조덕 교수

In multiple myeloma (MM), the impaired function of several types of immune cells favors the tumor’s escape from immune surveillance and, therefore, its growth and survival. Tremendous improvements have been made in the treatment of MM over the past decade but cellular immunotherapy using dendritic cells, natural killer cells, and genetically engineered T-cells represent a new therapeutic era. The application of these treatments is growing rapidly, based on their capacity to eradicate MM. In this

Background: Recurrent somatic SET-binding protein 1 (SETBP1) and splicing pathway gene mutations have recently been found in atypical chronic myeloid leukemia and other hematologic malignancies. These mutations have been comprehensively analyzed in adult AML, but not in childhood AML. We investigated possible alteration of the SETBP1, splicing factor 3B subunit 1 (SF3B1), U2 small nuclear RNA auxiliary factor 1 (U2AF1), and serine/arginine-rich splicing factor 2 (SRSF2) genes in childhood AML. M

D antigens are clinically significant, and routine tests on the D antigen requires the inclusion of weak D testing, which is performed using indirect antihuman immunoglobulin methods. On the other hand, exact typing of the D type of an individual can be done more precisely with RHD genotyping, which is a useful tool in cases where the RHD gene is intact. The majority of weak-D or partial-D cases are from single nucleotide changes or hybridization of RHD and RHCE genes. Nevertheless, frameshift m

RHD genotyping is a useful adjunct to serologic testing. Although the use of RHD genotyping in the detection of Asia type DEL in serological D negative Koreans is gradually increasing, it is rarely requested for patients with a known weak D phenotype. This paper reports the first Korean case of a 52-year-old female patient with serologic weak D phenotype and weak D type 33 (c.520G＞A at exon 4 of RHD) identified by RHD exon 1 to 10 sequencing. In silico analysis predicted that the RHD c.520G＞A (V

Background: Adverse transfusion reactions (ATRs) are clinically relevant to patients with significant morbidity and mortality. This study aimed to review the cases of ATR reported in the recipient-triggered trace back system for a recent nine-year period in Korea. Methods: Nine-year data obtained from 2006 to 2014 by the trace back system at the Division of Human Blood Safety Surveillance of the Korean Centers for Disease Control (KCDC) were reviewed. The suspected cases were assessed according

극히 낮은 D 항원을 발현하는 적혈구는 기본혈청학적 검사법으로는 검출할 수 없어 DEL 이라고 부른다. 대부분 DEL형은 D 음성으로 보고된다. 그러나, 이들 DEL 적혈구는 흡착 및 용출시험(adsorption-elution test) 혹은 RHD 유전자 검사로 이를 규명할 수 있다. RhD 음성 환자가 DEL 혈액 수혈 후 항-D항체가 발생됨이 보고되었기때문에, DEL형과 순수 D 음성의 감별이 임상적으로 중요하다. 본 원고에서는 한국인에서 DEL 형에 대한 수혈전략과 검사법의 최신지견을 다루고자 한다.

DEL type red blood cells (RBCs) are characterized by the expression of extremely low levels of D-antigen, and thus, they cannot be detected by routine serologic D typing or a weak D test but are revealed by RHD genotyping or adsorption-elution studies [1]. The most common DEL phenotype is RHD (NM_016124.4: c.1227G>A), which is also referred to as Asia type DEL [2] and accounts for 94.7% of all Korean DEL cases [1]. Although DEL is a rare phenotype in individuals of European ethnicity [3], it is

Cis-AB, a rare ABO variant, is caused by a gene mutation that results in a single glycosyltransferase enzyme with dual A and B glycosyltransferase activities. It is the most frequent ABO subgroup in Korea, and it occurs more frequently in the East Asian region than in the rest of the world. The typical phenotype of cis-AB is A2B3, but it can express various phenotypes when paired with an A or B allele, which can lead to misclassification in the ABO grouping and consequently to adverse hemolytic

Background: Although testing to detect weak D antigens using the antihuman globulin reagent is not required for D- patients in many countries, it is routinely performed in Korea. However, weak D testing can be omitted in D- patients with a C-E- phenotype as this indicates complete deletion of the RHD gene, except in rare cases. We designed a new algorithm for weak D testing, which consisted of RhCE phenotyping followed by weak D testing in C+ or E+ samples, and compared it with the current algor