Thrombocytopenia, a condition involving low platelet counts, is very common in cancer patients. Accordingly, platelet transfusions are performed quite frequently in this population. As a result, studies have been conducted to establish appropriate platelet transfusion practices for these patients, and guidelines have provided recommendations on the thresholds for prophylactic transfusion and appropriate dosing. In real-world clinical practice, however, inappropriate platelet transfusions that deviate from these guidelines remain common. These include transfusions administered despite the platelet counts being above the recommended thresholds, transfusions exceeding the standard recommended dose, and transfusions given to achieve platelet levels required for chemotherapy. Such practices may lead to the inefficient use of limited platelet resources without clear clinical benefit. Therefore, efforts to improve the adherence to established guidelines and optimize platelet utilization are warranted, particularly in cancer patients.

ABO genotyping was first attempted shortly after the ABO gene was identified in 1990, when PCR-based assays, including PCR-RFLP (restriction fragment length polymorphism), PCR-SSCP (single strand conformation polymorphism), and PCR-SSP (sequence-specific primer), enabled discrimination among the major alleles (A, B, and O).Because various point mutations in exons 6 and 7 underlying subgroup phenotypes were progressively elucidated, these variants also became the targets for genotyping assays. Nevertheless, PCR-based approaches are inherently limited to the detection of predefined variants and require additional allelic separation and direct sequencing to identify alleles corresponding to subgroup phenotypes. Since the 2010s, next-generation sequencing (NGS) has enabled comprehensive analysis of the genetic variation across the entire ABO gene through massively parallel sequencing, helping identify several novel alleles at the population level. On the other hand, its short-read architecture imposes limitations in haplotype phasing. Long-read sequencing technologies have recently been introduced to overcome these limitations and are increasingly being applied, allowing direct analysis of full-length haplotypes and offering advantages in detecting recombination events and characterizing repetitive regions. Although advances in molecular genetics have substantially improved the accuracy and convenience of genotyping methods, their clinical application remains limited.The advantages of serological testing—namely, accessibility, accuracy, and low cost—continue to support its primary role in routine practice. Although ABO genotyping cannot yet replace serological methods, it serves as a valuable complementary tool in resolving discrepant cases and in specialized settings such as organ transplantation. Its clinical utility is expected to expand further as technological advances continue.

Cell-based artificial platelet production has made remarkable progress over the past three decades, driven by the need for safe and stable platelet sources in the face of donor limitations and transfusion-related risks. This review provides a chronological overview of the evolution of in vitro platelet production from various cell sources (CD34+ hematopoietic stem cells, embryonic stem cells, induced pluripotent stem cells (iPSCs), and others) and highlights key advances in the field. We outline developments from the foundational experiments of the 1990s, through the introduction of iPSCs in the mid-2000s, to the adoption of three-dimensional culture and bioreactor technologies in the late 2010s and the emergence of clinical trials in the 2020s. In addition, we discuss future perspec‑ tives, including the role of advanced gene editing and scalable biomanufacturing technologies in accelerating clinical translation. This comprehensive review underscores the promise of artificial platelet production technologies for clini‑ cal applications and discusses the remaining challenges, such as scalability, cost-effectiveness, and regulatory hurdles.The recent completion of the first human clinical trials using iPSC-derived platelets marks a significant milestone, pointing to a future in which patient-specific or human leukocyte antigen-universal platelets may be transformed into transfusion medicine and regenerative therapies.

The Jr(a+) antigen is one of the high-frequency antigens belonging to the JR blood group system. Although the clinical significance of anti-Jra is not well defined, cases of hemolytic disease of the newborn and hemolytic transfusion reactions caused by anti-Jra have been reported. This review introduces the genetic background of the JR blood group, the frequency of Jr(a＋), and the clinical significance of anti-Jra based on existing literature.Additionally, it summarizes the identification of anti-Jra and the transfusion strategies that can be adopted for patients with anti-Jra alloantibodies.

Background: The Jr a antigen is a high-prevalence red blood cell (RBC) antigen. Reports on cases of fatal hemolytic disease of the fetus and newborn and acute hemolytic transfusion reactions suggest that antibodies against Jr a (anti-Jra ) have potential clinical significance.Identifying anti-Jra is challenging owing to a lack of commercially available antisera. We developed an alternative approach to rapidly predict the presence of anti-Jra using the TaqMan single-nucleotide polymorphism (SNP)-genotyping method. Methods: Residual peripheral blood samples from 10 patients suspected of having the anti-Jr a were collected. Two samples with confirmed Jr(a–) RBCs and anti-Jra were used to validate the TaqMan genotyping assay by comparing the genotyping results with direct sequencing. The accuracy of the assay in predicting the presence of anti-Jra was verified through crossmatching with in-house Jr(a–) O+ RBCs. Results: The TaqMan-genotyping method was validated with two Jr(a–) RBC- and anti-Jra -confirmed samples that showed concordant Jr a genotyping and direct sequencing results.Jra genotyping for the remaining samples and crossmatching the serum samples with inhouse Jr(a–) O+ RBCs showed consistent results. Conclusions We validated a rapid, simple, accurate, and cost-effective method for predicting the presence of anti-Jra using a TaqMan-based SNP-genotyping assay. Implementing this method in routine practice in clinical laboratories will assist in solving difficult problems regarding alloantibodies to high-prevalence RBC antigens and ultimately aid in providing safe and timely transfusions and proper patient care.

Background: The Jr a antigen is a high-prevalence red blood cell (RBC) antigen. Reports on cases of fatal hemolytic disease of the fetus and newborn and acute hemolytic transfusion reactions suggest that antibodies against Jr a (anti-Jra ) have potential clinical significance.Identifying anti-Jra is challenging owing to a lack of commercially available antisera. We developed an alternative approach to rapidly predict the presence of anti-Jra using the TaqMan single-nucleotide polymorphism (SNP)-genotyping method. Methods: Residual peripheral blood samples from 10 patients suspected of having the anti-Jr a were collected. Two samples with confirmed Jr(a–) RBCs and anti-Jra were used to validate the TaqMan genotyping assay by comparing the genotyping results with direct sequencing. The accuracy of the assay in predicting the presence of anti-Jra was verified through crossmatching with in-house Jr(a–) O+ RBCs. Results: The TaqMan-genotyping method was validated with two Jr(a–) RBC- and anti-Jra -confirmed samples that showed concordant Jr a genotyping and direct sequencing results.Jra genotyping for the remaining samples and crossmatching the serum samples with inhouse Jr(a–) O+ RBCs showed consistent results. Conclusions We validated a rapid, simple, accurate, and cost-effective method for predicting the presence of anti-Jra using a TaqMan-based SNP-genotyping assay. Implementing this method in routine practice in clinical laboratories will assist in solving difficult problems regarding alloantibodies to high-prevalence RBC antigens and ultimately aid in providing safe and timely transfusions and proper patient care.

Background: The Jr a antigen is a high-prevalence red blood cell (RBC) antigen. Reports on cases of fatal hemolytic disease of the fetus and newborn and acute hemolytic transfusion reactions suggest that antibodies against Jr a (anti-Jra ) have potential clinical significance.Identifying anti-Jra is challenging owing to a lack of commercially available antisera. We developed an alternative approach to rapidly predict the presence of anti-Jra using the TaqMan single-nucleotide polymorphism (SNP)-genotyping method. Methods: Residual peripheral blood samples from 10 patients suspected of having the anti-Jr a were collected. Two samples with confirmed Jr(a–) RBCs and anti-Jra were used to validate the TaqMan genotyping assay by comparing the genotyping results with direct sequencing. The accuracy of the assay in predicting the presence of anti-Jra was verified through crossmatching with in-house Jr(a–) O+ RBCs. Results: The TaqMan-genotyping method was validated with two Jr(a–) RBC- and anti-Jra -confirmed samples that showed concordant Jr a genotyping and direct sequencing results.Jra genotyping for the remaining samples and crossmatching the serum samples with inhouse Jr(a–) O+ RBCs showed consistent results. Conclusions We validated a rapid, simple, accurate, and cost-effective method for predicting the presence of anti-Jra using a TaqMan-based SNP-genotyping assay. Implementing this method in routine practice in clinical laboratories will assist in solving difficult problems regarding alloantibodies to high-prevalence RBC antigens and ultimately aid in providing safe and timely transfusions and proper patient care.

Background: The Jr a antigen is a high-prevalence red blood cell (RBC) antigen. Reports on cases of fatal hemolytic disease of the fetus and newborn and acute hemolytic transfusion reactions suggest that antibodies against Jr a (anti-Jra ) have potential clinical significance.Identifying anti-Jra is challenging owing to a lack of commercially available antisera. We developed an alternative approach to rapidly predict the presence of anti-Jra using the TaqMan single-nucleotide polymorphism (SNP)-genotyping method. Methods: Residual peripheral blood samples from 10 patients suspected of having the anti-Jr a were collected. Two samples with confirmed Jr(a–) RBCs and anti-Jra were used to validate the TaqMan genotyping assay by comparing the genotyping results with direct sequencing. The accuracy of the assay in predicting the presence of anti-Jra was verified through crossmatching with in-house Jr(a–) O+ RBCs. Results: The TaqMan-genotyping method was validated with two Jr(a–) RBC- and anti-Jra -confirmed samples that showed concordant Jr a genotyping and direct sequencing results.Jra genotyping for the remaining samples and crossmatching the serum samples with inhouse Jr(a–) O+ RBCs showed consistent results. Conclusions We validated a rapid, simple, accurate, and cost-effective method for predicting the presence of anti-Jra using a TaqMan-based SNP-genotyping assay. Implementing this method in routine practice in clinical laboratories will assist in solving difficult problems regarding alloantibodies to high-prevalence RBC antigens and ultimately aid in providing safe and timely transfusions and proper patient care.

The Jr(a+) antigen is one of the high-frequency antigens belonging to the JR blood group system. Although the clinical significance of anti-Jra is not well defined, cases of hemolytic disease of the newborn and hemolytic transfusion reactions caused by anti-Jra have been reported. This review introduces the genetic background of the JR blood group, the frequency of Jr(a＋), and the clinical significance of anti-Jra based on existing literature.Additionally, it summarizes the identification of anti-Jra and the transfusion strategies that can be adopted for patients with anti-Jra alloantibodies.

The Jr(a+) antigen is one of the high-frequency antigens belonging to the JR blood group system. Although the clinical significance of anti-Jra is not well defined, cases of hemolytic disease of the newborn and hemolytic transfusion reactions caused by anti-Jra have been reported. This review introduces the genetic background of the JR blood group, the frequency of Jr(a＋), and the clinical significance of anti-Jra based on existing literature.Additionally, it summarizes the identification of anti-Jra and the transfusion strategies that can be adopted for patients with anti-Jra alloantibodies.