16 results on '"E. Girodon-Boulandet"'
Search Results
2. Mid-trimester hyperechogenic bowel in a fetus of Japanese origin carrying a new mutation of CFTR gene (L548Q)
- Author
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M Yamamoto, B Simon-Bouy, Yves Ville, Jacqueline Selva, M Moulis, E Girodon-Boulandet, Brigitte Leroy, and D. Molina-Gomes
- Subjects
Adult ,Male ,congenital, hereditary, and neonatal diseases and abnormalities ,Pathology ,medicine.medical_specialty ,Pancreatic disease ,Cystic Fibrosis ,Cystic Fibrosis Transmembrane Conductance Regulator ,Prenatal diagnosis ,Genetic Counseling ,Compound heterozygosity ,medicine.disease_cause ,Cystic fibrosis ,Diagnosis, Differential ,Pregnancy ,Prenatal Diagnosis ,medicine ,Humans ,Abnormalities, Multiple ,Genetics (clinical) ,Ultrasonography ,Mutation ,Fetus ,biology ,Obstetrics and Gynecology ,medicine.disease ,digestive system diseases ,Cystic fibrosis transmembrane conductance regulator ,Intestines ,Pregnancy Trimester, Second ,biology.protein ,Gestation ,Female - Abstract
We present a case of a fetus with hyperechogenic bowel, in which the L548Q mutation was detected in the mother of Japanese origin and the deltaF508 mutation in the father of Caucasian origin. The fetus proved to be compound heterozygous. Research into cystic fibrosis transmembrane conductance regulator (CFTR) mutations in this case was triggered by the fact that the fetus had a characteristic hyperechogenic bowel image with normal karyotype and no indications of intrauterine infections. Hyperechogenic bowel is highly indicative of a CFTR gene mutation. The incidence of cystic fibrosis (CF) in fetuses with mid-trimester hyperechogenic bowel is 5%, but once the most frequent mutations have been accounted for, rarer mutations must be investigated.
- Published
- 2005
3. Cystic fibrosis patients with the 3272-26A>G splicing mutation have milder disease than F508del homozygotes: a large European study
- Author
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H. Cuppens, Cécile Cazeneuve, Javier Pérez-Frías, Stavros Doudounakis, Teresa Casals, Michel Goossens, Casilda Olveira, Thierry Bienvenu, De Boeck K, C. Vásquez, Jean-Claude Chomel, Dapena J, Emmanouel Kanavakis, I. Vieira, João Lavinha, Dominique Hubert, Christine Clavel, Burkhard Tümmler, Amaral, Maria Tzetis, R. Cabanas, E. Girodon-Boulandet, Deborah Penque, des Georges M, Mireille Claustres, S. Gartner, Martine Blayau, B. Lopes, P. Birembaut, M. Adoun, Thilo Dörk, Celeste Barreto, Sebastian Beck, C. Verlingue, Paula Pacheco, Xavier Estivill, Carlos M. Farinha, Paulo Nogueira, and Claude Férec
- Subjects
Point mutation ,Gene mutation ,Biology ,Apical membrane ,medicine.disease ,Molecular biology ,Cystic fibrosis ,Cystic fibrosis transmembrane conductance regulator ,Frameshift mutation ,Genetics ,biology.protein ,medicine ,Missense mutation ,Exocrine pancreatic insufficiency ,Letters to the Editor ,Genetics (clinical) - Abstract
Editor—Cystic fibrosis (CF, MIM 219700) is a common, severe, autosomal recessive disease caused by mutations in the CF transmembrane conductance regulator ( CFTR ) gene cloned in 1989.1-3The disease, characterised by chronic lung disease which is the main cause of morbidity and mortality, pancreatic dysfunction, raised electrolyte levels in sweat, and male infertility, is caused by altered chloride (Cl−) secretion across the apical membrane of epithelial cells.4 There is, however, substantial variability in the clinical manifestations affecting the various organs.4 5 One single mutation, F508del, generally associated with severe disease, accounts for about 70% of CF chromosomes world wide, although with a heterogeneous geographical distribution.5 Patients homozygous for the F508del mutation have the classical severe form of the disease which includes chronic mucous obstruction of the lung and conducting airways, followed by recurrent infections mostly by Pseudomonas aeruginosa (Pa) and Staphylococcus aureus (Sa), exocrine pancreatic insufficiency (PI), resulting in failure to gain weight and height, and raised levels of Cl−, sodium, and potassium in exocrine sweat.5 However, almost 1000 genetic alterations have been detected in the CFTR gene ( CFTR Mutation Database), most presumed to be disease causing mutations. About half of these are amino acid substitutions (missense mutations) and about 20% are splicing mutations. The remainder are nonsense, frameshift (including small deletions and insertions), and a small proportion of promoter mutations. The relationship between genotype, that is, the mutations in the CFTR gene, and the clinical phenotype of CF patients has been difficult to establish, in particular for lung disease. It was previously shown that the 3272-26A>G mutation leads to the creation of an alternative acceptor splice site competing with the normal one during RNA processing and resulting in the occurrence of an alternatively spliced mRNA with 25 extra nucleotides from …
- Published
- 2001
4. NF1 gene analysis focused on CpG-rich exons in a cohort of 93 patients with neurofibromatosis type 1
- Author
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E, Girodon-Boulandet, J, Pantel, C, Cazeneuve, M V, Gijn, D, Vidaud, S, Lemay, J, Martin, J, Zeller, J, Revuz, M, Goossens, S, Amselem, and P, Wolkenstein
- Subjects
Adult ,Electrophoresis, Agar Gel ,Neurofibromatosis 1 ,Adolescent ,DNA Mutational Analysis ,Exons ,Middle Aged ,Nucleic Acid Denaturation ,Cell Line ,Cohort Studies ,Genes, Neurofibromatosis 1 ,Mutation ,Humans ,CpG Islands ,Electrophoresis, Polyacrylamide Gel ,Child ,Aged - Abstract
We studied the NF1 gene in 93 unrelated patients with neurofibromatosis type1, focusing the analysis on four exons that contain the highest number of possible mutations occurring at CpG sites. We used denaturing gradient gel electrophoresis to analyse exons 16, 28, 29 and 49, which contain 45 (25%) of the 183 possible mutations that could occur at the 120 CpG dinucleotides of the coding sequence. Six different mutations were identified, five of which are novel: two truncating mutations, W1810X and 5448insG, located in exon29; two splice defects leading to exon29 skipping, 5206-2AG and 5546GA; and one missense mutation, L844F, located in exon16. The already described R1748X mutation located in exon29 was found in two unrelated patients. The 5546GA and R1748X mutations are located at CpG sites, whereas the W1810X involves a CpNpG site. Four novel polymorphisms, which may be helpful for family studies, were also identified. Overall, all but one mutations were found in exon29, a result which suggests that all the CpG sites of the NF1 coding sequence do not have the same mutability, and that exon29, the most CpG-rich exon, contains mutational hotspots associated with NF1.
- Published
- 2000
5. E2/327 – Cystic fibrosis in Algeria: clinical spectrum and genotypic data
- Author
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L. Smati, E. Girodon-Boulandet, F. Benhassine, K.N. Benhalla, A. Boufersaoui, O. Redjala, M. Baghriche, and R. Boukari
- Subjects
Pulmonary and Respiratory Medicine ,Pathology ,medicine.medical_specialty ,business.industry ,Pediatrics, Perinatology and Child Health ,Genotype ,Medicine ,business ,medicine.disease ,Cystic fibrosis - Published
- 2006
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6. Fatal intra cerebral hemorrhage due to severe vitamin K deficiency disclosing cystic fibrosis
- Author
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Marie Dreyfus, G. Tchernia, D. Devictor, S. Essouri, M. Fabre, C. Trichet, and E. Girodon-Boulandet
- Subjects
Pathology ,medicine.medical_specialty ,business.industry ,Vitamin K deficiency ,medicine ,Hematology ,medicine.disease ,business ,Cystic fibrosis - Published
- 2003
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7. Diagnostic yield of repeat genetic testing in idiopathic chronic pancreatitis.
- Author
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Dermine S, Masson E, Girodon-Boulandet E, Bienvenu T, Férec C, Lévy P, and Rebours V
- Subjects
- Humans, Female, Male, Middle Aged, Adult, High-Throughput Nucleotide Sequencing, Aged, Cohort Studies, Trypsin Inhibitor, Kazal Pancreatic genetics, Trypsin, Pancreatitis, Chronic genetics, Pancreatitis, Chronic diagnosis, Genetic Testing
- Abstract
Genetic testing is performed for unexplained pancreatitis. The aim of this study was to evaluate the diagnostic value of repeating genetic testing in idiopathic pancreatitis when new predisposing genes are identified. We investigated 330 patients who were initially screened for PRSS1, SPINK1 and CFTR genes. A new analysis was performed by Next-Generation Sequencing (NGS) for PRSS1, SPINK1, CFTR, CTRC, CASR, CPA1, TRPV6 genes and the CEL-HYB1 allele in clinical practice, and patients were included in our cohort study. Additional rare variants were identified in 7.3 % of the patients. Screening for new pancreatitis genes is recommended when initial screening is limited. Routine use of NGS is a useful diagnostic tool in these cases., Competing Interests: Declaration of competing interest The authors of this manuscript have no conflicts of interest to disclose as described by Clinics and Research in Hepatology and Gastroenterology., (Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)
- Published
- 2024
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8. Correction of CFTR function in nasal epithelial cells from cystic fibrosis patients predicts improvement of respiratory function by CFTR modulators.
- Author
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Pranke IM, Hatton A, Simonin J, Jais JP, Le Pimpec-Barthes F, Carsin A, Bonnette P, Fayon M, Stremler-Le Bel N, Grenet D, Thumerel M, Mazenq J, Urbach V, Mesbahi M, Girodon-Boulandet E, Hinzpeter A, Edelman A, and Sermet-Gaudelus I
- Subjects
- Aminopyridines pharmacology, Aminopyridines therapeutic use, Benzodioxoles pharmacology, Benzodioxoles therapeutic use, Biomarkers, Cell Culture Techniques, Cells, Cultured, Chlorides metabolism, Cystic Fibrosis drug therapy, Cystic Fibrosis physiopathology, Epithelial Cells metabolism, Homozygote, Humans, Indoles pharmacology, Indoles therapeutic use, Mutation, Respiratory Function Tests, Treatment Outcome, Cystic Fibrosis genetics, Cystic Fibrosis metabolism, Cystic Fibrosis Transmembrane Conductance Regulator genetics, Cystic Fibrosis Transmembrane Conductance Regulator metabolism, Nasal Mucosa metabolism
- Abstract
Clinical studies with modulators of the Cystic Fibrosis Transmembrane conductance Regulator (CFTR) protein have demonstrated that functional restoration of the mutated CFTR can lead to substantial clinical benefit. However, studies have shown highly variable patient responses. The objective of this study was to determine a biomarker predictive of the clinical response. CFTR function was assessed in vivo via nasal potential difference (NPD) and in human nasal epithelial (HNE) cultures by the response to Forskolin/IBMX and the CFTR potentiator VX-770 in short-circuit-current (∆I
scF/I+V ) experiments. CFTR expression was evaluated by apical membrane fluorescence semi-quantification. Isc measurements discriminated CFTR function between controls, healthy heterozygotes, patients homozygous for the severe F508del mutation and patients with genotypes leading to absent or residual function. ∆IscF/I+V correlated with CFTR cellular apical expression and NPD measurements. The CFTR correctors lumacaftor and tezacaftor significantly increased the ∆IscF/I+V response to about 25% (SEM = 4.4) of the WT-CFTR level and the CFTR apical expression to about 22% (SEM = 4.6) of the WT-CFTR level in F508del/F508del HNE cells. The level of CFTR correction in HNE cultures significantly correlated with the FEV1 change at 6 months in 8 patients treated with CFTR modulators. We provide the first evidence that correction of CFTR function in HNE cell cultures can predict respiratory improvement by CFTR modulators.- Published
- 2017
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9. Mosaicism in men in hemophilia: is it exceptional? Impact on genetic counselling.
- Author
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Costa C, Frances AM, Letourneau S, Girodon-Boulandet E, and Goossens M
- Subjects
- Family Health, Female, Humans, Male, Pedigree, Hemophilia A genetics, Mosaicism
- Published
- 2009
- Full Text
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10. Mid-trimester hyperechogenic bowel in a fetus of Japanese origin carrying a new mutation of CFTR gene (L548Q).
- Author
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Yamamoto M, Molina-Gomes D, Girodon-Boulandet E, Moulis M, Leroy B, Simon-Bouy B, Selva J, and Ville Y
- Subjects
- Abnormalities, Multiple diagnostic imaging, Abnormalities, Multiple genetics, Adult, Cystic Fibrosis genetics, Diagnosis, Differential, Female, Genetic Counseling, Humans, Intestines diagnostic imaging, Intestines embryology, Male, Pregnancy, Pregnancy Trimester, Second, Ultrasonography, Abnormalities, Multiple diagnosis, Cystic Fibrosis diagnosis, Cystic Fibrosis Transmembrane Conductance Regulator genetics, Intestines abnormalities, Prenatal Diagnosis
- Abstract
We present a case of a fetus with hyperechogenic bowel, in which the L548Q mutation was detected in the mother of Japanese origin and the deltaF508 mutation in the father of Caucasian origin. The fetus proved to be compound heterozygous. Research into cystic fibrosis transmembrane conductance regulator (CFTR) mutations in this case was triggered by the fact that the fetus had a characteristic hyperechogenic bowel image with normal karyotype and no indications of intrauterine infections. Hyperechogenic bowel is highly indicative of a CFTR gene mutation. The incidence of cystic fibrosis (CF) in fetuses with mid-trimester hyperechogenic bowel is 5%, but once the most frequent mutations have been accounted for, rarer mutations must be investigated., (2006 John Wiley & Sons, Ltd.)
- Published
- 2006
- Full Text
- View/download PDF
11. Familial Mediterranean fever among patients from Karabakh and the diagnostic value of MEFV gene analysis in all classically affected populations.
- Author
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Cazeneuve C, Hovannesyan Z, Geneviève D, Hayrapetyan H, Papin S, Girodon-Boulandet E, Boissier B, Feingold J, Atayan K, Sarkisian T, and Amselem S
- Subjects
- Adolescent, Adult, Aged, Arabs genetics, Armenia epidemiology, Child, Child, Preschool, Cytoskeletal Proteins, Familial Mediterranean Fever ethnology, Female, Genotype, Humans, Jews genetics, Male, Middle Aged, Mutation, Phenotype, Pyrin, Familial Mediterranean Fever diagnosis, Familial Mediterranean Fever genetics, Genetic Testing, Proteins genetics
- Abstract
Objective: Familial Mediterranean fever (FMF) is an autosomal-recessive disorder that is common in Armenian, Turkish, Arab, and Sephardic Jewish populations. Its clinical diagnosis is one of exclusion, with the patients displaying nonspecific symptoms related to serosal inflammation. MEFV gene analysis has provided the first objective diagnostic criterion for FMF. However, in the absence of an identified mutation (NI/NI genotype), both the sensitivity of the molecular analyses and the involvement of the MEFV gene in FMF are called into question. The present study was designed to further evaluate the diagnostic value of MEFV analysis in another population of Mediterranean extraction., Methods: The MEFV gene was screened for mutations in 50 patients living in Karabakh (near Armenia) who fulfilled the established criteria for FMF. In addition, we analyzed published series of patients from the above-mentioned at-risk populations., Results: The mutation spectrum in Karabakhian patients, which consisted of only 6 mutations (with 26% of NI alleles), differed from that reported in Armenian patients. Strikingly, among patients from Karabakh and among all classically affected populations, the distribution of genotypes differed dramatically from Hardy-Weinberg equilibrium (P = 0.0016 and P < 0.00001, respectively). These results, combined with other population genetics-based data, revealed the existence of an FMF-like condition that, depending on the patients' ancestry, was shown to affect 85-99% of those with the NI/NI genotype., Conclusion: These data illuminate the meaning of negative results of MEFV analyses and show that in all populations evaluated, most patients with the NI/NI genotype had disease that mimicked FMF and was unrelated to the MEFV gene. Our findings also demonstrate the high sensitivity of a search for very few mutations in order to perform a molecular diagnosis of MEFV-related FMF.
- Published
- 2003
- Full Text
- View/download PDF
12. Cystic fibrosis patients with the 3272-26A>G splicing mutation have milder disease than F508del homozygotes: a large European study.
- Author
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Amaral MD, Pacheco P, Beck S, Farinha CM, Penque D, Nogueira P, Barreto C, Lopes B, Casals T, Dapena J, Gartner S, Vásquez C, Pérez-Frías J, Olveira C, Cabanas R, Estivill X, Tzetis M, Kanavakis E, Doudounakis S, Dörk T, Tümmler B, Girodon-Boulandet E, Cazeneuve C, Goossens M, Blayau M, Verlingue C, Vieira I, Féréc C, Claustres M, des Georges M, Clavel C, Birembaut P, Hubert D, Bienvenu T, Adoun M, Chomel JC, De Boeck K, Cuppens H, and Lavinha J
- Subjects
- Alleles, Cystic Fibrosis pathology, DNA chemistry, DNA genetics, DNA Mutational Analysis, Europe, Female, Genotype, Haplotypes, Homozygote, Humans, Male, Phenotype, Point Mutation, Severity of Illness Index, Alternative Splicing genetics, Cystic Fibrosis genetics, Cystic Fibrosis Transmembrane Conductance Regulator genetics, Sequence Deletion genetics
- Published
- 2001
- Full Text
- View/download PDF
13. Identification of MEFV-independent modifying genetic factors for familial Mediterranean fever.
- Author
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Cazeneuve C, Ajrapetyan H, Papin S, Roudot-Thoraval F, Geneviève D, Mndjoyan E, Papazian M, Sarkisian A, Babloyan A, Boissier B, Duquesnoy P, Kouyoumdjian JC, Girodon-Boulandet E, Grateau G, Sarkisian T, and Amselem S
- Subjects
- Adolescent, Adult, Age of Onset, Aged, Aged, 80 and over, Amyloidosis complications, Amyloidosis epidemiology, Amyloidosis genetics, Apolipoprotein E4, Armenia, Child, Child, Preschool, Cohort Studies, Cytoskeletal Proteins, Familial Mediterranean Fever complications, Familial Mediterranean Fever epidemiology, Familial Mediterranean Fever etiology, Female, Genotype, Humans, Kidney Diseases metabolism, Kidney Diseases pathology, Logistic Models, Male, Middle Aged, Multivariate Analysis, Odds Ratio, Prevalence, Proteins physiology, Pyrin, Sex Factors, Apolipoproteins genetics, Apolipoproteins E genetics, Familial Mediterranean Fever genetics, Proteins genetics
- Abstract
Familial Mediterranean fever (FMF) is a recessively inherited disorder predisposing to renal amyloidosis and associated with mutations in MEFV, a gene encoding a protein of unknown function. Differences in clinical expression have been attributed to MEFV-allelic heterogeneity, with the M694V/M694V genotype associated with a high prevalence of renal amyloidosis. However, the variable risk for patients with identical MEFV mutations to develop this severe complication, prevented by lifelong administration of colchicine, strongly suggests a role for other genetic and/or environmental factors. To overcome the well-known difficulties in the identification of modifying genetic factors, we investigated a relatively homogeneous population sample consisting of 137 Armenian patients with FMF from 127 independent families living in Armenia. We selected the SAA1, SAA2, and APOE genes-encoding serum amyloid proteins and apolipoprotein E, respectively-as well as the patients' sex, as candidate modifiers for renal amyloidosis. A stepwise logistic-regression analysis showed that the SAA1alpha/alpha genotype was associated with a sevenfold increased risk for renal amyloidosis, compared with other SAA1 genotypes (odds ratio [OR] 6. 9; 95% confidence interval [CI] 2.5-19.0). This association, which was present whatever the MEFV genotype, was extremely marked in patients homozygous for M694V (11/11). The risk for male patients of developing renal amyloidosis was fourfold higher than that for female patients (OR=4.0; 95% CI=1.5-10.8). This association, particularly marked in patients who were not homozygous for M694V (34.0% vs. 11.6%), was independent of SAA1-allelic variations. Polymorphisms in the SAA2 or APOE gene did not appear to influence susceptibility to renal amyloidosis. Overall, these data, which provide new insights into the pathophysiology of FMF, demonstrate that susceptibility to renal amyloidosis in this Mendelian disorder is influenced by at least two MEFV-independent factors of genetic origin-SAA1 and sex-that act independently of each other.
- Published
- 2000
- Full Text
- View/download PDF
14. NF1 gene analysis focused on CpG-rich exons in a cohort of 93 patients with neurofibromatosis type 1.
- Author
-
Girodon-Boulandet E, Pantel J, Cazeneuve C, Gijn MV, Vidaud D, Lemay S, Martin J, Zeller J, Revuz J, Goossens M, Amselem S, and Wolkenstein P
- Subjects
- Adolescent, Adult, Aged, Cell Line, Child, Cohort Studies, DNA Mutational Analysis, Electrophoresis, Agar Gel methods, Electrophoresis, Polyacrylamide Gel, Genes, Neurofibromatosis 1, Humans, Middle Aged, Mutation, Nucleic Acid Denaturation genetics, CpG Islands genetics, Exons genetics, Neurofibromatosis 1 genetics
- Abstract
We studied the NF1 gene in 93 unrelated patients with neurofibromatosis type1, focusing the analysis on four exons that contain the highest number of possible mutations occurring at CpG sites. We used denaturing gradient gel electrophoresis to analyse exons 16, 28, 29 and 49, which contain 45 (25%) of the 183 possible mutations that could occur at the 120 CpG dinucleotides of the coding sequence. Six different mutations were identified, five of which are novel: two truncating mutations, W1810X and 5448insG, located in exon29; two splice defects leading to exon29 skipping, 5206-2A>G and 5546G>A; and one missense mutation, L844F, located in exon16. The already described R1748X mutation located in exon29 was found in two unrelated patients. The 5546G>A and R1748X mutations are located at CpG sites, whereas the W1810X involves a CpNpG site. Four novel polymorphisms, which may be helpful for family studies, were also identified. Overall, all but one mutations were found in exon29, a result which suggests that all the CpG sites of the NF1 coding sequence do not have the same mutability, and that exon29, the most CpG-rich exon, contains mutational hotspots associated with NF1., (Copyright 2000 Wiley-Liss, Inc.)
- Published
- 2000
- Full Text
- View/download PDF
15. Fetal bowel hyperechogenicity may indicate mild atypical cystic fibrosis: a case associated with a complex CFTR allele.
- Author
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Abramowicz MJ, Dessars B, Sevens C, Goossens M, and Girodon-Boulandet E
- Subjects
- Adult, Child, Child, Preschool, Female, Genetic Counseling, Heterozygote, Humans, Infant, Newborn, Male, Mutation, Pregnancy, Alleles, Cystic Fibrosis genetics, Cystic Fibrosis Transmembrane Conductance Regulator genetics, Intestines embryology
- Published
- 2000
- Full Text
- View/download PDF
16. Screening practices for mutations in the CFTR gene ABCC7.
- Author
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Girodon-Boulandet E, Cazeneuve C, and Goossens M
- Subjects
- Cystic Fibrosis Transmembrane Conductance Regulator metabolism, Family Health, Genetic Counseling, Genetic Testing trends, Heterozygote, Humans, Prenatal Diagnosis, Cystic Fibrosis diagnosis, Cystic Fibrosis genetics, Cystic Fibrosis Transmembrane Conductance Regulator genetics, Genetic Testing methods, Mutation genetics
- Abstract
Cystic fibrosis transmembrane conductance regulator (CFTR) gene studies are now one of the most frequent activities in clinical molecular genetics laboratories. The number of requests is growing, owing to the increasingly wide range of recognized CFTR gene diseases (cystic fibrosis, congenital bilateral absence of the vas deferens, disseminated bronchiectasis, allergic bronchopulmonary aspergillosis and chronic pancreatitis), and the availability of efficient molecular tools for detecting mutations. A growing number of tests capable of simultaneously detecting several frequent CF mutations are being developed, and commercial kits are now available. The most recent kits detect nearly 90% of defective alleles in Caucasians, a rate high enough for carrier screening and for the majority of diagnostic requests. However, because of the wide variety of molecular defects documented in the CFTR gene, only a limited number of laboratories have mastered the entire panoply of necessary techniques, while other laboratories have to refer certain cases to specialized centers with complementary and/or scanning tools at their disposal. A good knowledge of CFTR diseases and their molecular mechanisms, together with expertise in the various techniques, is crucial for interpreting the results. Diagnostic strategies must take into account the indication, the patient's ethnic origin, and the time available in the framework of genetic counseling. This review presents the methods most frequently used for detecting CFTR gene mutations, and discusses the strategies most suited to the different clinical settings., (Copyright 2000 Wiley-Liss, Inc.)
- Published
- 2000
- Full Text
- View/download PDF
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