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At least 19 recordsLinked to original sources
PubMed1976

Human tumors studied with genetic markers.

Genetic marker systems have been employed to investigate the origin and development of many human tumors. The type of information already gained with such systems includes the probable single cell origin of chronic myelocytic leukemia in a marrow stem cell. The G-6-PD system has also confirmed the hypothesis that at least some hereditary and viral tumors have multiple cell origin. However, Burkitt lymphoma, the malignancy in man for which there is a great amount of circumstantial evidence for a viral cancer, has a clonal origin. Of particular interest is the demonstration that early relapses after remissions of Burkitt lymphoma represent reemergence of the original malignant cell lines, whereas some late recurrences may be the result of newly induced malignant clones. Similarly, some recurrences of acute lymphoblastic leukemia in patients treated with marrow transplantation may be new occurrences of disease. These observations have important implications for the etiology and pathogenesis of Burkitt lymphoma and acute lymphoblastic leukemia.

Burkitt Lymphoma↗
PubMedDate not supplied

Diabetes mellitus: the search for genetic markers.

The search for genetic markers has established that idiopathic diabetes mellitus is a genetically heterogeneous group of disorders that have glucose intolerance in common. The types of genetic markers--subclinical linkage, and association--and how they are utilized to delineate the genetic basis of the diabetic syndrome are discussed. The use of such markers as insulin levels, pancreatic islet cell antibodies, and HLA antigens has permitted the separation of insulin-dependent (juvenile) and not insulin-dependent (maturity) diabetes. Such studies have also started to reveal heterogeneity within these broad groups of insulin-dependent and not insulin-dependent types. This extensive heterogeneity has major implications for understanding the pathogenesis and genetics of diabetic mellitus and is of potentially great clinical significance, since the natural history and complications may well differ between these different disorders.

Diabetes Mellitus↗
PubMed1979

Human saliva as a source of biochemical genetic markers. I. Techniques.

The number of genetic markers identified in human saliva is still small compared to known genetic markers of blood. Enzyme activities that can be detected in human saliva by spectrophotometric techniques are listed. The methodologies currently available for the detection of biochemical genetic markers by polyacrylamide-gel electrophoresis are summarized.

Electrophoresis, Polyacrylamide Gel↗
PubMed1979

[Geographical pathology and genetic markers: detection of associations (author's transl)].

The study of potential associations between genetic markers and various diseases is an important approach in epidemiology. With such studies it is possible to reveal an hereditary component for multifactorial diseases. There are three kinds of analyses: --comparisons of the frequency of the marker in patients and in a control group; --investigations of genetic markers in families with high incidence of disease; --studies of geographical clines between the incidence of the disease and the marker frequency. The interpretation of such geographical associations is difficult. These associations can be the reflect of the migration of susceptibility genes with genetic markers. The HLA system is the better for this kind of approach.

Breast Neoplasms↗
PubMed1977

Genetic markers and cancer epidemiology.

The study of potential associations between genetic markers and various cancers has a long history in cancer epidemiology. Such investigations are subject to serious problems of statistical significance and the choice of appropriate control populations. A promising future for the use of human population genetics in cancer epidemiology may be in the investigation of genetic markers (such as the HL-A complex) which code for proteins of potential immunological or physiological importance in susceptibility or resistance to cancer. The cerumen gentic marker has played a central part in a hypothesis formulated in our laboratory for the etiology of breast cancer. A second new development in this field is likely to be the investigation of genetic markers in families with high incidence of cancer. Such families permit the simultaneous study of genetic hypotheses of cancer inheritance and the association of marker genotypes with cancer through segregation and linkage analysis.

ABO Blood-Group System↗
PubMed1991

Genetic marker technology.

Advances in our understanding of polymorphisms found in eukaryotic genomes and improved methods for studying genetic markers should facilitate genetic linkage mapping and other applications. Progress within the past year includes characterization of the types, frequencies, and properties of tandemly repeated sequences, methods for obtaining the DNA sequence flanking genetic markers for use in the polymerase chain reaction, and new detection systems featuring automation and multiplexing.

Animals↗
PubMed1978

[Modifications of genetic markers during malignant blood disease].

Genetic marker changes in malignancy are related to an acquired disfunction of the genetic material in stem cells. This disfunction always leads to the lack of antigen; whenever we evidenced a new specificity it was an unconverted substrate. In malignant states modifications are multiple, polyclonal and independent. This least feature explains the extent of the process giving that disfunction. The evidence of a genetic defect is supported by the simultaneous decrease of the primary gene product: the glycosyl-transferase (ABO locus). In some other malignant carcinoma, blood group specificities were observed, their meaning is not well explained. Blood group specificities associated to carcino embryogenic antigen (CEA) or to some mucins could be related to the structure of macromolecular carriers.

ABO Blood-Group System↗
PubMed1992

Genetic markers in alcoholic liver cirrhosis.

11 genetic markers were typed in 157 individuals suffering from alcoholic cirrhosis, and compared with a random sample of healthy individuals. No significant differences were found for transferrin, specific group component, orosomucoid, esterase D, phosphogluconate dehydrogenase and adenylate kinase. Strong associations between alcoholic cirrhosis and alpha-1-antitrypsin PI*Z allele, haptoglobin HP*1 allele and acid phosphatase ACP AC phenotype were observed. The biological significance of these associations and their relationships with the development of alcoholic cirrhosis are also discussed.

Adult↗
PubMed1992

Absence of evidence for linkage between Booroola gene and genetic markers at 11 sheep blood polymorphic loci.

Genetic linkage between the Booroola locus (Fec) and 11 sheep blood polymorphic loci (i.e. Tf, Hb, CA, OLA, and A, B, C, D, M, R, F41 red cell blood groups) was investigated in six large sire families (163 informative female offspring). The six sires tested were heterozygous for the Booroola allele (FecB) and for several genetic markers. No evidence in favour of linkage was found. Moreover, depending on the marker locus considered, linkage closer than or as close as the recombination frequency of 10-30% was excluded.

Animals↗
PubMed1979

Optimization procedures in twin zygosity diagnosis by genetic markers. A cost-effectiveness analysis.

More and more genetic markers usable for twin zygosity determination have become available. A relatively small number of markers is sufficient to achieve a satisfactory probability of correctly classifying a twin pair. Previously only the genetic properties of markers have been considered when choosing the markers to be determined. A cost-effectiveness analysis, which considers both genetic properties and relative determination costs of markers, is presented and illustrated with data from the Finnish Twin Registry studies.

Cost-Benefit Analysis↗
PubMed1992

Novel genetic markers of rheumatoid arthritis in Chilean patients, by DR serotyping and restriction fragment length polymorphism analysis.

OBJECTIVE: The analysis of genetic markers of rheumatoid arthritis (RA) in a population in which the DR4 serotype is not strongly associated with the disease. METHODS: Chilean RA patients (56 seropositive and 22 seronegative) and 141 controls were studied by serotyping. Southern blot analysis of Bam HI restriction fragment length polymorphism (RFLP) was done in genomic DNA from 46 patients with seropositive RA, 17 patients with seronegative RA, and 45 controls, using a complementary DNA probe specific for DRB1 genes. RESULTS: The prevalence of the HLA-DR9 haplotype was strikingly higher in seropositive RA patients (21%) than in controls (3%) (Pcorr less than 0.0008, by Fisher's exact test; relative risk [RR] = 9.34). The prevalence of DR4 and DR1 haplotypes, although slightly increased, did not achieve a significant preponderance. The simultaneous presence of two Bam HI fragments (3.6 kb and 4.5 kb) was found with higher prevalence in seropositive patients (83%; RR = 9; Pcorr less than 0.00002) than in controls (36%), and seemed higher in seronegative RA patients as well (71%; RR = 4). Furthermore, its prevalence remained increased in comparisons of DR4 positive controls (36%) with DR4 positive seropositive patients (100%; RR = 67; Pcorr less than 0.0002) and DR4 positive seronegative patients (100%; RR = 36; Pcorr less than 0.006), even after excluding the DR9 positive individuals. A tendency toward higher association with DR1 seropositive RA patients (67%; RR = 12), a group with no DR4 or DR9 positive individuals, than in DR1 positive controls (14%), was also observed. CONCLUSION: The HLA-DR9 haplotype was definitively consolidated as a very strong genetic marker exclusively for seropositive RA in Chilean patients, as suggested by our previous observations. RFLP analysis showed that the simultaneous presence of 3.6-kb and 4.5-kb Bam HI fragments constituted a better RA marker than did any of the heretofore studied haplotypes. These fragments together would be linked to RA independently of the DR1, DR4, and DR9 haplotypes. The overall evidence indicates that Chilean seropositive RA patients display a genetic background that is different from that underlying RA susceptibility in other populations and suggests the existence of common, as well as distinct, genetic elements predisposing to seronegative and seropositive RA.

Adult↗
PubMed1977

Genetic markers in Herdwick sheep: no correlation with succeptibility or resistance to experimental scrapie.

Genetic markers were studied in Herdwick sheep, bred at Compton, with special reference to genetically selected lines which differ in susceptibility or resistance to experimentally produced scrapie. There were no correlations between susceptibility to the disease and albumin, pre-albumin, esterase and haemoglobin phenotypes, and between reduced glutathione levels and alpha-mannosidase isoenzymes, the latter possibly representing a previously undescribed genetic marker in sheep.

Animals↗
PubMed1991

Isolation and sequencing of a gene, C-ADE1, and its use for a host-vector system in Candida maltosa with two genetic markers.

The host-vector systems of an n-alkane-assimilating-yeast, Candida maltosa, that we previously constructed consisted of a vector replicating with an ARS region of this yeast, and C. maltosa strains J288 (leu2) or CH1 (his5) as hosts. Since each of these hosts has a single genetic marker, we have developed a new host-vector system using two genetic markers. By UV irradiation of strain CH1, an adenine auxotrophic mutant, CHA1, forming red colonies was isolated. A DNA fragment complementing this deficiency was isolated from the C. maltosa genome. Since the DNA fragment also complemented the ade1 mutation of S. cerevisiae, we termed a gene contained in this DNA fragment C-ADE1. The nucleotides of C-ADE1 were sequenced. The deduced amino acid sequence (291 residues) had 65.6% homology with that of ADE1 of S. cerevisiae (306 residues). Having the cloned C-ADE1 DNA, we improved the host-vector system of C. maltosa.

Adenine↗
PubMed1979

Genetic markers in depressive disorders.

1. Association or linkage between a known genetic marker and an illness with a presumed genetic etiology supports two conclusions: a) The genetic etiology would be considered definite, and b) the illness should be considered a homogeneous disease. 2. After separating depressions on the basis of gross familial differences, a finding of linkage or association in any subgroup would indicate that the particular illness is autonomous. Data on association between bipolar and unipolar depression and subtypes of the ABO system are given. 3. Methodological problems in association studies are discussed. 4. Preliminary data suggest the possibility of linkage between the alpha-haptoglobin locus and third component of complement locus and depression spectrum disease, a depression which is familially defined by the presence of alcoholism in the first-degree family member.

Depressive Disorder↗