Molecular genetic analysis of the human Lewis histo-blood group system.

Nishihara, Shoko; Narimatsu, Hisashi; Iwasaki, H.; Yazawa, Shin; Akamatsu, Suguru; Ando, Takao; Seno, Taiko; Narimatsu, Ikuyo

doi:10.1016/s0021-9258(19)62041-7

Cited by 145 publications

(16 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A mutation at 59T>G alone results in the functional allele Le 59 which has been commonly found in Caucasian Americans 13 and the Brazilian population. 17 SNP 59T>G, in conjunction with other SNPs such as 508G>A, results in a non-functional allele le 59,508 that has been commonly found in Lewisnegative Japanese 3 and Africans. 25 The non-functional allele le 59,1067 has been mainly found in Lewis-negative phenotype in Japanese 3 and Indonesians 1 and was seen also in our cohort.…”

Section: Discussionmentioning

confidence: 99%

“…17 SNP 59T>G, in conjunction with other SNPs such as 508G>A, results in a non-functional allele le 59,508 that has been commonly found in Lewisnegative Japanese 3 and Africans. 25 The non-functional allele le 59,1067 has been mainly found in Lewis-negative phenotype in Japanese 3 and Indonesians 1 and was seen also in our cohort. In addition, we found evidence of an association between the SNPs 59T>G and 1067T>A and the occurrence of the Lewis-negative phenotype, likely due to the high level of homozygosity in the overall Thai population.…”

Section: Discussionmentioning

confidence: 99%

“…1,2 The FUT2 and FUT3 enzymes function independently and are controlled by the FUT2 and FUT3 loci, respectively. 3,4 Individuals with a functional FUT3 enzyme will present with Le a or Le b depending on their FUT2 status, while a person with an inactivate FUT3 enzyme is considered as a Lewis-negative phenotype regardless of the FUT2 enzyme situation. In particular diseases, for example asthma 5 and coronary heart disease 6 , the Lewis-negative phenotype as well as mutations of the FUT3 gene have been shown to be associated with an increased prevalence and risk of these diseases.…”

Section: Introductionmentioning

confidence: 99%

“…It has been well demonstrated that FUT3 enzyme activity is regulated by single nucleotide polymorphisms (SNPs) of the Lewis gene (FUT3). The mutations 202T>C 7,8 , 508G>A 3,9,10 , and 1067T>A 1 encode non-functional alleles of the FUT3 gene designated as le 202 , le 508 , and le 1067 , respectively. Homozygous mutation of one of these alleles results in inactivation of catalytic domains of FUT3 enzyme and so leads to lack of enzyme activity to produce the Lewis antigen.…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Prevalence of Lewis Blood Group Polymorphisms in Southern Thai Blood Donors

Nanakorn

Boonthongkhao

Mitundee

et al. 2021

J Health Sci Med Res

View full text Add to dashboard Cite

Objective: To determine the frequencies of five of the most common (59T>G, 202T>C, 314C>T, 508G>A and 1067T>G) single nucleotide polymorphisms (SNPs) of the FUT3 gene in Thai blood donors and examine their associations with the presence or absence of Lewis antigens on red blood cells.Material and Methods: A total of 364 donor specimens from Songklanagarind Hospital and Regional Blood Centre XII Songkhla, Thailand, were recruited for the study. Molecular analysis of each SNP was performed by polymerase chain reaction amplification with sequence-specific primers (PCR-SSP). The Lewis phenotype was investigated in 159 individuals using the standard hemagglutination test.Results: The frequencies of the SNPs were 32.0% (59T>G), 46.6% (202T>C), 21.7% (314C>T), 37.9% (508G>A), and 25.0% (1067T>A). The prevalences of the Lewis phenotype were 61.0% for Le(a-b+), 7.6% for Le(a+b-), 11.3% for Le(a+b+), and 20.1% for Le(a-b-). The Lewis-negative phenotype was significantly associated with homozygosity in 59T>G and 1067T>A (χ2 =49.873, and χ2 =44.520, respectively).Conclusion: Our findings suggest that le59,1067 is largely responsible for the Lewis-negative phenotype in our southern Thai population. Genetic variations in FUT3 polymorphisms may be used as molecular markers for ethnicity and to help understand the roles of the Lewis blood group in infections or clinical diseases.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Prevalence of Lewis Blood Group Polymorphisms in Southern Thai Blood Donors

Nanakorn

Boonthongkhao

Mitundee

et al. 2021

J Health Sci Med Res

View full text Add to dashboard Cite

show abstract

“…There are 25 This allele is usually present with a second fully inactivating mutation. 48,53 A point mutation at nucleotide 385, which is expressed in a homozygous state, or in a heterozygous state with a nonsecretor allele, has now been identified in all Le(a+b+) or weaksecretor individuals tested of both Polynesian and Indonesian descent (unpublished observation).…”

Section: Molecular Geneticsmentioning

confidence: 95%

Review: phenotyping for Lewis and secretor histo-blood group antigens

Henry

1996

Immunohematology

View full text Add to dashboard Cite

Up-regulation of Lewis enzyme (Fuc-TIII) and plasma-type ?1,3Fucosyltransferase (Fuc-TVI) expression determines the augmented expression of sialyl Lewis x antigen in non-small cell lung cancer

et al. 1999

View full text Add to dashboard Cite

Sialyl Lewis a and x antigens are well‐known tumor‐associated antigens expressed in many cancer tissues. The expression of the genes encoding 5 α1,3fucosyltransferases, which are able to synthesize the sialyl Lewis antigens, was examined in normal and cancerous lung tissues of patients with non‐small cell lung carcinoma. In all 20 cases examined, the transcripts only for the Lewis gene, encoding the Lewis enzyme (α1,3/4fucosyltransferase, Fuc‐TIII), were abundantly expressed in lung tissue, and interestingly they were markedly up‐regulated in the lung cancer tissues of all 20 cases in comparison with normal lung tissues. Myeloid‐type α1,3fucosyltransferase (Fuc‐TIV) was expressed at an intermediate level but was not up‐regulated in lung cancer tissues. The transcripts for plasma‐type α1,3fucosyltransferase (Fuc‐TVI) gene were detected at a very low level but were apparently up‐regulated in cancer tissues. Fuc‐TVI was found to exhibit stronger relative activity for sialyl Lewis x synthesis (almost 6.4‐fold that of Fuc‐TIII). The amount of sialyl Lewis x antigen on mucins in the lung cancer tissues was found to be determined by both enzymes, the Lewis enzyme (Fuc‐TIII) and Fuc‐TVI. However, the amount of the sialyl Lewis a antigens was not determined by any of the α1,3‐fucosyltransferases, although the expression of sialyl Lewis a antigens definitely required the Lewis enzyme. Int. J. Cancer 83:70–79, 1999. © 1999 Wiley‐Liss, Inc.

show abstract

Molecular genetic analysis of the human Lewis histo-blood group system.

Cited by 145 publications

References 34 publications

Prevalence of Lewis Blood Group Polymorphisms in Southern Thai Blood Donors

Prevalence of Lewis Blood Group Polymorphisms in Southern Thai Blood Donors

Review: phenotyping for Lewis and secretor histo-blood group antigens

Up-regulation of Lewis enzyme (Fuc-TIII) and plasma-type ?1,3Fucosyltransferase (Fuc-TVI) expression determines the augmented expression of sialyl Lewis x antigen in non-small cell lung cancer

Contact Info

Product

Resources

About