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Favourable response to antithymocyte or antilymphocyte globulin in low‐risk myelodysplastic syndrome patients with a ‘non‐clonal’ pattern of X‐chromosome inactivation in bone marrow cells
Author(s) -
Aivado M.,
Rong A.,
Stadler M.,
Germing U.,
Giagounidis A.,
Strupp C.,
Novotny J.,
Josten K.M.,
Kobbe G.,
Hildebrandt B.,
Gattermann N.,
Aul C.,
Haas R.,
Ganser A.
Publication year - 2002
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1034/j.1600-0609.2002.01625.x
Subject(s) - clone (java method) , bone marrow , immunology , haematopoiesis , myelodysplastic syndromes , monoclonal , biology , medicine , antibody , monoclonal antibody , stem cell , gene , genetics
Objective: Antithymocyte and antilymphocyte globulin (ATG/ALG) have a therapeutic effect in about 30% of patients with myelodysplastic syndromes (MDS). We were interested to know whether responding patients achieve clonal or polyclonal remissions.Patients: Ten women with low‐risk MDS received either ALG or ATG. Before treatment and 3, 6, and 12 months later, X‐chromosome inactivation patterns of peripheral blood T lymphocytes were compared with those of peripheral blood granulocytes or bone marrow cells, using the human androgen receptor gene assay and the phosphoglycerate kinase‐1 assay.Results: Six women did not respond to therapy. Prior to treatment, four of them had a monoclonal, one had an oligoclonal, and one had a skewed X‐chromosome inactivation pattern (XCIP). Four patients responded to ATG/ALG. Three of them were informative in our X‐inactivation assays, and showed a non‐clonal XCIP which did not change significantly after treatment with ATG/ALG.Conclusion : A non‐clonal XCIP in the bone marrow was associated with a response to ATG/ALG. Non‐clonal XCIPs do not necessarily imply that there is no pathological clone. By definition, they just indicate that there is no evidence of a clone contributing more than 50% of cells in a sample. Non‐clonal XCIPs may therefore be attributable to incomplete clonal expansion. This, in turn, might be explained by a vigorous immune attack against the MDS clone, which simultaneously causes collateral damage in the remaining normal haemopoiesis. In such patients, ATG/ALG may improve normal haemopoiesis by relieving the immunological pressure on the innocent bystanders.