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HLA‐DPB1*05:01:18 differs from HLA‐DPB1*05:01:01:01 by one nucleotide in exon 4. [ABSTRACT FROM AUTHOR]

HLA‐A*24:02:160 differs from HLA‐A*24:02:01:01 by one nucleotide in exon 3. [ABSTRACT FROM AUTHOR]

HLA‐A*02:07:22 differs from HLA‐A*02:07:01:01 by one nucleotide in exon 3. [ABSTRACT FROM AUTHOR]

HLA‐C*04:490 differs from HLA‐C*04:01:01:01 by one nucleotide in exon 3. [ABSTRACT FROM AUTHOR]

HLA‐DQB1*03:03:29 differs from HLA‐DQB1*03:03:02:01 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

HLA‐DRB1*14:07:03 differs from HLA‐DRB1*14:07:01 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

HLA‐B*15:644 differs from HLA‐B*15:17:01:02 by one nucleotide in exon 4. [ABSTRACT FROM AUTHOR]

HLA‐DQB1*04:93 differs from HLA‐DQB1*04:01:01:01 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

HLA‐DRB1*14:246 differs from HLA‐DRB1*14:18 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

HLA‐DPB1*1352:01 differs from HLA‐DPB1*02:01:02:01 by one nucleotide in exon 4. [ABSTRACT FROM AUTHOR]

HLA‐B*15:638 differs from HLA‐B*15:01:01:01 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

Mastering the SNP content in the HLA region can be based on it to judiciously select unrelated donor stem cells with preferable MHC matching to lower postoperative complications. Herein, quantitative PCR‐based primers and probes were designed for 10 transplants outcome‐associated SNP loci with two‐allelic polymorphism, and then a new detection system ("HLA‐10‐SNP") was established. Compared with Sanger sequencing, its accuracy has been proven to reach 100%. Additionally, fluorescent PCR typing of 10 important SNPs via this system expressed excellent repeatability (sensitivity, 20 ng). Overall, the new system achieves single‐sample classification precision and easily distinguishable results, equipped with the advantages of simple, rapid, accurate, and effective, promising to acquire widespread popularization and application in clinical settings. [ABSTRACT FROM AUTHOR]

HLA‐C*04:01:152 differs from HLA‐C*04:01:01:01 by one nucleotide in exon 1. [ABSTRACT FROM AUTHOR]

HLA‐DRB1*14:251 differs from HLA‐DRB1*14:126:01 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

The killer cell immunoglobulin-like receptor (KIR), which mediates the killing function of NK cells, is an attractive candidate for adoptive cellular therapy. The ethnic distribution for China provides a unique opportunity to investigate KIR gene distribution. The aim of this study was to explore the relationship between population history and the rapidly evolving KIR genetic diversity. 8050 Chinese donors from 184 hospitals were included to analyse frequency, haplotype, and B-content data of 16 KIR genes, by PCR-SSP for KIR genotyping. KIR gene carrier frequencies were found similar to those observed in other studies on Han, but different from Thais, Japanese, Africans, and populations of West Eurasian ancestry. High-frequency KIR genotype profiles found in the present population were consistent with other studies on Han populations but different from those conducted on other cohorts. The majority of our cohort carried group A KIR gene motifs. Additionally, populations with similar geographic locations in China were shown clustered together, while Hainan and Xinjiang provinces were slightly separated from these. The distribution of KIR genes varies by geographic region, and different ethnic groups may be a confounding factor of KIR diversity. [ABSTRACT FROM AUTHOR]

HLA‐C*03:621 differs from HLA‐C*03:04:01:01 by one nucleotide in exon 1. [ABSTRACT FROM AUTHOR]

HLA‐B*13:176 differs from HLA‐B*13:02:01:01 by one nucleotide in exon 1. [ABSTRACT FROM AUTHOR]

HLA‐A*24:582 differs from HLA‐A*24:02:01:01 by one nucleotide in exon 1. [ABSTRACT FROM AUTHOR]

HLA‐C*15:02:58 differs from HLA‐C*15:02:01:01 by one nucleotide in exon 1. [ABSTRACT FROM AUTHOR]

HLA‐B*48:01:11 differs from HLA‐B*48:01:01:01 by one nucleotide in exon 4. [ABSTRACT FROM AUTHOR]

HLA‐A*24:561:02 differs from HLA‐A*24:02:01:01 by one nucleotide in exon 3. [ABSTRACT FROM AUTHOR]

HLA‐DRB1*12:01:12 differs from HLA‐DRB1*12:01:01:01 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

HLA‐C*07:1029 differs from HLA‐C*07:02:01:01 by one nucleotide in exon 5. [ABSTRACT FROM AUTHOR]

HLA‐DQB1*06:208:02 differs from HLA‐DQB1*06:02:02 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

HLA‐B*13:01:21 differs from HLA‐B*13:01:01:01 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

HLA‐B*35:568 differs from HLA‐B*35:03:01:01 by one nucleotide in exon 4. [ABSTRACT FROM AUTHOR]

HLA‐A*02:1075 differs from HLA‐A*02:07:01:01 by one nucleotide in exon 5. [ABSTRACT FROM AUTHOR]

HLA‐A*24:02:159 differs from HLA‐A*24:02:01:01 by one nucleotide in exon 3. [ABSTRACT FROM AUTHOR]

HLA‐C*01:239 differs from HLA‐C*01:02:01:01 by one nucleotide in exon 4. [ABSTRACT FROM AUTHOR]

HLA‐B*55:131 differs from HLA‐B*55:02:01:01 by one nucleotide in exon 4. [ABSTRACT FROM AUTHOR]

HLA‐DQB1*03:499N differs from HLA‐DQB1*03:01:01:01 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

HLA‐B*40:01:78 differs from HLA‐B*40:01:02:01 by one nucleotide in exon 3. [ABSTRACT FROM AUTHOR]

HLA‐DQB1*02:01:44 differs from HLA‐DQB1*02:01:01:01 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

HLA‐C*01:02:89 differs from HLA‐C*01:02:01:01 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

HLA‐C*03:04:74 differs from HLA‐C*03:04:01:01 by one nucleotide in exon 6. [ABSTRACT FROM AUTHOR]

HLA‐B*52:110N differs from HLA‐B*52:01:01:01 by one nucleotide in exon 3. [ABSTRACT FROM AUTHOR]

HLA‐B*55:130 differs from HLA‐B*55:35 by two nucleotides in exon 2. [ABSTRACT FROM AUTHOR]

HLA‐B*35:563 differs from HLA‐B*35:03:01:01 by one nucleotide in exon 4. [ABSTRACT FROM AUTHOR]

HLA‐DQB1*06:208:02 differs from HLA‐DQB1*06:02:02 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

HLA‐C*03:04:99 differs from HLA‐C*03:04:01:01 by one nucleotide in exon 5. [ABSTRACT FROM AUTHOR]

HLA‐B*35:501 differs from HLA‐B*35:02:01:01 by three nucleotides in exon 2. [ABSTRACT FROM AUTHOR]

HLA‐B*51:328 differs from HLA‐B*51:01:01:01 in exon 2 at position 241 by a single non‐synonymous mutation. [ABSTRACT FROM AUTHOR]

HLA‐B*46:85 differs from HLA‐B*46:01:01:01 in exon 3 at position 560 by a single non‐synonymous mutation. [ABSTRACT FROM AUTHOR]

HLA‐DRB1*13:306 differs from HLA‐DRB1*13:02:01:01 in exon 2 in codon 84 by a single coding change. [ABSTRACT FROM AUTHOR]

HLA‐A*69:01:04 differs from HLA‐A*69:01:01:01 in exon 2 at position 336 by a single synonymous mutation. [ABSTRACT FROM AUTHOR]

HLA‐A*68:302 differs from HLA‐A*68:01:02:01 by one nucleotide in exon 4. [ABSTRACT FROM AUTHOR]

HLA‐C*06:02:102 differs from HLA‐C*06:02:01:01 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

Several genes involved in the pathogenesis have been identified, with the human leukocyte antigen (HLA) system playing an essential role. However, the relationship between HLA and a cluster of hematological diseases has received little attention in China. Blood samples (n = 123913) from 43568 patients and 80345 individuals without known pathology were genotyped for HLA class I and II using sequencing-based typing. We discovered that HLA-A*11:01, B*40:01, C*01:02, DQB1*03:01, and DRB1*09:01 were prevalent in China. Furthermore, three high-frequency alleles (DQB1*03:01, DQB1*06:02, and DRB1*15:01) were found to be hazardous in malignant hematologic diseases when compared to controls. In addition, for benign hematologic disorders, 7 high-frequency risk alleles (A*01:01, B*46:01, C*01:02, DQB1*03:03, DQB1*05:02, DRB1*09:01, and DRB1*14:54) and 8 high-frequency susceptible genotypes (A*11:01-A*11:01, B*46:01-B*58:01, B*46:01-B*46:01, C*01:02-C*03:04, DQB1*03:01-DQB1*05:02, DQB1*03:03-DQB1*06:01, DRB1*09:01-DRB1*15:01, and DRB1*14:54-DRB1*15:01) were observed. To summarize, our findings indicate the association between HLA alleles/genotypes and a variety of hematological disorders, which is critical for disease surveillance. [ABSTRACT FROM AUTHOR]

HLA‐A*02:07:23 differs from HLA‐A*02:07:01:01 by one nucleotide in exon 2. [ABSTRACT FROM AUTHOR]

Post-transplantation cyclophosphamide (PTCy) can reduce the incidence of graft versus host disease (GVHD) and this intervention is often applied on adults with hematologic malignancy. However, the high relapse rate hinders the development of the intervention and data of PTCy used on children with hematologic malignancy remains limited. In order to overcome issue of high relapse rate in PTCy treatment, we used fludarabine (Flu), enhanced dose of cytarabine (Ara-C, 9 g/m2), busulfan (Bu), Cy, anti-thymocyte globulin (ATG) combined with PTCy for an intensified conditioning regimen. A total of 22 children with acute leukemia received intensified PTCy conditioning regimen (PTCy intensified group). We matched with 18 children who received modified Bu-Cy and ATG conditioning regimen in the same period (ATG group). The two-year cumulative incidences of grade II–IV acute GVHD was significantly lower in PTCy intensified group (13.6 ± 7.7% vs 38.9 ± 11.5%, P = 0.048). Two-year GVHD-free relapse free survival (GRFS) in PTCy seems to be better among the increment group despite not being significant (63.3 ± 10.3% vs 35.4 ± 11.9%, P = 0.092). The positive rate of minimal residual disease after transplantation was significantly lower than that before transplantation (20.0% vs 2.5%, P = 0.029). In conclusion, ATG and PTCy combined with Flu-based increased intensity conditioning regimen is effective for acute leukemia in children. It could reduce GVHD rate significantly and potentially improve GRFS. [ABSTRACT FROM AUTHOR]