, TUMOR necrosis factors, GENETIC polymorphisms, CYTOKINES
Abstract

Many cytokines have been thought to play important roles in the pathogenesis of oral submucous fibrosis (OSF), an areca nut chewing-specific pre-cancerous condition characterized by the deposition of collagen in oral submucosa. Tumor necrosis factor-α (TNF-α), situated in the class III region of human leukocyte antigen (HLA), is a mediator with multiple functions, including the regulation of inflammatory reaction and transcriptions of collagen and collagenase. In total, 809 male subjects were recruited for assessment of the association of OSF with a bi-allelic promoter-region (-308) polymorphism on the TNFA gene. The high production allele, TNF2, was significantly lower among OSF subjects (n =166) than in areca-chewing controls (n = 284). This association was independent of oral cancer status. The multivariate-adjusted odds ratio for the TNFA 11 genotype was 2.6 (95% confidence interval = 1.4-4.9; p = 0.004). The finding may imply a multifunctional etiological factor of TNF-α in OSF pathogenesis. [ABSTRACT FROM AUTHOR]

Published
2001
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26. Hepatocellular carcinoma associated with focal nodular hyperplasia. Report of a case with clonal analysis.

Author

Chen, Tse-Ching, Chou, Tze-Bin, Ng, Kwai-Fong, Hsieh, Ling-Ling, Chou, Yah-Huei, Chen, T C, Chou, T B, Ng, K F, Hsieh, L L, and Chou, Y H

Abstract

We describe a hepatocellular carcinoma partially surrounded by focal nodular hyperplasia in a 65-year-old female patient. In order to clarify the relationship of the hepatocellular carcinoma and the adjacent focal nodular hyperplasia, clonal analysis was conducted. The clonal analysis was based on the methylation pattern of the polymorphic X-chromosome-linked androgen receptor gene (HUMARA). The allelic bands from the amplification of the focal nodular hyperplasia and of the hepatocellular carcinoma showed a significant reduction in the intensity of one of the two alleles as compared with two alleles of equal intensity in the buff coat after HhaI digestion, which indicated that these two parts were monoclonal. However, the inactivated allele in the focal nodular hyperplasia and that in the hepatocellular carcinoma were not identical. Therefore, the focal nodular hyperplasia and hepatocellular carcinoma probably derived from the clonal expansion of two different clones. [ABSTRACT FROM AUTHOR]

Published
2001
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27. Hepatocellular carcinoma complicated with coexisting hepatolithiasis: pitfalls in diagnosis and management.

Author

Yeh, Ta-Sen, Chen, Tse-Ching, Hsieh, Ling-Ling, Jan, Yi-Yin, Jeng, Long-Bin, Hwang, Tsang-Long, Chen, Miin-Fu, Yeh, T S, Chen, T C, Hsieh, L L, Jan, Y Y, Jeng, L B, Hwang, T L, and Chen, M F

Abstract

Nineteen patients with hepatocellular carcinoma associated with hepatolithiasis were retrospectively analyzed. Eleven of the 19 patients presented with hepatolithiasis-related biliary infection. Diagnosis was erroneously assumed to be hepatolithiasis alone, liver abscess, or cholangiocarcinoma in five of 11 patients before surgery was attempted. Middle-age, male sex, liver cirrhosis, hepatitis B or C infection, abnormal alpha-fetoprotein, and negative carcinoembryonic antigen raised the suspicion of associated hepatocellular carcinoma rather than cholangiocarcinoma in patients with hepatolithiasis. Antibiotics and nonoperative methods to resolve biliary infection first, followed by hepatectomy, in selected cases, to eradicate hepatocellular carcinoma and hepatolithiasis simultaneously provides the best chance for long-term survival. Otherwise, patients often died of hepatolithiasis-related biliary sepsis rather than hepatocellular carcinoma per se in the long run. [ABSTRACT FROM AUTHOR]

Published
1998
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37. Metabolic gene polymorphism frequencies in control populations

Author

Garte, S., Gaspari, L., Alexandrie, A. -K, Rannug, A., Ingelman-Sundberg, M., Persson, I., Ambrosone, C., Autrup, H., Autrup, J. L., Baranova, H., Bathum, L., Boffetta, P., Breskvar, K., Dolzan, V., Brockmoller, J., Cascorbi, I., Clapper, M. L., Dresler, C. M., Coutelle, C., Daly, A., Dell’omo, M., Fryer, A., Strange, R. C., Haugen, A., Ryberg, D., Hein, D. W., Hildesheim, A., Hirvonen, A., Hsieh, L. -L, Kalina, I., Salagovic, J., Daehee Kang, Kihara, M., Noda, K., Kiyohara, C., Kremers, P., Roelandt, L., Lazarus, P., Le Marchand, L., Lechner, M. C., Lieshout, E. M. M., Peters, W. H. M., London, S., Manni, J. J., Maugard, C. M., Morita, S., Nazar-Stewart, V., Oda, Y., Parl, F. F., Pastorelli, R., Rebbeck, T., Risch, A., Romkes, M., Schoket, B., Seidegard, J., Shields, P. G., Sim, E., Sinnet, D., Sugimura, H., To-Figueras, J., Vineis, P., Yu, M. C., and Taioli, E.

42. Dosimetry study of diagnostic X-ray using doped iodide normoxic polymer gels.

Author

Huang, Y. R., Chang, Y. J., Hsieh, L. L., Liu, M. H., Liu, J. S., Chu, C. H., and Hsieh, B. T.

Subjects
*RADIATION dosimetry, *X-ray imaging, *IODIDES, *POLYMER colloids, *DIAGNOSTIC imaging, *RADIOTHERAPY
Abstract

In radiotherapy, polymer gel dosimeters are used for three-dimensional (3D) dose distribution. However, the doses are within the Gy range. In this study, we attempted to develop a low-dose 3D dosimeter within the mGy range for diagnostic radiology. The effect of the iodinated compound was used as a dose enhancement sensitizer to enhance the dose sensitivity of normoxic polymer gel dosimeters. This study aims to use N -isopropylacrylamide(NIPAM)-based and methacrylic acid (MAGAT)-based gels to evaluate the potential dose enhancement sensitizer, as well as to compare two gels that may be suitable for measuring diagnostic radiation doses. The suitable formulation of NIPAM gel [5% (w/w) gelatin, 5% (w/w) NIPAM, 3% (w/w) N , N ′-methylenebisacrylamide (BIS), 5 mM tetrakis (hydroxymethyl) phosphonium chloride (THPC), and 87% (w/w) deionized distilled water] and MAGAT gel (4% MAA, 9% gelatin, 87% deionized water, and 10 mM THPC) were used and loaded with clinical iodinated contrast medium agent (Iobitridol, Xenetix ® 350). Irradiation was conducted using X-ray computed tomography. The irradiation doses ranged from 0 mGy to 80 mGy. Optical computed tomography was the employed gel measurement system. The results indicate that the iodinated contrast agent yields a quantifiable dose enhancement ratio. The dose enhancement ratios of NIPAM and MAGAT gels are 3.35±0.6 and 1.36±0.3, respectively. The developed NIPAM gel in this study could be suitable for measuring diagnostic radiation doses. [ABSTRACT FROM AUTHOR]

Published
2014
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46. MMP-1(-1607G) polymorphism as a risk factor for fibrosis after pulmonary tuberculosis in Taiwan.

Author

Wang CH, Lin HC, Lin SM, Huang CD, Liu CY, Huang KH, Hsieh LL, Chung KF, and Kuo HP

Subjects
Adult, Aged, Antitubercular Agents therapeutic use, Female, Fibrosis, Follow-Up Studies, Humans, Male, Matrix Metalloproteinase 12 genetics, Matrix Metalloproteinase 9 genetics, Middle Aged, Polymorphism, Genetic, Prospective Studies, Risk Factors, Time Factors, Tuberculosis, Pulmonary drug therapy, Genetic Predisposition to Disease, Lung pathology, Matrix Metalloproteinase 1 genetics, Tuberculosis, Pulmonary complications
Abstract

Setting: Several matrix metalloproteinase (MMP) polymorphisms favouring the development of lung fibrosis after pulmonary tuberculosis (TB) have been described., Objective: To investigate the association of MMP-1, MMP-9 and MMP-12 polymorphisms with the development of fibrosis in pulmonary TB., Design: We studied 49 normal subjects and 98 TB patients. We analysed the association between MMP polymorphisms and clinical indices of lung fibrosis by serial chest radiography for 1 year after completion of treatment., Results: The frequency of the MMP-1(-1607G) polymorphism was significantly higher in TB patients with moderate to advanced pulmonary fibrosis than in those with minimal to mild fibrosis. Having at least one -1607G MMP-1 polymorphism increased the risk of moderate and advanced fibrosis respectively by 5.04 (95%CI 1.25-20.30) and 9.87 (95%CI 2.39-40.88) fold. There was no association of MMP-9(-1562T) and MMP-12(Asn357Ser) polymorphisms with lung fibrosis. The production of MMP-1 from monocytes stimulated by interleukin-1 beta was increased in subjects with the 1G allele genotype compared to the 2G/2G genotype., Conclusions: Patients with MMP-1(-1607G) polymorphism are more vulnerable to more extensive lung fibrosis 1 year after anti-tuberculosis treatment. This may be related to increased MMP-1 activity, leading to enhanced destruction of the matrix with subsequent fibrosis.

Published
2010

47. Humoral response to p53 in human colorectal tumors: a prospective study of 1,209 patients.

Author

Tang R, Ko MC, Wang JY, Changchien CR, Chen HH, Chen JS, Hsu KC, Chiang JM, and Hsieh LL

Subjects
Adult, Aged, Colorectal Neoplasms pathology, Female, Humans, Lymphatic Metastasis, Male, Middle Aged, Prospective Studies, Antibodies blood, Colorectal Neoplasms immunology, Tumor Suppressor Protein p53 immunology
Abstract

p53 Antibodies (p53-Abs) have been detected in the serum of a proportion of colorectal cancer (CRC) patients. It is not yet known at which stage during colorectal tumor progression p53-Abs appear in the serum. The utility of these antibodies as markers for CRC prognosis remains to be clarified. Using a quantitative enzyme-linked immunosorbent assay, we analyzed serum samples from 998 CRC patients and from 211 patients with polyp. Levels of p53-Abs were defined as negative (<10 U/microL), low (10-76 U/microL) and high (>76 U/microL). Overall, 13.0% of CRC patients and less than 1% of polyp patients had increased serum p53-Ab levels. High p53-Ab levels were only seen in patients with invasive carcinomas. The parameters that were significantly and independently associated with a greater frequency of high p53-Ab levels were the left colon (odds ratio [OR] = 3.4; 95% CI = 1.1-10.5), the rectum (OR = 2.9; 95% CI, 1.0-8.8) and advanced lymph node metastasis (OR = 4.6; 95% CI, 2.2-9.6). In univariate analysis, patients with high p53-Ab levels had a shorter survival times than did those without (p = 0.007). However, the significant effect disappeared in a Cox regression model adjusting for sex, age, tumor location, carcinoembryonic antigen levels, gross findings, histologic grade, mucin production and TNM stage. Thus, autoantibodies against p53 occur with tumor progression in multistep colorectal carcinogenesis and increase with advanced node metastasis. Furthermore, the seemingly adverse effect of high p53-Ab levels on the survival of CRC patients may be explained by other prognostic factors., (Copyright 2001 Wiley-Liss, Inc.)

Published
2001
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48. Association of aflatoxin B(1)-albumin adduct levels with hepatitis B surface antigen status among adolescents in Taiwan.

Author

Chen SY, Chen CJ, Chou SR, Hsieh LL, Wang LY, Tsai WY, Ahsan H, and Santella RM

Subjects
Adolescent, Aflatoxin B1 urine, Female, Hepatitis B, Chronic epidemiology, Humans, Linear Models, Male, Taiwan, Aflatoxin B1 metabolism, Albumins metabolism, DNA Adducts blood, Hepatitis B Surface Antigens blood, Hepatitis B, Chronic blood
Abstract

Chronic hepatitis B virus (HBV) infection and aflatoxin B(1) (AFB(1)) exposure interact synergetically to induce hepatocellular carcinoma. One suggested mechanism for this interaction is the enhanced activation of AFB(1) in chronically HBV-infected individuals. Whereas no associations between chronic HBV infection and AFB(1)-albumin adducts were observed in several studies in adults, hepatitis B surface antigen (HbsAg)-positive children were found to have elevated adducts in Gambia. To assess the association between chronic HBV infection and AFB(1)-albumin adduct level in Taiwan, 200 junior high school adolescents from 20 townships were assayed for HBsAg and AFB(1)-albumin adducts. The mean AFB(1)-albumin adduct level was higher in HBsAg-positive compared with HBsAg-negative subjects. The association between HBsAg status and AFB(1)-albumin adducts remained after multivariate adjustment. This finding additionally supports the synergetic interaction between HBV and AFB(1), but the mechanism remains to be elucidated.

Published
2001

49. Intraductal papillary neoplasia of the liver associated with hepatolithiasis.

Author

Chen TC, Nakanuma Y, Zen Y, Chen MF, Jan YY, Yeh TS, Chiu CT, Kuo TT, Kamiya J, Oda K, Hamaguchi M, Ohno Y, Hsieh LL, and Nimura Y

Subjects
Adult, Aged, Female, Humans, Male, Metaplasia, Middle Aged, Carcinoma, Intraductal, Noninfiltrating pathology, Carcinoma, Papillary pathology, Lithiasis pathology, Liver Diseases pathology, Liver Neoplasms pathology
Abstract

Intraductal papillary growth of neoplastic biliary epithelia with a fine fibrovascular stalk (intraductal papillary neoplasia of liver [IPN-L]) resembling intraductal papillary mucinous neoplasm of pancreas is occasionally associated with hepatolithiasis. In this study, 136 cases of hepatolithiasis in Taiwan, between January 1998 and March 2000, and an additional 21 cases of IPN-L before December 1998, were examined histologically. IPN-L was found in 41 of 136 hepatolithiasis cases (30.1%). Sixty-two IPN-L cases (42 women and 20 men; age range, 59.8 +/- 10 years) were divided into 4 types (type 1, IPN-L with low-grade dysplasia, 23 cases; type 2, IPN-L with high grade dysplasia, 11 cases; type 3, IPN-L with in situ and microinvasive carcinoma, 13 cases; and type 4, IPN-L of types 2 and 3 with distinct invasive carcinoma, 15 cases). Intraductal spreading and glandular involvement were commonly observed in all types. About half of types 3 and 4 cases had mucobilia, and mucinous carcinoma was variably found in two thirds of group 4 patients. IPN-L frequently showed variable gastroenteric differentiation such as goblet cells and foveolar and colon-like metaplasia. IPN-L with goblet cells and colon-like metaplasia was frequently associated with overproduction of mucin and mucobilia (P <.01). In Japan, IPN-L was not frequent in hepatolithiasis (12 of 135 cases). In conclusion, IPN-L forms a spectrum of biliary neoplasm in hepatolithiasis. It often displays variable gastroenteric metaplasia and significant intraductal spread. IPN-L tends to progress to mucinous carcinoma. Formerly reported "mucin-producing intrahepatic cholangiocarcinoma" with a favorable prognosis is included in IPN-L.

Published
2001
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50. Further characterization of apolipoprotein B genetic variations in Taiwanese.

Author

Wu JH, Lee YT, Hsu HC, Hsieh LL, Wen MS, Chern MS, and Wu D

Subjects
Analysis of Variance, Case-Control Studies, Female, Humans, Lipids blood, Male, Middle Aged, Taiwan, Apolipoproteins B genetics, Coronary Disease genetics, Polymorphism, Genetic
Abstract

Apolipoprotein B (apoB, protein; APOB, gene) is the main protein component of low-density lipoprotein (LDL) and plays an important role in blood lipid metabolism. Previously, we have reported four APOB coding regions, 5' signal peptide, and 3' repeat sequence polymorphisms in our population. In this report, we further characterize other APOB genetic variations. The results illustrate that the mutation frequencies for Arg3500Gln (1/846 alleles), Arg4019Trp (2/786 alleles), -265 C/T promoter region (0/264 alleles), and intron 2 A/G (0/450 alleles) are very low. Our population showed a frequency of 68.9% for the B4311 Ser allele. The B4311 Asn allele was associated with a higher apoB level than the Ser group (p < 0.05) in normal controls. In the normal controls, a higher B4311 Asn/Asn genotype frequency was found in the group with total cholesterol (TC) > 200 mg/dL and apoB concentration > 85 mg/dL than in the group with a TC < 200 mg/dL and apoB < 85 mg/dL (p = 0.03 for TC comparison).

Published
2001
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