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  • PATIENT  (39)
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  • 1
    Keywords: CELLS ; EXPRESSION ; SURVIVAL ; Germany ; GENE ; GENE-EXPRESSION ; GENES ; PROTEIN ; transcription ; PATIENT ; MECHANISM ; FAMILY ; TRANSCRIPTION FACTOR ; chromosome ; DELETION ; LYMPHOMA ; gene expression ; DISRUPTION ; UP-REGULATION ; MUTATION ; leukemia ; DELETIONS ; inactivation ; TUMOR-SUPPRESSOR GENE ; REGION ; B-CELLS ; point mutation ; TRANSCRIPTS ; molecular ; TUMOR-SUPPRESSOR ; ACUTE MYELOID-LEUKEMIA ; regulation ; ATM MUTATIONS ; B-CLL ; tumor suppressor gene ; transcript ; 11Q23 ; ATM ; CYCLIN-E ; GENOMIC REGION ; GTPASE-ACTIVATING PROTEIN ; INDUCED SKIN TUMORS ; MLL
    Abstract: Deletion of chromosome region 11q22-q23 defines a subgroup of patients with B-cell chronic lymphocytic leukemia (B-CLL) characterized by poor survival. Although the tumor-suppressor gene ATM in the consensus deletion region was found to be biallelically inactivated in about one third of B-CLL cases, in the majority of those who have this deletion, inactivation of the remaining ATM allele was not observed. To identify a second disease-associated gene, we investigated two B-CLL cases with translocation breakpoints in the critical 11q23 deletion region. In one case, a t(X;11)(q13;q23) was cloned and two novel genes were isolated. The breakpoint on 11q23 affected the ARHGAP20 gene, which encodes a protein predicted to be involved in the regulation of Rho family GTPases. The breakpoint on Xq13 occurred in BRWD3, which codes for a putative novel transcription factor. The rearrangement of ARHGAP20 and BRWD3 did not result in fusion transcripts, but it disrupted both genes. Mutation analysis of 28 B-CLL samples with monoallelic deletions and two B-CLL samples with 11q23 translocations detected no deleterious mutation in the remaining copy of ARHGAP20. Quantitative expression analysis in 22 B-CLLs revealed significant up-regulation of ARHGAP20 in CLL B cells, whereas BRWD3 was slightly down-regulated. Thus, deregulation of ARHGAP20 by altered gene expression or by gene disruption (but not point mutation) might be a general molecular mechanism of B-CLL leukemogenesis. (C) 2004 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 15543602
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  • 2
    Keywords: RECEPTOR ; EXPRESSION ; Germany ; KINASE ; TYROSINE KINASE ; GENE ; GENE-EXPRESSION ; GENES ; transcription ; ACCURACY ; TRANSDUCTION ; PATIENT ; ACTIVATION ; DOMAIN ; cell cycle ; CELL-CYCLE ; CYCLE ; signal transduction ; IDENTIFICATION ; PATTERNS ; gene expression ; MUTATION ; SIGNAL-TRANSDUCTION ; leukemia ; REGION ; MUTATIONS ; PROGNOSTIC-SIGNIFICANCE ; CONSTITUTIVE ACTIVATION ; SERIES ; point mutation ; gene expression profiling ; CYCLE CONTROL ; HEMATOLOGIC MALIGNANCIES ; GENE-MUTATIONS ; ACUTE MYELOGENOUS LEUKEMIA ; acute myeloid leukemia ; NORMAL CYTOGENETICS ; STUDY-GROUP ULM ; CANDIDATE GENES ; INTERNAL TANDEM DUPLICATION ; MYELOID-LEUKEMIA ; GENE-TRANSCRIPTION ; ADULT PATIENTS ; HIGH-DOSE CYTARABINE ; EXPRESSION PATTERNS ; SIGNATURE ; COOPERATIVE-GROUP ; FLT3-activating mutations ; normal karyotype ; NRAS-activating mutations ; SONIC-HEDGEHOG
    Abstract: In acute myeloid leukemia (AML), constitutive activation of the FLT3 receptor tyrosine kinase, either by internal tandem duplications (FLT3-ITD) of the juxtamembrane region or by point mutations in the second tyrosine kinase domain (FLT3-TKD), as well as point mutations of the NRAS gene (NRAS-PM) are among the most frequent somatic gene mutations. To elucidate whether these mutations cause aberrant signal transduction in AML, we used gene expression pro. ling in a series of 110 newly diagnosed AML patients with normal karyotype. The different algorithms used for data analysis revealed highly concordant sets of genes, indicating that the identified gene signatures are specific for each analysed subgroup. Whereas samples with FLT3-ITD and FLT3-TKD could be separated with up to 100% accuracy, this did not apply for NRAS-PM and wild-type samples, suggesting that only FLT3-ITD and FLT3-TKD are associated with an apparent signature in AML. The set of discriminating genes included several known genes, which are involved in cell cycle control (CDC14A, WEE1), gene transcription (HOXB5, FOXA1), and signal transduction (SMG1). In conclusion, we showed that unique gene expression patterns can be correlated with FLT3-ITD and FLT3-TKD. This might lead to the identification of further pathogenetic relevant candidate genes particularly in AML with normal karyotype
    Type of Publication: Journal article published
    PubMed ID: 15674343
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  • 3
    Keywords: PEPTIDE ; EXPRESSION ; INVASION ; Germany ; human ; COHORT ; DISEASE ; DISEASES ; POPULATION ; RISK ; GENE ; GENOME ; HYBRIDIZATION ; PATIENT ; DNA ; INDUCTION ; colon ; polymorphism ; COMPARATIVE GENOMIC HYBRIDIZATION ; COPY NUMBER ; NUMBER ; HUMAN GENOME ; PEPTIDES ; POLYMERASE-CHAIN-REACTION ; INDIVIDUALS ; ULCERATIVE-COLITIS ; inflammation ; INFLAMMATORY-BOWEL-DISEASE ; CLUSTER ; DNA-SEQUENCE ; INTERVAL ; LOCUS ; chronic inflammation ; DEFICIENT ; SEGMENTAL DUPLICATIONS ; odds ratio ; genomic ; ALPHA-DEFENSIN ; DEFENSIN DEFICIENCY ; healthy individuals ; NOD2 ; PANETH CELLS ; RESIDENT INTESTINAL FLORA
    Abstract: Defensins are endogenous antimicrobial peptides that protect the intestinal mucosa against bacterial invasion. It has been suggested that deficient defensin expression may underlie the chronic inflammation of Crohn disease ( CD). The DNA copy number of the beta-defensin gene cluster on chromosome 8p23.1 is highly polymorphic within the healthy population, which suggests that the defective beta-defensin induction in colonic CD could be due to low beta-defensin gene copy number. Here, we tested this hypothesis, using genomewide DNA copy number profiling by array-based comparative genomic hybridization and quantitative polymerase-chain-reaction analysis of the human beta-defensin 2 (HBD-2) gene. We showed that healthy individuals, as well as patients with ulcerative colitis, have a median of 4 ( range 2 - 10) HBD-2 gene copies per genome. In a surgical cohort with ileal or colonic CD and in a second large cohort with inflammatory bowel diseases, those with ileal resections/disease exhibited a normal median HBD-2 copy number of 4, whereas those with colonic CD had a median of only 3 copies per genome ( for the surgical cohort; P = .008 P = .032 for the second cohort). Overall, the copy number distribution in colonic CD was shifted to lower numbers compared with controls ( for both the surgical cohort and the cohort with inflammatory bowel diseases). Individuals with P = .002 〈= 3 copies have a significantly higher risk of developing colonic CD than did individuals with 〉= 4 copies ( odds ratio 3.06; 95% confidence interval 1.46 - 6.45). An HBD-2 gene copy number of 〈 4 was associated with diminished mucosal HBD-2 mRNA expression (P = 0.033). In conclusion, a lower HBD-2 gene copy number in the beta-defensin locus predisposes to colonic CD, most likely through diminished beta-defensin expression
    Type of Publication: Journal article published
    PubMed ID: 16909382
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  • 4
    Keywords: EXPRESSION ; GROWTH ; IN-VITRO ; INHIBITOR ; proliferation ; CELL ; CELL-PROLIFERATION ; Germany ; human ; IN-VIVO ; VITRO ; VIVO ; microarray ; PROTEIN ; PROTEINS ; RNA ; DRUG ; SURGERY ; PATIENT ; REDUCTION ; TRANSPLANTATION ; RAT ; CONTRAST ; mechanisms ; SKIN ; fibroblasts ; ACID ; PCR ; NUCLEOTIDES ; EXTRACELLULAR-MATRIX ; ADHESION ; MIGRATION ; cytoskeleton ; POLYMERASE-CHAIN-REACTION ; SMOOTH-MUSCLE ; COMPLICATIONS ; BIOPSY ; CHAIN ; fibroblast ; DEHYDROGENASE ; RECIPIENTS ; HUMAN FIBROBLASTS ; cell adhesion ; mycophenolic acid ; TECHNOLOGY ; B-LYMPHOCYTES ; ENGLAND ; ACTIN ; DYSFUNCTION ; synthesis ; NUCLEOTIDE ; CYCLOSPORINE ; MOFETIL ; KIDNEY-TRANSPLANT
    Abstract: Mycophenolic acid (MPA) is a potent inhibitor of the inosine monophosphate dehydrogenase and used as an immunosuppressive drug in transplantation. MPA inhibits proliferation of T- and B-lymphocytes by guanosine depletion. Since fibroblasts rely on the de novo synthesis of guanosine nucleotides, it is assumed that MPA interacts with fibroblasts causing an increased frequency of wound healing problems. We show a downregulation of the cytoskeletal proteins vinculin, actin and tubulin in fibroblasts exposed to pharmacological doses of MPA using microarray technology, real-time polymerase chain reaction (PCR) and Western blot. This reduction in RNA and protein content is accompanied by a substantial rearrangement of the cytoskeleton in MPA-treated fibroblasts as documented by immunofluorescence. The dysfunctional fibroblast growth was validated by scratch test documenting impaired migrational capacity. In contrast, cell adhesion was increased in MPA-treated fibroblasts. The results of the cultured human fibroblasts were applied to skin biopsies of renal transplant recipients. Skin biopsies of patients treated with MPA expressed less vinculin, actin and tubulin as compared to control biopsies that could explain potential wound healing problems posttransplantation. The perspective of MPA-induced cytoskeletal dysfunction may go beyond wound healing disturbances and may have beneficial effects on (renal) allografts with respect to scarring
    Type of Publication: Journal article published
    PubMed ID: 18786225
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  • 5
    Keywords: CANCER ; EXPRESSION ; CELL ; Germany ; IN-VIVO ; THERAPY ; DISEASE ; RISK ; GENE ; GENE-EXPRESSION ; GENES ; PATIENT ; ASSOCIATION ; DELETION ; COMPARATIVE GENOMIC HYBRIDIZATION ; gene expression ; DIFFERENCE ; NUMBER ; genetics ; leukemia ; DELETIONS ; REGION ; REGIONS ; HIGH-RISK ; CHILDREN ; CHRONIC MYELOGENOUS LEUKEMIA ; PROGNOSTIC FACTOR ; heredity ; ONCOLOGY ; CHILDHOOD ; THERAPIES ; PROGNOSTIC IMPACT ; CELL LYMPHOMA ; PROGNOSTIC-FACTOR ; USA ; LOSSES ; ARRAY-CGH ; PROFILE ; DERIVATIVE CHROMOSOME-9 ; EARLY TREATMENT RESPONSE ; INTRACHROMOSOMAL AMPLIFICATION ; TRANSLOCATION T(1/19)
    Abstract: In vivo response to initial therapy, as assessed by determination of minimal residual disease (MRD) after 5 and 12 weeks of treatment, has evolved as a strong prognostic factor in children with acute lymphoblastic leukemia (ALL) treated according to the BFM regime. Individual treatment response may be influenced by copy number alterations (CNA) leading to altered gene expression. We aimed to evaluate CNA using high-resolution array-comparative genomic hybridization (array-CGH) in different treatment-response groups. Leukemic genomic profiles of 25 standard risk (MRD-SR) and 25 high risk (MRD-HR) patients were compared. CNAs were found in 46/50 patients (92%). The most significant difference was a gain of 1q23-qter because of an unbalanced t(1; 19), found in 10/25 MRD-SR patients, but in none of the MRD-HR patients (P 〈 0.001). The most frequent Cl in the MRD-HR group were deletions of genomic regions harboring the immunoglobulin genes (1g), e.g., 2p11.2 in 60% of MRD-HR compared to 28% of MRD-SR (P = 0.045). Combining all 1g loci, significantly more MRD-HR than MRD-SR patients displayed deletions (17:8 patients, P = 0.02). Frequency of other CNAs, such as loss of 9p21 or gains of 21q, did not differ strongly between the two patient groups. This is the first study evaluating the clinical significance of CNA as detected by array-CGH in childhood ALL and the first to suggest that such analyses may provide clinically important data. This article contains Supplementary Material available at http://www.interscience.wiley.com/jpages/1045-2257/suppmat. (C) 2008 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 18311775
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  • 6
    Keywords: brain ; tumor ; Germany ; MODEL ; MODELS ; ALGORITHM ; screening ; SYSTEM ; COHORT ; RISK ; HYBRIDIZATION ; TUMORS ; PATIENT ; ACTIVATION ; DNA ; MARKER ; IMPACT ; prognosis ; BIOLOGY ; DELETION ; IN-SITU ; AMPLIFICATION ; COMPARATIVE GENOMIC HYBRIDIZATION ; NUMBER ; ABERRATIONS ; MARKERS ; ONCOGENE ; beta-catenin ; PROGNOSTIC VALUE ; OUTCOMES ; CHILDREN ; ONCOLOGY ; ADULT ; ADULTS ; CHILDHOOD ; brain tumor ; GENOMIC ABERRATIONS ; DNA COPY NUMBER ; medulloblastoma ; methods ; PROGNOSTIC MARKER ; RISK STRATIFICATION ; LOCI ; MYC ; outcome ; TUMOR BIOLOGY ; Genetic ; NUCLEAR BETA-CATENIN ; clinical oncology ; STRATIFICATION
    Abstract: Purpose Medulloblastoma (MB) is the most common malignant brain tumor in children, whereas it rarely presents in adults. We aimed to identify genetic aberrations in 146 adult MBs to evaluate age-dependent differences in tumor biology and adapt age-specific risk stratification models. Methods As a screening set, we studied a cohort of 34 adult MBs by using array-based comparative genomic hybridization comparing molecular results with clinical data. DNA copy number aberrations identified as possible prognostic markers were validated in an independent cohort of 112 adult patients with MB by fluorescent in situ hybridization analysis. Results were compared with the data obtained from 404 pediatric patients with MB. Results CDK6 amplification, 10q loss, and 17q gain are the most powerful prognostic markers in adult MB. Whereas MYC/MYCN oncogene amplifications had a high prognostic value in pediatric MB, these aberrations were rarely observed in adult tumors. Surprisingly, adult MBs with 6q deletion and nuclear beta-catenin activation did not share the excellent prognosis with their pediatric counterparts. Conclusion Adult MB is distinct from pediatric MB in terms of genomic aberrations and their impact on clinical outcomes. Therefore, adult MBs require age-specific risk stratification models. We propose a molecular staging system involving three distinct risk groups based on DNA copy number status of 10q and 17q
    Type of Publication: Journal article published
    PubMed ID: 20479417
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  • 7
    Keywords: CANCER ; EXPRESSION ; IN-VITRO ; VITRO ; DISEASE ; RISK ; GENE ; PROTEIN ; validation ; PATIENT ; DNA ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; BREAST ; BREAST-CANCER ; TRIAL ; CARCINOMA CELLS ; OVARIAN-CANCER ; SNP ; PCR ; PROGNOSTIC-FACTORS ; PROGNOSTIC FACTORS ; P-SELECTIN ; POOR-PROGNOSIS ; MULTIPLE-SCLEROSIS ; PATIENT SURVIVAL ; AUTOIMMUNE-DISEASES ; PROGNOSTIC MARKER ; NEOADJUVANT CHEMOTHERAPY ; AUTOREACTIVE T-CELLS ; pathologic complete response ; primary breast cancer ; LYMPHOCYTE ; ANTICANCER CHEMOTHERAPY ; Predictive marker
    Abstract: Overexpression of CD24 is an independent prognostic factor for breast cancer. Recently, two polymorphisms in the CD24 gene were linked to disease risk and progression in autoimmune diseases. Here, we evaluated the clinical relevance of these polymorphisms with respect to their potential to predict a pathologic complete response (pCR) to neoadjuvant chemotherapy (NCT) for primary breast cancer (PBC), one of the strongest prognostic factors in this setting. A total of 257 patients were randomized to either doxorubicin/cyclophosphamide (AC) or doxorubicin/pemetrexed (AP), both followed by docetaxel (Doc) as NCT for T2-4 N0-2 M0 PBC as part of an international, multicenter, randomized phase II trial. CD24 polymorphisms were analyzed on germ line DNA and correlated with clinicopathologic variables and pCR. No significant associations were found between either of the polymorphisms and any of the clinicopathologic variables. In a multivariate analysis, CD24 Val/Val genotype was the only significant predictor of pCR (OR: 4.97; P = 0.003). The predictive potential was significant in both treatment arms and in the hormone receptor-positive subgroup. There was no correlation between CD24 3'UTR (TG/Del) genotype and pCR. We did not observe any association between CD24 genotype and CD24 protein expression or in vitro chemosensitivity, but there was a significant correlation between CD24 Val/Val and intratumoral lymphocyte aggregates. In conclusion, CD24 Ala/Val SNP is a strong and independent predictor of pCR after NCT for PBC and may affect immune functions rather than tumor characteristics. Further evaluation of the CD24 function and validation of its predictive potential are clearly warranted.
    Type of Publication: Journal article published
    PubMed ID: 21960110
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  • 8
    Keywords: EXPRESSION ; SURVIVAL ; BLOOD ; CELL ; Germany ; GENE ; GENES ; PATIENT ; recombination ; ANTIGEN ; ASSOCIATION ; LYMPHOMA ; DIFFERENCE ; MUTATION ; ABERRATIONS ; DELETIONS ; B-CELLS ; AGGRESSIVE VARIANTS ; ATM GENE ; CD38 EXPRESSION ; CENTROCYTIC LYMPHOMA ; CHROMOSOMAL IMBALANCES ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; COMPLETE REMISSION ; IMMUNOGLOBULIN GENES ; MAJOR TRANSLOCATION CLUSTER ; SOMATIC HYPERMUTATION
    Abstract: Immunoglobulin variable heavy chain gene (V-H) mutation status and VDJ rearrangement structure were analyzed in 141 patients with mantle cell lymphoma (MCL) and correlated with biologic and clinical characteristics; 29% of the MCLs displayed mutated V-H using a 98% germline homology cutoff. Striking differences occurred in the VH mutation subgroups with respect to the use of specific V genes. Rearrangements involving V4-34 and V3-21 were almost exclusively unmutated, whereas rearrangements using V4-59 and V3-23 were typically mutated. Significant association occurred between mutated V-H with shorter CDR3 lengths and the use of J(H)4b. V3-21 and V4-59 were involved in highly characteristic rearrangements, implying that antigen specificity might have been involved in MCL development. There was no evidence for isotype switch recombination or Bcl-6 expression in any MCL. ZAP70 expression was not different in V-H-mutated or unmutated MCL. Although the deletions 11q- and 17p- showed a balanced distribution, an overrepresentation was observed for trisomies +3q, +8q, and tetraploidy in the V-H-unmutated subgroup and +12q in the V-H-mutated subgroup. Clinically, mutated V-H was associated with a higher rate of complete remission, but there was no correlation between VH mutation status and other clinical characteristics or overall survival. (Blood. 2003; 102:3003-3009) (C) 2003 by The American Society of Hematology
    Type of Publication: Journal article published
    PubMed ID: 12842981
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  • 9
    Keywords: CANCER ; IRRADIATION ; Germany ; EXPOSURE ; MORTALITY ; RISK ; GENE ; PROTEIN ; MICE ; radiation ; PATIENT ; LYMPHOMA ; MALIGNANCIES ; ENCODES ; MUTATION ; REPAIR ; leukemia ; inactivation ; MANTLE CELL LYMPHOMA ; ATAXIA-TELANGIECTASIA ; MALIGNANCY ; ATM ; ionising radiation ; predisposition of heterozygotes ; somatic mutation
    Abstract: Predisposition to lymphomagenesis is a well-known phenomenon of ataxia-telangiectasia, a recessive disorder caused by germline inactivation of ATM. ATM encodes a protein implicated in the repair of radiation induced double-strand breaks. Biallelic ATM inactivation was described also in sporadic lymphoid malignancies, supporting a role of ATM as a tumour suppressor gene. It is, however, still unclear whether ATM heterozygotes are at higher risk of tumours. We describe an ATM heterozygous patient, who developed a mantle cell lymphoma (MCL) after occupational exposure to ionising radiation and somatic mutation of the second ATM allele supporting the contention that heterozygous germline ATM alterations in combination with irradiation exposure predisposes to sporadic MCL. (c) 2005 Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 16387360
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  • 10
    Keywords: brain ; EXPRESSION ; Germany ; human ; MODEL ; SYSTEM ; DISEASE ; GENE ; GENES ; HYBRIDIZATION ; transcription ; DIFFERENTIATION ; PATIENT ; TRANSCRIPTION FACTOR ; DOMAIN ; BINDING ; BIOLOGY ; MOLECULAR-BIOLOGY ; DELETION ; NERVOUS-SYSTEM ; IN-SITU ; COMPARATIVE GENOMIC HYBRIDIZATION ; PROMOTER ; genetics ; PATHOGENESIS ; REGION ; REGIONS ; Jun ; PHENOTYPE ; CENTRAL-NERVOUS-SYSTEM ; DE-NOVO ; ABNORMALITIES ; FLUORESCENCE ; fluorescence in situ hybridization ; heredity ; DOMAINS ; in situ hybridization ; SINGLE ; molecular biology ; molecular ; FEATURES ; PATTERN ; PH ; development ; analysis ; female ; MOLECULAR PATHOGENESIS ; genomic ; RARE ; MENTAL-RETARDATION ; central nervous system ; correlates ; VERTEBRATE ; E-BOX ; E2-2 ; LOOP-HELIX FACTORS ; muscular
    Abstract: Pitt-Hopkins syndrome (PHS) is a rare syndromic mental disorder, which is mainly characterized by severe motor and mental retardation including absent language development, a characteristic facial gestalt and episodes of hyperventilation. We report on a female patient with PHS showing severe mental retardation with absent speech, pronounced muscular hypotonia, ataxia, distinctive facial features, such as a coarse face, a broad nasal bridge and a wide mouth, and hyperventilation attacks. In this patient, genomic profiling by array-based comparative genomic hybridization and fluorescence in situ hybridization studies detected and confirmed a de novo 0.5 Mb deletion in 18q21.2 containing a single gene, the basic helix-loop-helix transcription factor TCF4. cDNA and genomic analyses in the patient and her parents demonstrated TCF4 haploinsufficiency as the underlying cause of the disease. Analysis of the embryonal expression pattern of the Danio rerio ortholog, tcf4, by whole-mount in situ hybridization showed a highly specific expression domain in the pallium of the telencephalon during late somitogenesis, when the patterning of the zebrafish brain is advanced and neural differentiation commences. Later expression domains were restricted to several regions in the central nervous system, including continued expression in the pallium of the telencephalon, and starting expression in the diencephalon (thalamus, ventral thalamus and posterior tuberculum), the midbrain tegmentum, the hindbrain and the branchial arches. This expression pattern correlates with the clinical phenotype. Our results show that haploinsufficiency of TCF4 causes PHS and suggest that D. rerio, is a valuable model to study the molecular pathogenesis of PHS and the role of TCF4 in brain development
    Type of Publication: Journal article published
    PubMed ID: 17478476
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