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M Petrini, MT Quaranta, U Testa, P Samoggia, E Tritarelli, A Care, L Cianetti, M Valtieri, C Barletta and C Peschle
Department of Hematology-Oncology, Istituto Superiore di Sanita, Rome,
Italy.
Although the key role of human homeobox (HOX) genes in development is well
established, their function in adult cells is still under scrutiny. We have
analyzed, in normal adult blood cell subpopulations, acute lymphoid
leukemia (ALL) cells lines, and primary blasts, the RNA expression of all
HOX-2 cluster genes (5'-2.5, 2.4, 2.3, 2.2, 2.1, 2.6, 2.7, 2.8, 2.9, 3')
and nine genes in the HOX-1, -3, and -4 cluster by Northern blotting, RNAse
protection, and/or reverse transcriptase polymerase chain reaction
(RT-PCR). The analyzed HOX-1, -3, and -4 genes were never expressed in all
tested cell populations. Natural killer (NK) cells activated in
interleukin-2 (IL-2)/IL-1 beta-treated cultures exhibit a gradually
increasing, abundant expression of three HOX-2 genes (2.2, 2.6, 2.8), while
three other genes (2.3, 2.1, 2.7) are expressed at a lower level at late
culture times. However, no HOX-2 gene is expressed in quiescent lymphocytes
(NK, B and T [T-cell receptor (TCR) alpha/beta, gamma/delta lymphocytes,
thymocytes] cells), granulocytes, and monocytes. In B- and T-ALL cell
lines, HOX-2 genes are expressed according to different patterns: (1)
widespread transcription (seven of nine genes, including 2.3 and 2.6) in
the Peer line bearing the TCR gamma/delta; (2) expression of 2.5, 2.2, and
2.6 in the SEZ 627 line, which derives from an HTLV-1+ T-helper leukemia;
(3) transcription of 2.3 and 2.6 in both the T-ALL CEM line and four B- ALL
lines (interestingly, CALLA- B-ALL lines are constantly 2.3/2.6 RNA+); (4)
no HOX-2 gene expression was detected in one T- and two B- ALL lines.
Primary blasts from five T- and five pre-B-ALL showed selective expression
of one or more HOX-2 genes, namely 2.5, 2.2, 2.6, and 2.7. Our data are
compatible with the hypothesis that selected HOX- 2 genes play a role in
the IL-2/IL-1 beta-induced activation and/or proliferation of normal NK
lymphocytes and possibly in the oncogenetic process of some T- and B-ALL.
This article has been cited by other articles:
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