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Antoine Blancher - One of the best experts on this subject based on the ideXlab platform.
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Evolutionary dynamics of the human ABO Gene
Human Genetics, 2008Co-Authors: Francesc Calafell, Francis Roubinet, Anna Ramírez-Soriano, Jaume Bertranpetit, Naruya Saitou, Antoine BlancherAbstract:The ABO polymorphism has long been suspected to be under balancing selection. To explore this possibility, we analyzed two datasets: (1) a set of 94 23-Kb sequences in European- and African-Americans produced by the Seattle SNPs project, and (2) a set of 814 2-Kb sequences in O alleles from seven worldwide populations. A phyloGenetic analysis of the Seattle sequences showed a complex pattern in which the action of recombination and Gene conversion are evident, and in which four main lineages could be individuated. The sequence patterns could be linked to the expected blood group phenotype; in particular, the main mutation giving rise to the null O allele is likely to have appeared at least three times in human evolution, giving rise to allele lineages O02, O01, and O09. However, the Genealogy changes along the Gene and variations of both numbers of branches and of their time depth were observed, which could result from a combined action of recombination and selection. Several neutrality tests clearly demonstrated deviations compatible with balancing selection, peaking at several locations along the Gene. The time depth of the Genealogy was also incompatible with neutral evolution, particularly in the region from exons 6 to 7, which codes for most of the catalytic domain.
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long term evolution of the cazy glycosyltransferase 6 ABO Gene family from fishes to mammals a birth and death evolution model
Glycobiology, 2007Co-Authors: Annelaure Turcotdubois, Francis Roubinet, Stéphanie Despiau, Nicolai V. Bovin, Beatrice Le Moullacvaidye, Jacques Le Pendu, Antoine BlancherAbstract:Functional glycosyltransferase 6 (GT6) family members catalyze the transfer of galactose or N-acetylgalactosamine in α1,3 linkage to various substrates and synthesize structures related to the A and B histo-blood group antigens, the Forssman antigen, αGal epitope, and iGb3 glycolipid. In rat, mouse, dog, and cow genomes, we have identified three new mammalian Genes (GT6m5, GT6m6, and GT6m7) encoding putative proteins belonging to the GT6 family. Among these, GT6m6 protein does not display major alterations of the GT6 motifs involved in binding of the divalent cation and the substrate. Based on protein sequence comparison, Gene structure, and synteny, GT6 homologous sequences were also identified in bird, fish, and amphibian genomes. Strikingly, the number and type of GT6 Genes varied widely from species to species, even within phyloGenetically related groups. In human, except ABO functional alleles, all other GT6 Genes are either absent or nonfunctional. Human, mouse, and cow have only one ABO Gene, whereas rat and dog have several. In the chicken, the Forssman synthase-like is the single GT6 family member. Five Forssman synthase-like Genes were found in zebrafish, but are absent from three other fishes (fugu, puffer fish, and medaka). Two iGb3 synthase-like Genes were found in medaka, which are absent from zebrafish. Fugu, puffer fish, and medaka have an additional GT6 Gene that we termed GT6m8, which is absent from all other species analyzed here. These observations indicate that individual GT6 Genes have expanded and contracted by recurrent duplications and deletions during vertebrate evolution, following a birth-and-death evolution type.
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Long-term evolution of the CAZY glycosyltransferase 6 (ABO) Gene family from fishes to mammals—a birth-and-death evolution model
Glycobiology, 2007Co-Authors: Anne-laure Turcot-dubois, Francis Roubinet, Béatrice Le Moullac-vaidye, Stéphanie Despiau, Jacques Le Pendu, Nicolai V. Bovin, Antoine BlancherAbstract:Functional glycosyltransferase 6 (GT6) family members catalyze the transfer of galactose or N-acetylgalactosamine in α1,3 linkage to various substrates and synthesize structures related to the A and B histo-blood group antigens, the Forssman antigen, αGal epitope, and iGb3 glycolipid. In rat, mouse, dog, and cow genomes, we have identified three new mammalian Genes (GT6m5, GT6m6, and GT6m7) encoding putative proteins belonging to the GT6 family. Among these, GT6m6 protein does not display major alterations of the GT6 motifs involved in binding of the divalent cation and the substrate. Based on protein sequence comparison, Gene structure, and synteny, GT6 homologous sequences were also identified in bird, fish, and amphibian genomes. Strikingly, the number and type of GT6 Genes varied widely from species to species, even within phyloGenetically related groups. In human, except ABO functional alleles, all other GT6 Genes are either absent or nonfunctional. Human, mouse, and cow have only one ABO Gene, whereas rat and dog have several. In the chicken, the Forssman synthase-like is the single GT6 family member. Five Forssman synthase-like Genes were found in zebrafish, but are absent from three other fishes (fugu, puffer fish, and medaka). Two iGb3 synthase-like Genes were found in medaka, which are absent from zebrafish. Fugu, puffer fish, and medaka have an additional GT6 Gene that we termed GT6m8, which is absent from all other species analyzed here. These observations indicate that individual GT6 Genes have expanded and contracted by recurrent duplications and deletions during vertebrate evolution, following a birth-and-death evolution type.
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Evolution of the O alleles of the human ABO blood group Gene
Transfusion, 2004Co-Authors: Francis Roubinet, Francesc Calafell, Naruya Saitou, Stéphanie Despiau, Fen Jin, Jaume Bertanpetit, Antoine BlancherAbstract:It is the most important blood group system in transfusion and transplantation practices. It was also the first human Genetic system to be applied to anthropologic studies. The A and B alleles of the ABO Gene code for glycosyltransferases that either add an N -acetylgalactosamine or a galactose to various glycoconjugates. These products result in A or B bloodgroup-specific antigens. The O allele corresponds to a silent (null) allele of the ABO Gene. The cDNAs of the three major alleles of the human blood group ABO system were first described by Yamamoto and coworkers.
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Cloning of a rat Gene encoding the histo-blood group B enzyme: rats have more than one ABO Gene.
Glycobiology, 2003Co-Authors: Anne Laure Turcot, Francis Roubinet, Antoine Blancher, Béatrice Le Moullac-vaidye, Stéphanie Despiau, Jézabel Rocher, Claude Szpirer, Jacques Le PenduAbstract:A genomic DNA fragment corresponding to exon 7 of the human ABO Gene was amplified from rats of several inbred and outbred strains. Five different sequences were obtained, four of them corresponding to A-type sequences and one to a B-type sequence based on the amino acids equivalent to residues at positions 266 and 268 of the human enzymes. In rats from inbred strains, a single A-type sequence and the unique B-type sequence were found, whereas some animals of outbred strains presented two or three A-type sequences along with the B-type sequence. The complete coding sequence of the B-type Gene was obtained; identification of the exon‐intron boundaries, determined by comparison with rat genomic sequences from data banks, revealed that the rat B-type Gene structure is identical with that of the mouse ABO Gene. Compared with the human ABO Gene and the rat A Gene, it lacks exon 4. Like the rat A Gene (symbol: ABO), the rat B Gene (symbol: ABO2) is located on chromosome 3q11‐q12. It could be shown by transfection experiments that the B-type cDNA encodes an active B transferase. A transcript of the B Gene was found ubiquitously, whereas the B antigen was only detected in a restricted set of tissues. These data indicate that rats have at least two distinct ABO Genes, one monomorphic Gene encoding a B-specific enzyme and one or more Genes in some cases encoding an A-specific enzyme.
Hans Wolf - One of the best experts on this subject based on the ideXlab platform.
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The blood group ABO Gene transcript is down-regulated in human bladder tumors and growth-stimulated urothelial cell lines.
Cancer research, 1996Co-Authors: Torben F. Ørntoft, Peter Meldgaard, Bent Pedersen, Hans WolfAbstract:The molecular mechanism that in human bladder tumors leads to the loss of blood group ABO glycosyltransferase activity and, thereby, the loss of ABO antigens was investigated. In 15 tumors and 3 normal biopsies from blood group AB individuals and 7 tumors and 3 normal biopsies from blood group O individuals, mRNA was detected by a reverse transcription PCR (RT-PCR) assay, and the ABO blood group structure was determined by immunohistology. The RT-PCR spanned several introns in the ABO Gene to exclude DNA contamination, and the RT-PCR product was shown to reflect the ABO Gene message by dideoxy sequencing. The ABO mRNA was present in normal urothelium and low-grade tumors but disappeared from high grade tumors. This correlation to tumor grade was significant (P
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the blood group ABO Gene transcript is down regulated in human bladder tumors and growth stimulated urothelial cell lines
Cancer Research, 1996Co-Authors: Torben F. Ørntoft, Peter Meldgaard, Bent Pedersen, Hans WolfAbstract:The molecular mechanism that in human bladder tumors leads to the loss of blood group ABO glycosyltransferase activity and, thereby, the loss of ABO antigens was investigated. In 15 tumors and 3 normal biopsies from blood group AB individuals and 7 tumors and 3 normal biopsies from blood group O individuals, mRNA was detected by a reverse transcription PCR (RT-PCR) assay, and the ABO blood group structure was determined by immunohistology. The RT-PCR spanned several introns in the ABO Gene to exclude DNA contamination, and the RT-PCR product was shown to reflect the ABO Gene message by dideoxy sequencing. The ABO mRNA was present in normal urothelium and low-grade tumors but disappeared from high grade tumors. This correlation to tumor grade was significant (P<0.04). Immunohistochemistry with monoclonal anti-blood group antibodies showed a complete correlation between the presence of mRNA and the presence of AB carbohydrate structures on cell surfaces. In two urothelial cell lines, genotyped as A/- and A/A, growth stimulation with the cholera toxin B subunit led to a total loss of ABO mRNA, and epidermal growth factor stimulation had an identical effect on one of the cell lines. We conclude that the ABO glycosylation in normal and malignant urothelium is regulated at the mRNA level, and that a mechanism associated with cell proliferation may trigger down-regulation of ABO mRNA.
Rainer Blasczyk - One of the best experts on this subject based on the ideXlab platform.
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weak blood group b phenotypes may be caused by variations in the ccaat binding factor nf y enhancer region of the ABO Gene
Transfusion, 2007Co-Authors: Axel Seltsam, Franz F. Wagner, Daniela Grüger, Christa Das Gupta, Christina Badedoeding, Rainer BlasczykAbstract:BACKGROUND: Binding of CCAAT-binding factor NF-Y (CBF/NF-Y) to a 43-bp repeat unit in the minisatellite region in the 5′ region of the ABO Gene (CBF/NF-Y enhancer region) plays an important role in regulating the transcription of ABO Genes. The common ABO alleles were found to have CBF/NF-Y enhancer regions with specific numbers of 43-bp minisatellite repeats. MATERIAL AND METHODS: Blood samples from four healthy blood donors with weak B phenotypes were subjected to extensive ABO genotyping, including nucleotide sequencing of the 5′ regulatory region containing the CBF/NF-Y enhancer. RESULTS: The coding region of the ABO Genes exhibited common ABO*B101-heterozygous genotypes in all samples, but unexpected variations were observed in the CBF/NF-Y enhancer region. In two cases, the CBF/NF-Y enhancer motifs did not exhibit the expected ABO allele dependency. One, an ABweak sample was heterozygous for ABO*A101 and ABO*B101 but homozygous for the ABO*B101-specific CBF/NF-Y motif. The second had a common ABO*B101/ABO*O01 genotype but was heterozygous for ABO*A101- and ABO*O01-specific enhancer motifs. In the other two samples, novel CBF/NF-Y motifs were found. One contained a shortened version of an otherwise ABO*B101-specific CBF/NF-Y motif, and the other had a single-base substitution located 12 bp upstream from the beginning of the first 43-bp repeat of an ABO*B101-specific CBF/NF-Y enhancer sequence. CONCLUSION: The frequency of variations in the CBF/NF-Y region of the ABO Gene in these samples with presumably common ABO*B101 alleles suggests that weak blood group B phenotypes may be caused by sequence variations in the CBF/NF-Y regulatory region.
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Weak blood group B phenotypes may be caused by variations in the CCAAT‐binding factor/NF‐Y enhancer region of the ABO Gene
Transfusion, 2007Co-Authors: Axel Seltsam, Franz F. Wagner, Daniela Grüger, Christa Das Gupta, Christina Bade-doeding, Rainer BlasczykAbstract:BACKGROUND: Binding of CCAAT-binding factor NF-Y (CBF/NF-Y) to a 43-bp repeat unit in the minisatellite region in the 5′ region of the ABO Gene (CBF/NF-Y enhancer region) plays an important role in regulating the transcription of ABO Genes. The common ABO alleles were found to have CBF/NF-Y enhancer regions with specific numbers of 43-bp minisatellite repeats. MATERIAL AND METHODS: Blood samples from four healthy blood donors with weak B phenotypes were subjected to extensive ABO genotyping, including nucleotide sequencing of the 5′ regulatory region containing the CBF/NF-Y enhancer. RESULTS: The coding region of the ABO Genes exhibited common ABO*B101-heterozygous genotypes in all samples, but unexpected variations were observed in the CBF/NF-Y enhancer region. In two cases, the CBF/NF-Y enhancer motifs did not exhibit the expected ABO allele dependency. One, an ABweak sample was heterozygous for ABO*A101 and ABO*B101 but homozygous for the ABO*B101-specific CBF/NF-Y motif. The second had a common ABO*B101/ABO*O01 genotype but was heterozygous for ABO*A101- and ABO*O01-specific enhancer motifs. In the other two samples, novel CBF/NF-Y motifs were found. One contained a shortened version of an otherwise ABO*B101-specific CBF/NF-Y motif, and the other had a single-base substitution located 12 bp upstream from the beginning of the first 43-bp repeat of an ABO*B101-specific CBF/NF-Y enhancer sequence. CONCLUSION: The frequency of variations in the CBF/NF-Y region of the ABO Gene in these samples with presumably common ABO*B101 alleles suggests that weak blood group B phenotypes may be caused by sequence variations in the CBF/NF-Y regulatory region.
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Systematic analysis of the ABO Gene diversity within exons 6 and 7 by PCR screening reveals new ABO alleles.
Transfusion, 2003Co-Authors: Axel Seltsam, Michael Hallensleben, Anke Kollmann, Jürgen Burkhart, Rainer BlasczykAbstract:BACKGROUND: Mutations critical for ABO blood group phenotypes have predominantly been found in exons 6 and 7 of the ABO Gene, both of which encode the catalytic domain of ABO glycosyltransferase. To design rapid and reliable ABO genotyping assays, a profound knowledge of the prevalent alleles is required and a reliable sequence database needs to be established. STUDY DESIGN AND METHODS: A PCR screening system was established consisting of 102 different PCRs, each specific for a single nucleotide (nt) variation. The primer mixes were developed to walk from the 5′ to the 3′ end of exons 6 and 7 of the ABO Gene to screen for nt mutations at 50 known polymorphic sites. A total of 109 unrelated individuals with common and rare ABO characteristics were screened. All blood samples in which the PCR results were inconclusive or inconsistent with the ABO phenotypes were subjected to sequence analysis of exons 6 and 7. RESULTS: The results of PCR screening were conclusive and consistent with the ABO phenotypes in 90 cases. In the remaining 19 cases, PCR screening revealed unusual allele combinations or amplification results that were incompatible with known ABO allele combinations or subgroups predicted by serologic analysis. In these 19 cases, sequencing revealed new ABO alleles (one ABO*Ael allele, one ABO*B(A) allele and two ABO*O alleles) in two individuals with common and seven individuals with variant ABO phenotypes. CONCLUSION: This PCR screening strategy is an effective tool for obtaining deeper insight into the ABO Gene diversity and diversification and may be useful to increase the quality of the ABO sequence database.
Yoshihiko Kominato - One of the best experts on this subject based on the ideXlab platform.
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the 3 flanking region of the human ABO histo blood group Gene is involved in negative regulation of Gene expression
Legal Medicine, 2011Co-Authors: Rie Sano, Tamiko Nakajima, Rieko Kubo, Shin Yazawa, Keiko Takahashi, Yoshihiko KominatoAbstract:Abstract Gene expression is driven by promoters, enhancers, silencers, and other cis -regulatory elements upstream and downstream of the Gene. Previous studies of the regulation of human ABO Gene transcription have focused mainly on the 5′ region, including the core promoter and the region proximal to it. However, as the involvement of the 3′ flanking region in transcriptional regulation has not yet been examined, we focused on this issue. The 3′ region approximately 2.2 kb downstream of the ABO Gene was PCR-amplified and inserted into a cloning vector, followed by sequence determination and preparation of luciferase reporter vectors. Transient transfections into KATOIII and K562 cells were performed using various reporter plasmids containing the 3′ region. The 3′ region of the ABO Gene, which was characterized by a high degree of sequence repetition, was effectively cloned by a single-copy cloning method. Transfections in KATOIII and K562 cells showed that negative elements were demonstrable within the 3′ region. These observations suggest that negative regulatory elements seem to be present in the 3′ region of ABO in both epithelial and erythroid lineages. As we had observed a negative region just upstream of the ABO promoter, transcription from ABO could be negatively regulated by repressive regions just upstream of the promoter and downstream of the Gene. Further studies of the enhancer will be required for elucidating the molecular basis of ABO Gene expression.
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The 3′ flanking region of the human ABO histo-blood group Gene is involved in negative regulation of Gene expression
Legal Medicine, 2010Co-Authors: Rie Sano, Tamiko Nakajima, Rieko Kubo, Shin Yazawa, Keiko Takahashi, Yoshihiko KominatoAbstract:Abstract Gene expression is driven by promoters, enhancers, silencers, and other cis -regulatory elements upstream and downstream of the Gene. Previous studies of the regulation of human ABO Gene transcription have focused mainly on the 5′ region, including the core promoter and the region proximal to it. However, as the involvement of the 3′ flanking region in transcriptional regulation has not yet been examined, we focused on this issue. The 3′ region approximately 2.2 kb downstream of the ABO Gene was PCR-amplified and inserted into a cloning vector, followed by sequence determination and preparation of luciferase reporter vectors. Transient transfections into KATOIII and K562 cells were performed using various reporter plasmids containing the 3′ region. The 3′ region of the ABO Gene, which was characterized by a high degree of sequence repetition, was effectively cloned by a single-copy cloning method. Transfections in KATOIII and K562 cells showed that negative elements were demonstrable within the 3′ region. These observations suggest that negative regulatory elements seem to be present in the 3′ region of ABO in both epithelial and erythroid lineages. As we had observed a negative region just upstream of the ABO promoter, transcription from ABO could be negatively regulated by repressive regions just upstream of the promoter and downstream of the Gene. Further studies of the enhancer will be required for elucidating the molecular basis of ABO Gene expression.
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Identification and characterization of a novel antisense RNA transcribed from the opposite strand of the human blood group ABO Gene.
Transfusion, 2007Co-Authors: Yukiko Hata, Yoshihiko Kominato, Hisao TakizawaAbstract:BACKGROUND: To elucidate the molecular basis of control of the ABO Gene in cell type-specific expression, during normal cell differentiation, and in cancer cells lacking A/B antigen, the mechanisms responsible for regulation of human ABO Gene expression have been studied. Recently, naturally occurring antisense transcriptions have been reported to regulate Gene expression through a variety of biological mechanisms. Therefore, RNA transcribed from the opposite strand of the ABO Gene was investigated. STUDY DESIGN AND METHODS: The presence of antisense RNA to the ABO-coding strand in human cancer cell lines and normal tissues was examined by strand-specific reverse transcription-polymerase chain reaction. The 5'- and 3'-ends of the transcript were determined by the rapid amplification of cDNA ends (RACE) system. KATOIII cells were treated with mithramycin A, followed by quantitative analysis of both sense and antisense ABO transcripts. RESULTS: The endogenous antisense RNA to the ABO coding strand was found to start within the first intron of the ABO Gene, and the expression coincided with ABO Gene expression in various cultured cells and normal tissues. This novel Gene was named ABOAS. Treatment of KATOIII cells with mithramycin A repressed transcription from the ABO exon 1 promoter, while it increased the ABOAS transcript. CONCLUSION: These results suggest that ABOAS transcribed from the opposite strand of the ABO Gene might be involved in the regulation of ABO Gene expression.
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Regulation of ABO Gene expression.
Legal medicine (Tokyo Japan), 2005Co-Authors: Yoshihiko Kominato, Yukiko Hata, Kazuhiro Matsui, Hisao TakizawaAbstract:The ABO blood group system is important in blood transfusions and in identifying individuals during criminal investigations. Two carbohydrate antigens, the A and B antigens, and their antibodies constitute this system. Although biochemical and molecular Genetic studies have demonstrated the molecular basis of the histo-blood group ABO system, some aspects remain to be elucidated. To explain the molecular basis of how the ABO Genes are controlled in cell type-specific expression, during normal cell differentiation, and in cancer cells with invasive and metastatic potential that lack A/B antigens, it is essential to understand the regulatory mechanism of ABO Gene transcription. We review the transcriptional regulation of the ABO Gene, including positive and negative elements in the upstream region of the Gene, and draw some inferences that help to explain the phenomena described ABOve.
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Transcriptional regulation of the human ABO histo-blood group Genes is dependent on the N box upstream of the proximal promoter.
Transfusion, 2004Co-Authors: Yoshihiko Kominato, Tamiko Nakajima, Yukiko Hata, Kazuhiro Matsui, Hisao Takizawa, Junichi Tsukada, Yasushi Kaneko, Koichiro KishiAbstract:BACKGROUND: Our previous studies of the transcriptional regulation of the human ABO Gene indicated that negative regulatory elements are present in the sequence just upstream from the proximal promoter. The role of the -275 to -118 region in regulation of ABO Gene transcription is further characterized. STUDY DESIGN AND METHODS: Transient transfection experiments into various cells were performed with luciferase reporter plasmids carrying ABO upstream sequences, and electrophoretic mobility shift assay was carried out with a nuclear extract prepared from the human gastric cancer KATOIII cells. RESULTS: It is shown that the -202 to -118 region is involved in the negative regulation of ABO Gene transcription in all cell lines examined. Transient transfection experiments in KATOIII cells with a reporter plasmid carrying mutated N box at -196 to -191 demonstrate that the N box is a negative regulatory element in the -202 to -118 sequence. Electrophoretic mobility shift assays indicate that the N box binds with a nuclear factor from KATOIII cells. CONCLUSION: These results indicate that repression of transcription from the ABO proximal promoter is partially dependent upon the N box. Therefore, reduced binding of the protein with the N box might play a direct role in ABO Gene expression.
Torben F. Ørntoft - One of the best experts on this subject based on the ideXlab platform.
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The blood group ABO Gene transcript is down-regulated in human bladder tumors and growth-stimulated urothelial cell lines.
Cancer research, 1996Co-Authors: Torben F. Ørntoft, Peter Meldgaard, Bent Pedersen, Hans WolfAbstract:The molecular mechanism that in human bladder tumors leads to the loss of blood group ABO glycosyltransferase activity and, thereby, the loss of ABO antigens was investigated. In 15 tumors and 3 normal biopsies from blood group AB individuals and 7 tumors and 3 normal biopsies from blood group O individuals, mRNA was detected by a reverse transcription PCR (RT-PCR) assay, and the ABO blood group structure was determined by immunohistology. The RT-PCR spanned several introns in the ABO Gene to exclude DNA contamination, and the RT-PCR product was shown to reflect the ABO Gene message by dideoxy sequencing. The ABO mRNA was present in normal urothelium and low-grade tumors but disappeared from high grade tumors. This correlation to tumor grade was significant (P
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the blood group ABO Gene transcript is down regulated in human bladder tumors and growth stimulated urothelial cell lines
Cancer Research, 1996Co-Authors: Torben F. Ørntoft, Peter Meldgaard, Bent Pedersen, Hans WolfAbstract:The molecular mechanism that in human bladder tumors leads to the loss of blood group ABO glycosyltransferase activity and, thereby, the loss of ABO antigens was investigated. In 15 tumors and 3 normal biopsies from blood group AB individuals and 7 tumors and 3 normal biopsies from blood group O individuals, mRNA was detected by a reverse transcription PCR (RT-PCR) assay, and the ABO blood group structure was determined by immunohistology. The RT-PCR spanned several introns in the ABO Gene to exclude DNA contamination, and the RT-PCR product was shown to reflect the ABO Gene message by dideoxy sequencing. The ABO mRNA was present in normal urothelium and low-grade tumors but disappeared from high grade tumors. This correlation to tumor grade was significant (P<0.04). Immunohistochemistry with monoclonal anti-blood group antibodies showed a complete correlation between the presence of mRNA and the presence of AB carbohydrate structures on cell surfaces. In two urothelial cell lines, genotyped as A/- and A/A, growth stimulation with the cholera toxin B subunit led to a total loss of ABO mRNA, and epidermal growth factor stimulation had an identical effect on one of the cell lines. We conclude that the ABO glycosylation in normal and malignant urothelium is regulated at the mRNA level, and that a mechanism associated with cell proliferation may trigger down-regulation of ABO mRNA.
