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Fred Gilbert

Publications and source records attributed to Fred Gilbert.

11 recordsLinked to original sources

TBX5 genetic testing validates strict clinical criteria for Holt-Oram syndrome.

Holt-Oram syndrome (HOS) is an autosomal dominant heart-hand syndrome characterized by congenital heart disease (CHD) and upper limb deformity, and caused by mutations in the TBX5 gene. To date, the sensitivity of TBX5 genetic testing for HOS has been unclear. We now report mutational analyses of a nongenetically selected population of 54 unrelated individuals who were consecutively referred to our center with a clinical diagnosis of HOS. TBX5 mutational analyses were performed in all individuals, and clinical histories and findings were reviewed for each patient without reference to the genotypes. Twenty-six percent of the complete cohort was shown to have mutations of the TBX5 gene. However, among those subjects for whom clinical review demonstrated that their presentations met strict diagnostic criteria for HOS, TBX5 mutations were identified in 74%. No mutations were identified in those subjects who did not meet these criteria. Thus, these studies validate our clinical diagnostic criteria for HOS including an absolute requirement for preaxial radial ray upper limb malformation. Accordingly, TBX5 genotyping has high sensitivity and specificity for HOS if stringent diagnostic criteria are used in assigning the clinical diagnosis.

Abnormalities, Multiple↗

Preimplantation genetic diagnosis of human congenital heart malformation and Holt-Oram syndrome.

Holt-Oram syndrome (HOS) is a multiple malformation syndrome associated with congenital heart malformation (CHM) and caused by mutations in the TBX5 transcription factor. Effective prenatal genetic diagnosis of HOS is limited by factors that modify clinical manifestations and confound prediction of an individual's phenotype. Although preimplantation genetic diagnosis (PGD) has been applied to complex disorders with some cardiovascular manifestations, its utility in Mendelian CHM has not been previously demonstrated. We tested whether PGD and in vitro fertilization (IVF) technology, including oocyte donation, can identify fertilized eggs affected by HOS for potential embryo selection. Five donor oocytes were fertilized in vitro with sperm from a HOS patient heterozygous for a Glu69ter-TBX5 mutation and then underwent embryo biopsy and genotyping. One carried the Glu69ter-TBX5 mutation; all others had wildtype genotypes. Two wildtype blastocysts were transferred to the mother, and the resulting singleton pregnancy was successfully delivered. Mutational analysis of fetal amniocytes and postpartum umbilical cord blood confirmed PGD. Fetal ultrasonography as well as postpartum electrocardiography and echocardiography also validated accurate prediction of normal skeletal and cardiac phenotypes. We conclude that PGD is an effective reproductive strategy for HOS patients. As more genetic etiologies for CHM are identified, application of PGD as adjunctive therapy to IVF will be increasingly available to prevent transmission of such diseases from affected parents to their children. Clinical application of PGD must balance the benefits of avoiding disease transmission with the medical risks and financial burdens of IVF.

Adult↗

Correlation between rare chromosomal abnormalities and prenatal ultrasound findings.

Our objective was to examine ultrasound findings with outcomes in cases of rare chromosomal abnormalities diagnosed during pregnancy. Results of cytogenetic studies obtained from amniocenteses and chorionic villus samplings (CVS) from 1994-2000 were reviewed. Only those examples of rare chromosomal abnormalities with little information on the associated outcome were included. Cases of autosomal trisomy (13, 18, and 21), sex chromosome aneuploidy, and reciprocal or Robertsonian translocations were excluded. Ultrasound findings and outcomes were reviewed. In all, 8,642 procedures of amniocenteses and 557 of CVS were performed; 21 cases met the inclusion criteria. Parental karyotypes were obtained for 19 couples and the karyotypic abnormalities were de novo in 13. Abnormal ultrasound findings were present in 14 pregnancies, with the following outcomes: seven underwent dilatation and evacuation (D&E), with abnormal findings in two (although examination was limited by fragmentation); one medical termination with micrognathia and low-set ears; one fetal demise; one neonatal demise; three surviving neonates with abnormalities (one each with congenital kyphosis, hydronephrosis, and hypotonia), and one newborn was normal. There were seven patients without abnormal ultrasound findings with the following outcomes: three underwent D&E, with abnormal findings in two, one child with a colobomatous optic nerve, and two apparently normal infants. Follow-up was not available in one patient. We conclude that when rare karyotypes and ultrasound abnormalities are present, poor outcomes are likely. Even with normal ultrasound findings, abnormalities may be present. These data may assist in counseling patients when testing reveals such chromosomal abnormalities.

Adult↗

Allelic imbalance in selected chromosomal regions in ovarian cancer.

Ovarian cancer (OC) is often asymptomatic at the initial stage. When diagnosed, up to 75% of the patients present grade III or IV tumors with metastasis in nearby organs of the abdomen. Genetic imbalance is abundant in OC, and allelic loss (AL) of specific chromosomal regions is considered an early event. To establish association between genetic markers for early diagnosis/prognosis of OC, our target was to define narrow specific regions of AL. We analyzed 65 ovarian carcinomas by using 19 microsatellite markers located in three different chromosomes. First, a 7.6-Mb region containing the estrogen receptor (ESR1) and the tumor suppressor gene LATS1 was analyzed. Several chromosomal breakpoints flanking ESR1 affecting the region harboring LATS1 were found. Second, we found chromosomal breakpoints on 13q13.1 approximately q13.3 that defined two narrow regions flanking the BRCA2 locus. Third, our ovarian tumors exhibited a very high frequency of AL on 16q and chromosomal breakpoints defining two narrow regions within 16q22.2 approximately q24.3. In this article, we report three new polymorphic microsatellite markers and strong evidence of AL of narrow well-defined regions in hot spots on 6q, 13q, and 16q in ovarian tumors.

Allelic Imbalance↗

Chromosome 7.

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Chromosome Mapping↗

Chromosome 6.

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Chromosome Mapping↗

Frequent LOH at hMLH1, a highly variable SNP in hMSH3, and negligible coding instability in ovarian cancer.

BACKGROUND: Molecular alterations such as DNA microsatellite instability (MSI/RER), single nucleotide polymorphism (SNP) and loss of heterozygosity (LOH) can occur throughout the genome and be associated with different types of cancer. In the present study, we aimed at detecting molecular alterations within the mismatch DNA repair genes in ovarian cancer (OC), using a sensitive, accurate and reliable protocol we have developed. MATERIALS AND METHODS: A combination of high-resolution GeneScan software analysis and automated DNA cycle sequencing was used. RESULTS: Negligible coding MSI was observed in selected sequences of mismatch DNA repair genes in our series of sixty-two ovarian tumors and matched blood DNAs. Unlike MSI, loss of one hMLH1 allele was scored in almost half (47%) of the informative cases. In addition, an SNP in hMSH3/intron 5 was found to be highly variable in OC patients. CONCLUSION: 1) Coding DNA instability is likely to be a very rare event in OC and, therefore, may not significantly contribute to the development of OC, and 2) the high frequency of LOH at hMLH1 observed in our ovarian tumors suggests that further investigation is needed to determine if such a trend exists in other mismatch DNA repair and/or critical genes.

Adaptor Proteins, Signal Transducing↗