2009 Vienna - European Society of Human Genetics

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Cancer genetics versity of Mashhad, Mashhad, Islamic Republic of Iran. BMI1, a Polycomb group repressor protein, represses the genes that induce cellular senescence and cell death, and it can contribute to cancer when improperly expressed. We aimed to evaluate the expression and tissue distribution of BMI1 in bladder tumors. Tissue specimens containing bladder tumor were evaluated and compared with intact tissues from tumor margins and normal bladders. Tumor specimens of patients with transitional cell carcinoma of the bladder, and tumorfree tissues taken from the margin of the tumors were obtained and tested for the expression of BMI1 gene and protein. Specific primers for BMI1 and B2M (as an internal control) were used for reverse transcript polymerase chain reaction technique. The production and distribution of BMI1 protein was also examined by immunohistochemistry and western blotting techniques. Polymerase chain reaction generated a 683-bp product, corresponding to the expected size of BMI1 amplified region. The identity of the amplified fragment was then confirmed by direct DNA sequencing. The mean of expression of BMI1 detected in tumor tissues was significantly higher than that in intact tissues, and there was also a significant association between the mean of gene expression and the stage of malignancy (P < .001). The expression of BMI1 at protein level was further confirmed by western blotting and immunohistochemistry. BMI1 is a potent repressor of retinoblastoma and p53 pathways, and hence, elucidating its role in tumorigenesis is very important. We reported for the first time the expression of BMI1 and its correlation with incidence and progress of bladder tumors. P06.010 the role of the CYP A , GSTM , GSTP gene polymorphisms in formation of predisposition to bladder cancer A. A. Izmailov1 , S. Izmailova1 , L. Akhmadishina2 , T. V. Victorova1 , V. Pavlov1 ; 1 2 Bashkortostan State Medical University, Ufa, Russian Federation, Institute of Biochemistry and Genetics, Ufa, Russian Federation. Bladder cancer is a wide spread oncological disease with numerous risk factors. Such factors include cancinogens of tobacco smoke, polyaromatic hydrocarbons and other substances, collectively named xenobiotics. Xenobiotics become active in hypersensitive organisms, sensitivity of which is formed under a specific genetic background. That is the reason for the importance of studying peculiarities of genetic systems, which take part in detoxication of xenobiotics. To detect associations of polymorphisms of the P450 cytochrome (CYP1A1(Ile462Val)) and glutathione-S-transferases (GSTM1(del), GSTP1(Ile105Val)) genes in formation of predisposition to bladder cancer we genotyped 145 patients (77 patients had surface form, and 68 had invasive form of this desease) and 241 controls by PCR-RFLP analysis. All individuals were citizens of the Republic of Bashkortostan selected on the basis of age, sex and ethnicity. That genotypes Ile/Val of CYP1A1 gene (OR=8.6, p=0.0005), Val/Val of CYP1A1 we found gene (OR=7.8, p=0.006), Val/Val of GSTP1 gene (OR=3.3, p=0.01) were significantly associated with bladder cancer. A positive association were found between a CYP1A1 Val/Val genotype, a GSTP1 Val/Val genotype and urinary bladder carcinoma invasive forms (OR=10.9, p=0.01 и 5.2, p=0.01 respectively). There were no differences in GSTM1 gene deletion frequency distribution groups in both. The data shown that polymorphisms of the P450 cytochrome and glutathione-S-transferases can be important components of the genetic structure of predisposition to the development of cancerous neoformations. P06.011 investigation of cytochrome P-450 Polymorphisms in turkish Bladder cancer Patients K. Incekara, N. Ersoy; Halic University, Istanbul, Turkey. Bladder cancer is the fourth most common cancer in men and the seventh in women globally. Well-known etiological risk factors are occupational exposure to certain carcinogens and cigarette smoking. It is thought that the interaction between genetic factors and the environment accounts for the different levels of susceptibilities to the development of bladder cancer. The cytochrome P-450 (CYP) superfamily of enzymes catalyses one of the first steps in the metabolism of carcinogens such as polycyclic aromatic hydrocarbons, nitroaromatic compounds and arylamines. This enzyme system is highly polymorphic and these polymorphisms within CYP genes have been found to be associated with many cancer types. In addition, frequency of CYP polymorphisms shows ethnic variations among populations, so it necessitates population based studies. In this study, CYP1A1 (m1, m2, m3, m4), CYP1B1 (Leu432Val), CY- P2D6 (int3/ex4) and CYP2E1 (PstI, RsaI, DraI) polymorphisms and their interaction with environmental factors such as sex, age and smoking are studied in Turkish population and association between these polymorphisms and bladder cancer is investigated. Investigated CYP1A1, CYP2D6 and CYP2E1 genes are shown not to be associated with the disease, however, it is found that CYP1B1 432Val allele increases the risk of bladder cancer (adjusted OR = 3,080, 95% CI: 1,204 - 7,874). Age, sex and smoking are also found to be associated with increased risk of bladder cancer. P06.012 Gene expression in superficial bladder cancer using microarrays J. Mares 1 , M. Szakacsova 2 , C. Guelly 3 , A. Sartori 4 , V. Soukup 2 , J. Duskova 2 , F. Zelezny 5 , J. Klema 5 , M. Babjuk 2 ; 1 2nd Medical Faculty, Prague 5, Czech Republic, 2 1st Medical Faculty, Prague 2, Czech Republic, 3 Center for Medical Research, Graz, Austria, 4 Applied Biosystems, Darmstadt, Germany, 5 Dept. Cybernetics, Czech Tech. University, Prague 2, Czech Republic. Non-muscle invasive bladder cancer is a heterogenous disease whose molecular phenotypes are being elucidated. Treatment of these superficial tumours is dependent on the risk of recurrence. To improve the accuracy of progression prediction various molecular markers have been evaluated by gene expression microarrays but to date no molecular markers have been used in clinical practice. For the improvement of recurrence prognosis we analysed gene expression and identified differences between superficial bladder tumours in a non-recurrence cohort during period of two years (19 patients) and early recurrence cohort (18 patients), which might explain differences in the biology and clinical outcomes. Data from microarrays containing 29,019 targets (Applied Biosystems) were subjected to a panel of statistical analyses to identify bladder cancer recurrence-associated gene signatures. Initial screening using the GeneSpring and Bioconductor software tools revealed a putative set of about 120 genes associating with the early recurrence cohort. Significant differences were observed by CDKN2A, CDKN1C, HOXA10, GPNMB, TCN1, INA, H19, AURKC, FABP3 and PLOD2 genes. Besides, we integrated the microarray dataset with additional background knowledge, in order to algorithmically mine for differential-expression patterns in terms of the Gene Ontology functions and processes as well as known regulatory pathway memberships. Our results indicate that it may be possible to identify patients with a high risk of disease recurrence at an early stage using a molecular profile present already in the superficial tumours. Research was supported by MSM 0021620808. P06.013 investigation of the relationship between mitochondrial DNA and transitional cell carcinoma of the bladder D. Ergeç 1 , H. Tavukçu 2 , G. Koç 3 , M. Özyürek 2 , D. Javadova 3 , K. Ulucan 4 , D. Kıraç 5 , L. Türkeri 2 , I. Güney 3 ; 1 Maltepe University, Faculty of Medicine, Department Medical Biology and Genetics, İstanbul, Turkey, 2 Marmara University, Faculty of Medicine, Department of Urology, İstanbul, Turkey, 3 Marmara University, Faculty of Medicine, Department of Medical Genetics, İstanbul, Turkey, 4 Maltepe University, Faculty of Dentistry, Department of Medical Biology and Genetics, İstanbul, Turkey, 5 Yeditepe University, Faculty of Medicine, Department of Biochemistry, İstanbul, Turkey. Mitochondrial DNA mutations have been described recently in different tumors, whereas similar studies focusing on bladder cancer are scarce. In an effort to understand the significance of mtDNA mutations in bladder cancer, we investigated the mtDNA alterations. It has been suggested that the extent of mitochondrial DNA mutations might be useful in the prognosis of cancer and the response to certain therapies. In an attempt to progress in the understanding of the relationship of mtDNA alterations and bladder tumorigenesis, we studied the mtDNA in 38 bladder tumors and 21 microdissected normal bladder tissues. Mitochondrial genes ATPase6, Cytb, ND1 and D-loop region were amplified by PCR. The results of DNA sequencing revealed numerous point mutations in mtDNA genes. We detected 40 mutations in the pa-
Cancer genetics tient group in which 19 of them resulted in aa substitution. Our findings indicate that G8697A, G14905A, C15452A and A15607G mutations are frequent in bladder cancers (P< 0.05). These mutations are belong to mtDNA haplogroup T. No association was found between mtDNA mutations and the patients’ gender, tumor stage or grade, recurrence and progression. In conclusion, the high incidence of mtDNA mutations in bladder cancer suggests that mtDNA and mitochondria could play an important role in the process of carcinogenesis process. Especially, mtDNA haplogroup T may be important to detect the cancer risk. More extensive biochemical and molecular studies and further studies in larger groups are necessary to determine the pathological significance of these mutations. P06.014 molecular genetic alterations and their predictive values in superficial bladder cancer. A. Y. Babayan 1,2,3 , S. V. Bashkatov 4 , O. B. Karyakin 4 , A. A. Teplov 5 , D. V. Zaletaev 1,3 , M. V. Nemtsova 1,3 ; 1 Sechenov Moscow Medical Academy, Moscow, Russian Federation, 2 Russian State Medical University, Moscow, Russian Federation, 3 Medical Genetic Research Centre, Moscow, Russian Federation, 4 Medical Radiology Research Centre, Obninsk, Russian Federation, 5 Moscow Herzen Oncological Research Institute, Moscow, Russian Federation. Conventional histopathologic and morphologic factors are widely used to predict poor prognosis in patients with superficial bladder cancer (BC) underwent transurethral resection. But this system is not able accurately predict the behavior of the most bladder tumors and need additional factors. Our purpose was to establish associations between some genetic alterations in respect to unfavorable clinical phenotype (recurrence rate, invasion, high grade) and to determine the prognostic significance of these genetic alterations. We have studied 108 matched samples (blood and tumor tissue) from patients with superficial BC, of which 12 patients demonstrated recurrence within one year, and 10 samples from patients with invasive BC. The panel included loss of heterozygosity at 3p14, 9p21, 9q34, p53 locus, activating mutation in 7 exon FGFR3 and RASSF1A, p16, p14, RARb, CDH1 promoter hypermethylation. Methods: microsatellite analysis, SSCP and direct sequencing and methyl-sensitive PCR. Statistical analysis included comparison of the patients’ clinical groups by Fisher’s exact test, calculation of odds ratios and corresponding 95% confidence intervals. Results: 9p21- locus deletions are significantly more frequent in primary tumors with high recurrence rate (within one year) (p=0.049. OR=8.70). FGFR3 mutations are associated with Ta stage (p=0.0042. OR=5.00). 3p14 locus deletions (p=0.042. OR=5.71), RARb (p=0.016. OR=3.91) and p16 (p=0.055. OR=4.17) promoter hypermethylation are associated with high grade tumors. P53 locus deletions (p=0.006. OR=8.10) and p16 hypermethylation (p=0.05. OR=4.09) are significantly more frequent in invasive bladder tumors than in superficial tumors. Conclusion. Revealed genetic alterations could be used as additional prognostic markers to predict tumor’s behavior more accurately. P06.015 Diagnostic and prognostic molecular markers in brain tumors A. R. Lincesso 1 , D. Marchetti 1 , S. Pericotti 2 , D. Barachetti 1 , L. Pezzoli 1 , R. Merli 3 , M. Iascone 1 ; 1 Genetica Molecolare - USSD Lab. Genetica Medica, Ospedali Riuniti, Bergamo, Italy, 2 Anatomia Patologica, Ospedali Riuniti, Bergamo, Italy, 3 Neurochirurgia, Ospedali Riuniti, Bergamo, Italy. Malignant gliomas are associated with high morbidity and mortality. Despite optimal treatment, the survival is often very low. Recently, there have been advances in our understanding of the molecular pathogenesis of gliomas and progress in treating them. This work summarizes preliminary results of molecular markers routinely used to help diagnosis and management of these tumours in adults. Loss of heterozygosity (LOH) on 1p and 19q seem to be a predictor of good prognosis and chemosensitivity. Conversely, 10q LOH predicts rather poor outcome. Moreover, epigenetic silencing of the MGMT promoter predicts response to alkylating agents. We have analyzed 32 cases: 18 glioblastomas, 10 oligodendrocitomas and 4 astrocitomas. After DNA extraction from peripheral blood and microdissected-FFPE samples, we analyzed by microsatellite LOH on 1p, 19q and 10q and the MGMT promoter by methylation-sensitive PCR. Two cases (1 astrocitoma and 1 glioblastoma) were not analyzable due to low quality of tumor DNA. All astrocitomas did not show LOH on chromosomes 1p, 19q and 10q. Among the 17 glioblastomas, two did not show LOH, three showed 1p LOH, two 1p+19q LOH, one 1p+10q LOH, one 19q+10q LOH and eight 10q LOH. All oligodendrogliomas exhibited 1p+19q LOH. MGMT promoter resulted methylated in all oligodendrogliomas and astrocitomas, while among glioblastomas only 6 were methylated. As reported in literature, 1p and 19q LOH are hallmarks of oligodendrogliomas, while LOH do not seem to be associated to astrocitomas. These results confirm the correlation between histological diagnosis and genetic molecular markers; follow up on treatment response is underway. P06.016 Polymorphisms in DNA BER genes XRcc1 and PARP1 increase the risk of adult brain tumors G. Kanigur 1 , E. Yosunkaya 2 , B. Küçükyürük 3 , H. Biçeroğlu 3 , M. Uzan 3 , Ç. Gürel 1 , &. Onaran 1 ; 1 Department of Medical Biology, Cerrahpasa Medical School, Istanbul University, TURKEY, İstanbul, Turkey, 2 Department of Medical Genetics, Cerrahpasa Medical School, Istanbul University, TURKEY, İstanbul, Turkey, 3 Department of Neurosurgery, Cerrahpasa Medical School, Istanbul University, İstanbul, Turkey. Cancer development is a multi-step process, in which polygenetic and environmental factors play important roles. Allelic polymorphisms of genes that code for DNA repair enzymes could also determine genetic susceptibility or resistance to cancer in most instances. XRCC1 and PARP1 are two important proteins in base excision repair. In this hospital-based case-control study, consisted of 137 patients with primary brain tumors and 244 cancer-free control subjects, we sought to determine possible associations between XRCC1 Arg399Gln and PARP1 Val762Ala polymorphisms and primary brain tumors. We also searched for any possible relation between the tumor grade and these polymorphisms. The results indicated a significant association between the occurrence of primary brain tumor and the existence of XRCC1 Arg399Gln and PARP1 Val762Ala polymorphisms (OR: 2,113; 95% CI: 1,069-4,176; p=0.041 and OR: 3,720; 95% CI: 1,673-8,273; p=0.001, respectively). However, there was no statistically significant relationship between the tumor grade and the polymorphisms studied. We conclude that XRCC1 Arg399Gln and PARP1 Val762Ala polymorphisms might play role in the initial stages but have no effect on the progression of brain tumor development. P06.017 cancer genes mutation testing - an improved sequencing workflow for quality-assured, clinical-grade results using improved technology capillary electrophoresis T. Schäfer, K. O. Wesche; Applied Biosystems GmbH, Darmstadt, Germany. It was found that the range of mutations that can drive cancer growth could be much wider than initially expected. An international research effort, the Cancer Genome Project, has identified around 120 genes that may contain mutations promoting the disease. Moreover, in the recent years it has been demonstrated that cancer gene mutations can not only report about cancer predisposition like in BRCA1 and BRCA2 genes but that they can also serve as biomarkers for therapy decisions and so in clinical practice mutations in the genes KRAS, EGFR and more recently BRAF are being used for that purpose. This has brought cancer gene mutation analysis from a research study to a clinical management practice. For this reason also the needs for the technology capable of performing genetic analysis changed from high productivity features to an easy to use technology. Here we describe the results of independent collaborative studies to develop improved sequencing workflows on several selected cancer genes. These protocols take advantage of new reagents for better sensitivity and the latest generation capillary electrophoresis instruments, easy to use and with new level of data quality. Quality control features built in this new technology will offer new solutions to the clinical laboratory for obtaining results with the highest level of reliability and quality.
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Volume 17 Supplement 2 May 2009 www
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European Society of Human Genetics
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Table of Contents spoken Presentati
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Plenary Lectures PL2.2 massive para
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Concurrent Symposia s01.1 Genome va
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Concurrent Symposia Monogenic diabe
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Concurrent Symposia invariable in t
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Concurrent Symposia s11.2 clinical,
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Concurrent Symposia s13.2 A novel g
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Concurrent Sessions c01.1 mRNA-seq
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Concurrent Sessions velopmental del
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Concurrent Sessions development of
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Concurrent Sessions c04.6 Duplicati
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Concurrent Sessions genes to be rec
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Concurrent Sessions c07.5 Prenatal
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Concurrent Sessions with familial h
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Concurrent Sessions University of W
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Concurrent Sessions with this, we f
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Concurrent Sessions had immotile ci
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Concurrent Sessions abnormal glycos
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Concurrent Sessions showers’ and
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Concurrent Sessions partial gene de
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Concurrent Sessions leads to distre
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Genetic counseling Genetics educati
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Clinical genetics and Dysmorphology
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Cytogenetics P03. cytogenetics Recu
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Cytogenetics use of metaphase analy
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Cytogenetics 2: mother’s age < fa
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Cytogenetics P03.028 HLA B27 allele
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Cytogenetics karyotype revealed a p
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Cytogenetics drome is estimated at
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Cytogenetics P03.057 Pathological c
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Cytogenetics grandmother and 2 mate
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Page 123 and 124: Cytogenetics P03.082 High-resolutio
Page 125 and 126: Cytogenetics All detected anomalies
Page 127 and 128: Cytogenetics somy for chromosome 2.
Page 129 and 130: Cytogenetics cially in chromosome 4
Page 131 and 132: Cytogenetics (59.390.122 to 62.021.
Page 133 and 134: Cytogenetics For further characteri
Page 135 and 136: Cytogenetics 9p duplication. This c
Page 137 and 138: Cytogenetics regions with mental /d
Page 139 and 140: Cytogenetics donation program of po
Page 141 and 142: Cytogenetics P03.165 interpretation
Page 143 and 144: Cytogenetics P03.174 Deletion of th
Page 145 and 146: Cytogenetics P03.183 An atypical 7q
Page 147 and 148: Cytogenetics spermia, 11 oligosperm
Page 149 and 150: Reproductive genetics and social fa
Page 151 and 152: Reproductive genetics mosomal chang
Page 153 and 154: Reproductive genetics two cohorts w
Page 155 and 156: Reproductive genetics the 147 SC ch
Page 157 and 158: Prenatal and perinatal genetics P05
Page 159 and 160: Prenatal and perinatal genetics and
Page 161 and 162: Prenatal and perinatal genetics fro
Page 163 and 164: Prenatal and perinatal genetics dev
Page 165 and 166: Prenatal and perinatal genetics in
Page 167 and 168: Prenatal and perinatal genetics obj
Page 169 and 170: Prenatal and perinatal genetics P05
Page 171: Cancer genetics P06.005 tiling reso
Page 175 and 176: Cancer genetics chronic inflammatio
Page 177 and 178: Cancer genetics licular thyroid can
Page 179 and 180: Cancer genetics also studied. In 31
Page 181 and 182: Cancer genetics tile polyposis. We
Page 183 and 184: Cancer genetics Upon recombinant ex
Page 185 and 186: Cancer genetics variant allele was
Page 187 and 188: Cancer genetics from patients with
Page 189 and 190: Cancer genetics tion (PAX5 and GATA
Page 191 and 192: Cancer genetics scribed underexpres
Page 193 and 194: Cancer genetics of the ZIC gene fam
Page 195 and 196: Cancer genetics Materials and metho
Page 197 and 198: Cancer genetics the past and it is
Page 199 and 200: Cancer genetics P06.130 spectrum an
Page 201 and 202: Cancer genetics P06.139 the role of
Page 203 and 204: Cancer genetics and MSH2 germline m
Page 205 and 206: Cancer genetics P06.155 New roles f
Page 207 and 208: Cancer genetics screening was perfo
Page 209 and 210: Cancer genetics val (DFI) than pati
Page 211 and 212: Cancer genetics is hTERC gene ampli
Page 213 and 214: Cancer genetics on chromosome regio
Page 215 and 216: Cancer genetics preferentially dupl
Page 217 and 218: Cancer cytogenetics mutations in co
Page 219 and 220: Cancer cytogenetics P07.08 molecula
Page 221 and 222: Statistical genetics, includes Mapp
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Statistical genetics, includes Mapp
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Complex traits and polygenic disord
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Evolutionary and population genetic
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Genomics, Genomic technology and Ep
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Molecular basis of Mendelian disord
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Metabolic disorders P12.167 Pattern
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Metabolic disorders PKU. BH4 challe
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Metabolic disorders catepe Universi
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Metabolic disorders respectively. G
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Metabolic disorders enzymaticaly co
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Metabolic disorders Normal Affected
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Therapy for genetic disorders in th
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Therapy for genetic disorders P14.0
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Therapy for genetic disorders of me
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Laboratory and quality management P
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Laboratory and quality management T
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Molecular and biochemical basis of
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Genetic analysis, linkage ans assoc
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Author Index Allanson, J.: P02.140
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Author Index 0 Barbacioru, C.: C01.
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Author Index 0 Bonneau, D.: C16.2,
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Author Index 0 Chakravarti, A.: C13
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Author Index 0 Dan, D.: P01.39, P14
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Author Index 0 Duskova, J.: P06.012
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Author Index Franke, A.: P09.056 Fr
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Author Index Grasso, R.: P02.025 Gr
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Author Index Holder-Espinasse, M.:
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Author Index Jurkiewicz, E.: C14.5
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Author Index Kooper, A. J. A.: P05.
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Author Index Li, K. J.: P11.086 Li,
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Author Index Martinet, D.: P03.095
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Author Index Moorman, A. F. M.: P16
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Author Index P10.57, P10.82 Oguzkan
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Author Index P09.054, P09.085, P09.
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Author Index P16.01 Renieri, A.: P0
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Author Index Santorelli, F.: P08.55
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Author Index Sinke, R. J.: P02.020
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Author Index Taheri, M.: P04.33, P0
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Author Index Valentino, P.: P02.064
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Author Index Wiemer-Kruel, A.: P14.
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Keyword Index 1 10q22 deletions: P0
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Keyword Index autosomal dominant re
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Keyword Index CLA: P06.073 CLCN1 ge
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Keyword Index DMD: P16.40, P16.41,
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Keyword Index gene networks: S12.2
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Keyword Index hydrocephaly: P05.11
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Keyword Index malignant hyperthermi
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Keyword Index NAT2: P12.118 natridi
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Keyword Index Polymalformations: P0
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Keyword Index Sardinia: C09.6 Sardi
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Keyword Index TNFalpha: P08.61, P09
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