Interstitial 9q deletion in T‐lymphoid/myeloid biphenotypic leukaemia

Koichi Akashi, Tsunefumi Shibuya, Mine Harada, Akiko Oogami, Takanori Teshima, Yasushi Takamatsu, Masahiro Kikuchi, Yoshiyuki Niho

研究成果: ジャーナルへの寄稿学術誌査読

20 被引用数 (Scopus)

抄録

Summary. We report the biological characteristics of leukaemic blasts from two cases of acute leukaemia with an interstitial deletion of the long arm of chromosome 9 (9q). Case 1 (FAB: M1) showed del(9)(q12q22) as the sole karyotypic anomaly, and case 2 (FAB: M1) presented del(9) (q12q22) in association with trisomy 10. In both cases, leukaemic blasts presented unique cytological features, such as prominent vacuoles on Giemsa staining, or strong localization of myeloperoxidase resembling ‘pseudo‐Chediak‐Higashi’ granules. Immunophenotyping of blasts revealed the biphenotypic expression of T‐lymphoid/myeloid antigens (CD2, CD7/CD33) in addition to CD34. Neither T‐cell receptor β (TCRB), T‐cell receptor γ (TCRG) nor Ig heavy chain (IGH) genes were clonally rearranged. Furthermore, there was neither rearrangement nor expression of ABL, which is located at 9q34, indicating that the deletion involved bands centrometric to 9q34 did not induce the activation of ABL. DNA synthesis of the blasts was stimulated (stimulation index > 2·0) in the presence of interleukin (IL)‐3, IL‐4, granulocyte colony‐stimulating factor or erythropoietin (Epo). IL‐3 and IL‐4 could also support the in vitro growth of leukaemic blast colonies, and the IL‐3‐ or IL‐4‐dependent blast colony growth was synergistically enhanced by the addition of IL‐6 or Epo. These observations imply that T‐lymphoid/myeloid or pluripotent stem cells may be closely involved in the development of 9q AML. 1992 Blackwell Publishing Ltd

本文言語英語
ページ(範囲)172-177
ページ数6
ジャーナルBritish Journal of Haematology
80
2
DOI
出版ステータス出版済み - 2月 1992

!!!All Science Journal Classification (ASJC) codes

  • 血液学

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