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Blood, Vol. 92 No. 8 (October 15), 1998:
pp. 2688-2695
RAPID COMMUNICATION
The Cryptic inv(2)(p23q35) Defines a New Molecular Genetic Subtype
of ALK-Positive Anaplastic Large-Cell Lymphoma
Iwona Wlodarska,
Chris De Wolf-Peeters,
Brunangelo Falini,
Gregor Verhoef,
Stephan W. Morris,
Anne Hagemeijer, and
Herman Van denBerghe
From the Center for Human Genetics, Department of Pathology, and
Department of Hematology, K.U. Leuven, Leuven, Belgium; the Institute
of Hematology, University of Perugia, Perugia, Italy; and the
Department of Experimental Oncology, St. Jude Children's Research
Hospital, Memphis, TN.
Recently, a distinctive entity characterized by expression of the
anaplastic lymphoma kinase (ALK) protein [most frequently due to the
t(2;5)(p23;q35)-associated NPM-ALK fusion] has emerged within the
heterogenous group of non-Hodgkin's lymphomas (NHL) classified as
anaplastic large-cell lymphoma (ALCL). Sporadic variant
2p23/ALK abnormalities identified in ALK-positive ALCL indicate that genes other than NPM may also be involved in the deregulation of ALK and lymphomagenesis. We report here three cases with an inv(2)(p23q35) detected by fluorescence in situ hybridization (FISH) in young male patients with
ALK-positive ALCL. In contrast to ALCL cases with the
classical t(2;5)(p23;q35) that usually show both cytoplasmic and
nuclear or predominantly nuclear alone localization of the NPM-ALK
chimeric product, in all three cases with an inv(2)(p23q35) the ALK
protein accumulated in the cytoplasm only, supporting the previous
assumption that the oncogenic potential of ALK may not be dependent on
its nuclear localization. As the first step to identify the
ALK partner gene involved in the inv(2)(p23q35), we
performed extensive FISH studies and demonstrated that the 2q35
breakpoint occurred within the 1,750-kb region contained within the
914E7 YAC. Moreover, a striking association of the inv(2)(p23q35) with
a secondary chromosomal change, viz, ider(2)(q10)inv(2)(p23q35),
carrying two additional copies of the putative ALK-related
fusion gene, was found in all three patients, suggesting that, in
contrast to the standard t(2;5)/NPM-ALK fusion, multiple copies
of the putative 2q35-ALK chimeric gene may be required for
efficient tumor development. In summary, we demonstrate that the
inv(2)(p23q35), a variant of the t(2;5)(p23;q35), is a recurrent
chromosomal abnormality in ALK-positive ALCL, the further
characterization of which should provide new insight into the
pathogenesis of these lymphomas.
© 1998 by The American Society of Hematology.
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