Hello again, and thank you CrystalRiver.

I don't know if this may be of any help,- there's a lot to it, and this is but one excerpt;

Abstract

We report a female patient whose Rh phenotype shifted from RhD-positive to RhD-negative over a 3-year period (1991–94), during which time she was treated with mastectomy (1992) and local irradiation for a low-grade recurrent breast cancer. She was diagnosed with chronic myeloid leukaemia in 1994, and has since then received chemotherapy. The patient was repeatedly typed as O, RhD-positive between 1965 and 1991 and was repeatedly found RhD-negative after 1994. Bcr-Abl transcripts typical of Ph1 chromosome were detected. Molecular analysis indicated that the patient was heterozygous at the RH locus, carrying one haplotype in which the RHD gene exhibited a single nucleotide deletion (G600) resulting in a frameshift and premature stop codon, and a normal RHCE gene (allele Ce). The second haplotype contained only the RHCE gene (allele ce) and was normal. Further analysis carried out on total leucocytes, purified neutrophils, EBV-lymphoblastoid cell line and cultured erythroblasts indicated that the G600 deletion was restricted to the myeloid lineage. No modification of other blood group antigens could be detected. These findings suggest a somatic mutation which most probably occurred in a stem cell common to the myeloid lineage.

Abnormal expression of blood group antigens with disease has been recognized for a long time. The first example reported concerned the ABH system and associated antigen changes in haematological disorders such as leukaemia and myeloproliferative disorders (for reviews see Salmon et al, 1969 ; Garratty, 1977), and in solid tumours ( Hakomori & Young, 1978; Hakomori, 1981; Hakomori & Kannagi, 1983). Less frequently, Rh blood group changes, characterized by the presence of two populations of red cells of different Rh phenotype (Rh mosaicism) in the blood from patients suffering from acute and chronic myelogenous leukaemia (AML, CML), myeloid metaplasia, polycythaemia or myelofibrosis, have been described ( Tovey et al, 1961 ; Leven et al, 1964 ; Majsky, 1967; Mannoni et al, 1970 ; Callender et al, 1971 ; Habibi et al, 1974 ; Fisher et al, 1984 ; Van Brockstaele et al, 1986 ). In a CML patient, both the RH and MNS loci were affected ( Bracey et al, 1983 ). On several occasions there was a complete loss of Rh antigens ( Marsh et al, 1974 , 1980; Cooper et al, 1979 ; Garner et al, 1980 ; Mohandas et al, 1993 ; Mertens et al, 1997 ). Although in some cases there was an association of the Rh loss with chromosome aberrations ( Marsh et al, 1974 ; Cooper et al, 1979 ; Mohandas et al, 1993 ), no detectable abnormality of chromosome 1, where the RH locus is located (1p34-p36), was noticed in other instances. In these examples the Rh mosaicism most probably resulted in the expansion of an abnormal clone of stem cells (somatic mutation, monosomy for RH?), which occasionally disappeared during clinical remission with a return to a normal Rh phenotype ( Bracey et al, 1983 ; Mohandas et al, 1993 ). However, it is not clear whether these changes in Rh blood group expression are caused by the leukaemic process itself. Rh mosaicism, was also found in apparently healthy individuals in whom chimaerism or dispermia could be eliminated as a possible explanation ( Race & Sanger, 1975; Mertens et al, 1997 ; Salaru & Lay, 1985). In one case a somatic mutation affecting only one of the monozygotic twins was suspected ( Muller et al, 1978 ). In a healthy donor and a patient suffering from a non-haematological disease (prolapse of an invertebral disc), respectively, a mosaicism for the blood group RH and FY locus (chromosome 1q) was noticed ( Jenkins & Marsh, 1965; Northoff et al, 1984 ).

The molecular changes of blood group ABH and associated antigens were best investigated in carcinomas ( Hakomori, 1995), but the alterations, if any, of the primary gene products, the glycosyltransferases, are still unknown. Similarly, there is currently no information available regarding the molecular alterations causing Rh blood group changes in malignant diseases, although the molecular basis of the RH genes has been largely determined (for reviews see Cartron & Agre, 1993; Anstee & Tanner, 1993; Cartron, 1994).

In this report we show that the loss of RhD antigen in a patient suffering a chronic myeloid leukaemia resulted from a somatic mutation within the RHD gene (single nucleotide deletion) which affected the erythroid but not the lymphoid lineage.

http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2141.1998.00895.x/full

Amazing days.

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Fox.