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PubMed2003

Possible maternal inheritance of breast muscle morphology in turkeys at sixteen weeks of age.

During the study of inheritance of breast muscle morphology of turkeys during embryonic development and posthatch in two experiments, interesting results were obtained at 16 wk of age. In experiment 1, an experimental line (F) selected long term for increased 16-wk BW was crossed reciprocally with a commercial sire line (B). Samples of pectoralis major muscle were obtained from three males and three females of each genetic group. The F line was reciprocally crossed with a randombred control line (RBC2) in experiment 2, and p. major muscle samples were taken from 10 males and 10 females of each genetic group. The RBC2 line was the base population for the F line. The muscle samples were obtained in a manner to avoid contraction. After fixing, the muscle samples were stained with hematoxylin and eosin to view muscle morphology. Distinct morphological types were observed in the muscle samples for the B, F, and RBC2 lines. The pectoralis major muscle from the B line was, in general, characterized by large fibers with a well-defined extracellular matrix (perimysial and endomysial spaces). Similar to the B line, representative samples of the RBC2 line had a well-defined extracellular matrix but muscle fiber size was not as large as that of the B line. Representative samples of the F line were characterized by a greatly reduced extracellular matrix with the muscle fibers not well defined. For the reciprocal crosses in both experiments, representative samples indicated the offspring had breast muscle morphology similar to that of the female parent, suggesting maternal inheritance. There was no sex effect on breast muscle morphology in either experiment. In order to study the consistency of the results, muscle morphology of representative sections of muscle were subjectively rated by four individuals. The ratings ranged from 1 (little extracellar matrix and indistinct muscle fibers) to 5 (large extracellular space and distinct muscle fibers). Ratings of 2 to 4 were intermediate to these extremes. In experiment 1, ratings of the pure B line and the F sire x B dam cross were similar and higher than that of the pure F line and B sire x F dam cross, which did not differ in average rating. The results for experiment 2 were similar to those for experiment 1 in that the average ratings of the reciprocal crosses were similar to that of the female parental line. The results from the ratings support maternal inheritance of breast muscle morphology.

Animals↗

PubMed1993

Both inherited HLA-haplotypes are important in the predisposition to rheumatoid arthritis.

The distribution of the HLA-DR allele frequencies of 105 RA patients has been compared with the expected distribution under recessive and dominant modes of inheritance using control data from 2041 controls and the antigen genotype frequency among patients methodology. The observed distribution was compatible with a recessive mode of HLA-linked inheritance in RA, with a dominant mode rejected, whether HLA-DR4 was considered alone, or HLA-DR4 and HLA-DR1 were combined as if they were behaving as a single predisposing gene. Mean sibship concordance rates (MSCRs) were calculated for categories of proband HLA-DR genotypes. The highest MSCR was for HLA-DR4 homozygous probands, and the lowest for HLA-DR2 or 7/non-4 genotypes. These combined observations suggest that interactions between both inherited HLA-haplotypes are important in the predisposition to RA.

Alleles↗

PubMed1994

An overview of the mechanism of action of antithrombin and its inherited deficiency states.

Antithrombin is the most important physiological inhibitor of the various activated serine protease clotting factors, particularly thrombin. In vitro, the inhibition of thrombin by antithrombin is very slow; but greatly enhanced by heparin and related glycosaminoglycans. When a serine protease interacts with antithrombin, the two proteins form a covalent stable stoichiometric 1:1 complex that is rapidly removed from the circulation. The formation of this stable covalent complex involves the cleavage of the reactive centre of the inhibitor at arginine 393-serine 394 by the active site serine residue of the protease. This is followed by the formation of an ester linkage between the active site serine residue of the protease and the arginine 393 residue of the cleaved antithrombin molecule. The existence of an antithrombin deficiency state was first recognized in 1965, in a family some of whose members suffered from recurrent episodes of venous thrombosis. Subsequently, many kindreds with antithrombin deficiency have been described from diverse geographic locations. Moreover, the prevalence of antithrombin deficiency in the general population has been reported to vary from 1:500 to 1:5000. With the advent of recombinant DNA techniques, the definition of the molecular pathology of antithrombin deficiency has allowed the characterization of the specific mutation in more than 150 kindreds. Approximately 60 different mutations, resulting in either an absent or a pathological antithrombin gene product, have been reported. Inherited antithrombin deficiency is a well-recognized cause of predisposition to venous thrombosis and in a large type 2 antithrombin-deficient kindred with an alanine 382 threonine mutation (antithrombin-Hamilton), less than 20% of affected individuals were found to have objective evidence for past thrombotic events. In most of these, the initial thrombotic episode occurred when a predisposing factor was present (pregnancy, surgery, oral contraception, trauma, etc.). The incidence of thrombotic events in subjects with inherited antithrombin deficiency thus appears to be significantly lower than heretofore estimated; moreover, such events appear to occur predominantly in association with predisposing factors. Insights from studies of patients with inherited antithrombin deficiency could provide useful information in the management of those with acquired antithrombin deficiency.

Amino Acid Sequence↗

PubMed1996

Low thrombosis rate seen in blood donors and their relatives with inherited deficiencies of antithrombin and protein C: correlation with type of defect, family history, and absence of the factor V Leiden mutation.

We have previously identified a group of blood donors with inherited deficiencies of either antithrombin (AT) or protein C who appear to have a relatively low thrombosis rate. In the 5 years that have elapsed since initial identification of these individuals, resistance to activated protein C (APC resistance), which is associated with the factor V Leiden gene mutation, has emerged as an important and highly prevalent inherited thrombophilic risk factor. We have followed 28 donors/relatives with deficiency of AT (median age 48 years, range 16-77) and 23 with deficiency of protein C (median age 44 years, range 15-79) over a period of 5 years. During the study period only one individual, who was previously symptomatic, has suffered a thrombotic event which occurred spontaneously whilst on warfarin. We have now excluded coinheritance of APC resistance due to the factor V Leiden mutation in our cohort. Our findings demonstrate that individuals with single inherited thrombophilic defects are not uncommon and are frequently asymptomatic. The absence of the factor V Leiden mutation may in part explain the low thrombosis rate observed, and lends support to the hypothesis that multiple thrombophilic defects may be necessary for the development of thrombosis.

Adolescent↗

PubMed2001

Risk of venous thromboembolism in carriers of factor V Leiden with a concomitant inherited thrombophilic defect: a retrospective analysis.

Factor V Leiden is the most common genetic defect associated with venous thromboembolism. Its clinical expression is limited and shows a wide intrafamilial and interfamilial variation, which might be explained by the influence of other genetic risk factors. We retrospectively studied 226 patients with factor V Leiden and documented venous thromboembolism (probands) and 400 first-degree carrier relatives to assess the contribution of concomitant genetic risk factors to the occurrence of venous thromboembolism. The prothrombin G20210A mutation was found in 8.3%, homozygosity of factor V Leiden in 7.2%, and inherited deficiencies of antithrombin, protein C or protein S in 4.7% of symptomatic carriers (probands and relatives), as compared with 6.0, 3.4 and 0.9% of asymptomatic carriers, respectively. The total follow-up time in relatives was 11 049 years. Prevalences of venous thromboembolism were 10.8% in single heterozygous factor V Leiden carrier relatives, 16.0% in double-heterozygotes for factor V Leiden and the prothrombin mutation, 36.8% in homozygotes for factor V Leiden, and 40.0% in double-heterozygotes for factor V Leiden and an inherited deficiency of protein C or protein S. Annual incidences in these groups were 0.39, 0.57, 1.41, and 4.76%, respectively. Multivariate analysis showed a small, non-significant additional effect of the prothrombin mutation on the risk of venous thromboembolism in heterozygotes for factor V Leiden [adjusted hazard ratio, 1.3; 95% confidence interval (CI), 0.5-3.8]. This effect was more pronounced for homozygosity of factor V Leiden (adjusted hazard ratio, 3.9; 95% CI, 1.7-9.0) and inherited protein C or protein S deficiencies (adjusted hazard ratio, 17.5; 95% CI, 3.8-81.2). Our data provide evidence of clustering of the evaluated genetic thrombophilic defects in symptomatic factor V Leiden carriers and support the assumption that the clinical expression of factor V Leiden depends on clustering in a part of carriers.

Adult↗

PubMed2001

Caspr1/Paranodin/Neurexin IV is most likely not a common disease-causing gene for inherited peripheral neuropathies.

Contactin associated protein 1 (Caspr1/Paranodin/Neurexin IV) is an axonal transmembrane molecule mainly localised at the paranodal junction. Since molecular alterations in septate-like junctions at the paranodes might have important consequences for the function of the nerve fiber, we considered that Caspr1 could be involved in the pathogenesis of inherited peripheral neuropathies. In this study, we physically mapped the Caspr1 gene on chromosome 17q21.1 and determined its genomic structure. We performed a mutation analysis of the Caspr1 gene in a cohort of 64 unrelated patients afflicted with distinct inherited peripheral neuropathies. Since no disease causing mutations were found, we suggest that Caspr1 is probably not a common cause of inherited peripheral neuropathies.

Cell Adhesion Molecules, Neuronal↗

PubMed1995

Inherited and noninherited risk factors in rheumatoid arthritis.

Rheumatoid arthritis (RA) is likely the result of a concerted action of several inherited and noninherited factors. Although there is a high suspicion that environmental factors are important, proof is missing. Most information has been collected on genetic risk factors. The inheritance pattern for RA is complex, and there is good evidence that HLA as well as non-HLA genes are involved. Almost all racial-ethnic groups share the association of RA with the HLA-DRB1-encoded sequence motif QKRAA or QRRAA. However, the completeness of the association varies significantly in different ethnic cohorts, as can be expected in a multigene model. The sequence motif translates into a pocket in the antigen-binding site of the HLA-DR molecule. The "rheumatoid pocket" accommodates peptide side chains and has distinct binding characteristics. Epidemiologic evidence points toward a role for non-HLA genes. Candidate genes, such as transporter in antigen processing (TAP) genes are currently explored. Major advances in defining and understanding the contribution of inherited and noninherited factors in RA may come from abandoning the concept of RA as a single entity and accepting a heterogeneity model for RA. Distributions of HLA-DR genes indicate that several subsets of RA patients exist. Seronegative (prognostically good) and seropositive (prognostically worse) patients can be distinguished by the arginine versus lysine substitution at position 71 of the HLA-DRB1 gene. A different dimension of disease, rheumatoid organ disease, appears to be reached in patients with two HLA-DRB1*0401 alleles. Identification of distinct RA subsets may allow us to stratify patients into categories that differ with respect to etiology, disease course, clinical pattern, and treatment response.

Amino Acid Sequence↗

PubMed1998

Inherited predisposition to colon cancer.

Colorectal cancer is one of the most common malignancies in the United States. Although both genetic and environmental factors play a role in colorectal tumorigenesis, recent advances in genetics have more clearly defined the impact of inheritance in the multistep process of the disease. Researchers have identified single genes that confer a susceptibility to familial adenomatous polyposis (FAP) and hereditary nonpolyposis colorectal cancer (HNPCC). Because these genes are inherited in an autosomal dominant fashion, offspring of carriers have a 50% chance of inheriting the gene mutation and its associated risk. The FAP gene, when mutated, initiates the neoplastic process. HNPCC gene mutations disrupt mismatch repair, thus inducing progression of tumor formation. Discovery of these genes has helped our understanding of sporadic colon cancer as well. Genetic testing for the FAP and HNPCC genes is now available, and results of this testing have implications for surveillance and management. In addition, testing raises complex psychosocial and ethical issues. At present, genetic testing is primarily conducted in the research setting, but it will soon be available in the clinical arena. To prepare for the challenges that these new advances will present, nurses must begin now to enhance their knowledge of genetics and its application to oncology.

Adenomatous Polyposis Coli↗

PubMed1993

The inheritance pattern of dysplastic naevi in families of dysplastic naevus patients.

Dysplastic naevi (DN) are the major precursor lesions of malignant melanoma, yet the presumed mode of inheritance or genetic aetiology of DN remains controversial. The inheritance pattern of DN in families from a randomly selected population of 26 dysplastic naevus patients was investigated by estimating the segregation ratio in families ascertained through an offspring with DN (incomplete ascertainment). For families ascertained through a parent with DN (complete ascertainment) the transmission pattern was examined by comparing the observed number of affected offspring to the expected number using a chi 2 goodness-of-fit test. Results from the chi 2 tests and the estimated segregation ratio of 0.52 (95% confidence interval: 0.31, 0.73) suggest that the inheritance pattern for dysplastic naevi in these families is consistent with autosomal dominant transmission, although the present study was limited because of a small sample size. The findings, therefore, need to be confirmed by a much larger study that is able to test more rigorously specific genetic hypotheses.

Dysplastic Nevus Syndrome↗

PubMed2004

Inherited thrombocytopenias: toward a molecular understanding of disorders of platelet production.

PURPOSE OF REVIEW: To review the defined syndromes of inherited thrombocytopenia and discuss new genetic data for several disorders that shed light on the process of megakaryopoiesis. RECENT FINDINGS: The genes responsible for several inherited thrombocytopenias have been recently discovered, including congenital amegakaryocytic leukemia, amegakaryocytic thrombocytopenia with radio-ulnar synostosis, familial platelet syndrome with predisposition to acute myelogenous leukemia, Paris-Trousseau, Wiskott-Aldrich syndrome, and the May-Hegglin, Sebastian, Epstein, and Fechner syndromes. These clinical syndromes, combined with studies in mouse and in vitro models, reveal the importance of these genes for normal hematopoiesis. SUMMARY: Although inherited syndromes of thrombocytopenia are rare, characterization of mutations in these disorders has contributed greatly to our understanding of megakaryocyte and platelet development. A systematic registry of congenitally thrombocytopenic individuals would almost certainly lead to new genetic discoveries.

Animals↗

PubMed1999

Molecular basis of inherited neuropathies.

Considerable advances in our knowledge of the most frequently encountered group of inherited neuropathies, Charcot-Marie-Tooth neurpathy (CMT) and related disorders, have recently been made by genetic studies demonstrating that these disorders are caused by duplication, deletion or point mutations of specific genes of the peripheral myelin. The present classification of CMT and related disorders is based on a combination of clinical, neurophysiological, and genetic findings, and new genes and distinct mutations responsible for different clinical phenotypes are continuously being added. The genes that encode peripheral myelin protein of 22 kDa, protein zero, connexin-32 and early growth response-2 are the genes known to be involved in the pathogenesis of inherited neuropathies. Overexpression or underexpression of peripheral myelin protein of 22 kDa are causative for the most frequent forms of CMT-CMT1A and hereditary neuropathy with liability to pressure palsies--but the mechanisms that lead to incorrect myelin formation and maintenance are still unknown. Point mutations in the myelin genes can determine a loss of function, but in some cases an aberrant protein can act through a dominant negative or a toxic gain of function mechanism, disrupting the regular and precise relationship between the different myelin genes. Animal and in-vitro models of inherited neuropathies have been developed and will probably give the information that is necessary to clarify the pathogenetic mechanisms of demyelination.

Animals↗

PubMed2003

The evolution of juvenile myelomonocytic leukemia in a female patient with paternally inherited neurofibromatosis type 1.

The most common myeloid malignancy seen in children with neurofibromatosis type 1 (NF-1) is juvenile myelomonocytic leukemia (JMML), a myeloproliferative disease. The vast majority of these children have inherited the neurocutaneous disease from an affected mother; boys are more often affected than girls. We present the rare finding of a 7-year-old girl with NF-1 who developed JMML. She inherited her NF-1 from the father. At the time of her initial presentation, clonogenic assays of bone marrow mononuclear cells did not show the spontaneous growth of granulocyte-macrophage colony-forming units or hypersensitivity to granulocyte-macrophage colony-stimulating factor that is characteristic of this disorder. After 1 month, repeat evaluations of the patient's clinical and laboratory test results became fully consistent with those for a diagnosis of JMML. This illustrates the stepwise evolution of this myeloproliferative disorder in NF-1 and the importance of close follow-up and reassessment of these patients. Our case is only the second report of JMML in a girl who inherited NF-1 from her father.

Bone Marrow↗

PubMedDate not supplied

Inherited susceptibility for pediatric cancer.

The percentage of childhood cancers that are caused by a clearly inherited predisposition varies significantly from only a few percent to more than 50% with individual tumor types. Recent advances in genetic testing and studies of cohorts of cancer patients have demonstrated the likelihood of identifying a cancer susceptibility mutation for numerous childhood cancers. Inherited predisposition to cancer is frequently the result of dominant constitutional mutations in tumor suppressor genes, which can be inherited from an affected parent or occur de novo during gametogenesis. In this article, we review the childhood malignancies that are associated with at least a 10% likelihood of being caused by a genetic susceptibility to cancer and therefore warrant consideration for a genetic evaluation; these malignancies include retinoblastoma, adrenocortical carcinoma, atypical teratoid and malignant rhabdoid tumors, optic pathway tumors, juvenile myelomonocytic leukemia, malignant peripheral nerve sheath tumors, vestibular schwannomas, endolymphatic sac tumors, hemangioblastomas, medullary thyroid cancer, pheochromocytomas, and paragangliomas. Children with other malignancies may also warrant genetic evaluation if there is the co-occurrence of malignancy and two or more congenital anomalies, or malignancy and a significant family history of related cancers. We also review the importance of the correct genetic diagnosis in order to ensure appropriate treatment and ongoing cancer surveillance for the child with cancer and closely related family members (e.g., parents and siblings).

Child↗

PubMedDate not supplied

Role of the geneticist in testing and counseling for inherited thrombophilia.

Within the past decade, the identification of two mutations that are relatively prevalent among the white population (the factor V Leiden and prothrombin G20210A gene mutations) has paved the way for a number of large cohort studies that have greatly advanced our understanding of the pathogenesis of venous thromboembolism (VTE). VTE is clearly a multigenic disorder, with well-characterized examples of gene-gene and gene-environment interactions underlying its pathogenesis. Increasing numbers of patients are being referred for testing, and many more diagnoses of inherited thrombophilia are being made. The purpose of this article is to discuss the practical applications of both diagnostic testing and genetic counseling for the major inherited thrombophilias: inherited resistance to activated protein C/factor V Leiden, prothrombin G20210A mutation, protein C deficiency, protein S deficiency, and antithrombin deficiency. A description of each entity is included along with a discussion of the indications for testing, selection of the most appropriate screening test, and proper interpretation of test results. Informed consent for testing, screening of asymptomatic individuals in special circumstances (such as during pregnancy or before initiation of estrogen therapy), screening of family members, and posttest education are also addressed. This article emphasizes that these polymorphisms should be regarded as risk factors for thrombosis whose clinical expression generally depends on the coexistence of additional thrombophilic mutations or environmental conditions that provoke the development of VTE.

Environment↗

PubMed2004

Familial multiple sclerosis and other inherited disorders of the white matter.

BACKGROUND: An objective demonstration of lesions disseminated in time and space remains the core of the last revision of diagnostic criteria for multiple sclerosis (MS), but this update is now empowered by a weighted use of magnetic resonance imaging (MRI), which results in an earlier and more unambiguous diagnosis ("MS," "not MS," or "possible MS"). Nevertheless, the exclusion of other entities still remains an integral element of the diagnostic process. REVIEW SUMMARY: Exclusion of genetic disorders can be challenging in some cases with familial recurrence of MS, particularly when the transmission is mimicking a mendelian or a maternal pattern of inheritance. Vice versa, many forms of mendelian leukodystrophies and leukoencephalopathies present with juvenile or adult onset, progressive or relapsing-remitting courses, intrafamilial phenotypic heterogeneity and MRI signs of multifocal white matter (WM) pathology, features potentially leading to a temporary confusion with MS. With the recent availability of disease modifying medications in MS, the development of specific molecular therapies in inherited WM disorders, and the general recognition of the effectiveness of early treatments, the accuracy of initial diagnostic assessment has become critical. CONCLUSION: Considering the importance of disease specific treatments, here we review the major characteristics of familial MS and some of the inheritable diseases of the WM. Although no direct genetic link between MS and these WM abnormalities is known, molecular data from the field of rare genetic disorders may also provide some experimental paradigms to a further exploration of MS.

Brain↗

PubMed2005

Living donor liver transplantation for noncirrhotic inheritable metabolic liver diseases: impact of the use of heterozygous donors.

BACKGROUND: In living donor liver transplantation (LDLT), the liver donor is almost always a blood relative; therefore, the donor is sometimes a heterozygous carrier of inheritable diseases. The use of such carriers as donors has not been validated. The aim of the present study was to evaluate the outcome of LDLT for noncirrhotic inheritable metabolic liver disease (NCIMLD) to clarify the effects of using a heterozygous carrier as a donor. METHODS: Between June 1990 and December 2003, 21 patients with NCIMLD underwent LDLT at our institution. The indications for LDLT included type II citrullinemia (n = 7), ornithine transcarbamylase deficiency (n = 6), propionic acidemia (n = 3), Crigler-Najjar syndrome type I (n = 2), methylmalonic acidemia (n = 2), and familial amyloid polyneuropathy (n = 1). Of these 21 recipients, six underwent auxiliary partial orthotopic liver transplantation. RESULTS: The cumulative survival rate of the recipients was 85.7% at both 1 and 5 years after operation. All surviving recipients are currently doing well without sequelae of the original diseases, including neurological impairments or physical growth retardation. Twelve of the 21 donors were considered to be heterozygous carriers based on the modes of inheritance of the recipients' diseases and preoperative donor medical examinations. All donors were uneventfully discharged from the hospital and have been doing well since discharge. No mortality or morbidity related to the use of heterozygous donors was observed in donors or recipients. CONCLUSIONS: Our results suggest that the use of heterozygous donors in LDLT for NCIMLD has no negative impact on either donors or recipients, although some issues remain unsolved and should be evaluated in further studies.

Acidosis↗

PubMed1999

Enhanced proteasomal degradation of mutant human thiopurine S-methyltransferase (TPMT) in mammalian cells: mechanism for TPMT protein deficiency inherited by TPMT2, TPMT3A, TPMT3B or TPMT3C.

Inheritance of the TPMT*2, TPMT*3A and TPMT*3C mutant alleles is associated with deficiency of thiopurine S-methyltransferase (TPMT) activity in humans. However, unlike TPMT*2 and TPMT*3A, the catalytically active protein coded by TPMT*3C does not undergo enhanced proteolysis when heterologously expressed in yeast, making it unclear why this common mutant allele should be associated with inheritance of TPMT-deficiency. To further elucidate the mechanism for TPMT deficiency associated with these alleles, we characterized TPMT proteolysis following heterologous expression of wild-type and mutant proteins in mammalian cells. When expressed in COS-1 cells, proteins encoded by TPMT*2, TPMT*3A, and TPMT*3C cDNAs had significantly reduced steady-state levels and shorter degradation half-lives compared with the wild-type protein. Similarly, in rabbit reticulocyte lysate (RRL), these mutant TPMT proteins were degraded significantly faster than the wild-type protein. Thus, enhanced proteolysis of TPMT*3C protein in mammalian cells is in contrast to its stability in yeast, but consistent with TPMT-deficiency in humans. Proteolysis was ATP-dependent and sensitive to proteasomal inhibitors MG115, MG132 and lactacystin, but not to calpain inhibitor II. We conclude that all of these mutant TPMT proteins undergo enhanced proteolysis in mammalian cells, through an ATP-dependent proteasomal pathway, leading to low or undetectable levels of TPMT protein in humans who inherit these mutant alleles.

Adenosine Triphosphate↗

PubMed2002

Variable modes of inheritance of morphometrical traits in hybrids between Drosophila melanogaster and Drosophila simulans.

We investigated body-size inheritance in interspecific sterile hybrids by crossing a Drosophila simulans strain with 13 strains of Drosophila melanogaster, which were of various origins and chosen for their broad range of genetic variation. A highly significant parent-offspring correlation was observed, showing that the D. melanogaster genes for size are still expressed in a hybrid background. Superimposed on to this additive inheritance, the size of hybrids was always less than the mid-parent value. This phenomenon, which at first sight might be described as dominance or overdominance, is more precisely interpreted as a consequence of a hybrid breakdown, that is, a dysfunction of the parental genes for size when put to work together. This interpretation is enforced by the fact that phenotypic variability was much more prevalent in hybrids than in parents. We also analysed body pigmentation inheritance in the same crosses and got a very different picture. There was no increase in the phenotypic variance of F(1) hybrids and only a low parent-offspring correlation. Apparent overdominance could be observed but in opposite directions, with no evidence of hybrid breakdown. Our data point to the possibility of analysing a diversity of quantitative traits in interspecific hybrids, and indicate that breakdown might be restricted to some traits only.

Animals↗