| Research Abstract |
Results of the transformation in genetic markers before and after BMT in recipients with different phenotypes from the donor follows. The red cell antigens transformed as follows ; type O to type A, type O to type B, type AB to type A and type A to type O (the pre-BMT recipient type to the post-BMT donor type), MN/ss to M/ss, MN/ss to N/ss, NSs to Nss, CcDEe to CCDee, CcDee to CCDee, CCDee to CcDEe, CcDEe to ccDEE, Pl(+) to Pl(-), Pl(-) to Pl(+), Jk(a+b+) to Jk(a+b-), Jk(a+b+) to Jk(a-B+), Jk(a-b+) to Jk(a+b+), Jk(a+b-) to Jk(a+b+), Fy(a+b+) to Fy(a+b-), Xg(a+) to Xg(a-), Xg(a-) to Xg(a+). The red cell enzyme types transformed as follows ; EsD 2-1 to EsD 1-1, EsD1-2 to EsD1-1, PGM2-1 to PGM1-1, PGM1(1+1-) to PGM2-1(2+1+), PGM2-1(2-1+) to PGM1-1(1-1-), ACP A to ACP AB.Some genetic markers which did not transform when the donor phenotypes differed from the recipient phenotypes include the Lewis, Hp, Tf, FXIII-B, Se, Pa, Pr, Db, and PmF markers. Other genetic markers, including the Luther
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an, Kell-Cellano, Xa, HLA, Ge, Gm, Km, Bf, PLG, GLO, 6PGD, Pb, PIF, Amyl, and various complementing systems could not be evaluated because the donor and recipient phenotypes were identical.
Many transformations in genetic markers which accompany BMT illustrate the relationship between gene products and the bone marrow. Various antigens from red cell membrane substances of the glycolipid and glycophorin systems are produced primarily in the bone marrow. However, production of the Lewis antigen, blood-group-related substances secreted in saliva, and salivary polymorphic protein appear to take place in the bone maeeow.
Chenges in the red blood cell agglutinin appear to be related to antibody production under gene control and are presumably produced by the transformed Gm system (immunogloblin allotype) rather than being the result of serum antibody absorption by antigens, which leaves only nonself antibodies. The transformation of the red cell enzyme EsD, PGM, ACP, PGD markers provides a useful clue for therapy for enzyme defects. RFLP analysis using DPbeta, DQbeta, and DRbeta cDNA as a probe was carried out in a case which showed the high MLC activity although Class I and Class II on HLA typing were coincident each other. The recipient showed some specific bands which were not observed in the donor and her patients, that suggested the relationship between the specific bands and high MLC activity.
BMT between family memberns may lead to transformation in the gene markers, but within a pattern compatible with family inheritance patterns, and no genetic paradox will be found in later surveys of familial genetic relationships. However in a personal identification system in forensic medicine using genetic markers as an index, the appearance of a phenotype incompatible with a blood relationship is possible after BMT from a donor who is not a blood relative. This result is similar to the inheritance pattern observed after artificial insemination by a donor, a more complete out-of-family cross.
As development of immune suppressants such as cyclosporins improves, BMT will be preformed more frequently based upon HLA histocompatibility alone. Care will be required to track the transformation in personal identification and paternity testing based on genetic markers. Less
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