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Clonality in myelodysplastic syndromes: demonstration of pluripotent stem cell origin using X‐linked restriction fragment length polymorphisms
Author(s) -
Tsukamoto Norifumi,
Morita Kimio,
Maehara Tadashi,
Okamoto Kiyoshi,
Karasawa Masamitsu,
Omine Mitsuhiro,
Naruse Takuji
Publication year - 1993
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1993.tb04695.x
Subject(s) - restriction fragment length polymorphism , myelodysplastic syndromes , hypoxanthine guanine phosphoribosyltransferase , biology , microbiology and biotechnology , myeloid , monoclonal , x chromosome , clone (java method) , stem cell , lymphocyte , genetics , immunology , monoclonal antibody , genotype , gene , bone marrow , antibody , mutant
Restriction fragment length polymorphisms (RFLP) of the X‐chromosome genes phosphoglycerate kinase (PGK) and hypoxanthine phorphoribosyltransferase (HPRT) were used to determine the clonal nature of myelodysplastic syndromes (MDS) in 22 patients. These included eight with refractory anaemia (RA), four with RA with ring sideroblasts (RARS), six with RA with an excess of blasts (RAEB), three with RAEB in transformation (RAEB‐T), and one with chronic myelomonocytic leukaemia (CMML). Monoclonal X‐inactivation patterns were observed in 19/22 patients. The remaining three cases, one each with RA, RARS and RAEB, were of polyclonal composition. Separated T‐lymphocyte and granulocyte fraction analyses in six patients of the former cases revealed that T‐lymphocyte as well as granulocyte fractions showed a monoclonal pattern of X‐inactivation. These results support the view that the majority of MDS arise from a pluripotent stem cell capable of myeloid and lymphoid differentiation.