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Blood, Vol. 95 No. 12 (June 15), 2000:
pp. 4014-4015
CORRESPONDENCE
 |
To the Editor: |
Translocation t(11;18) absent in early gastric marginal zone
B-cell lymphoma of MALT type responding to eradication of
Helicobacter pylori infection
Malignant lymphomas are characterized by specific gene
rearrangements that result in particular fusion transcripts and
proteins. For example, follicular lymphoma harbors the translocation
t(14;18) while mantle cell lymphoma bears the translocation t(11;14).
Both translocations result in specific gene fusions (Bcl-2 activation and cyclin D1 overexpression, respectively) that render the respective lymphoma cells resistant to apoptotic stimuli. The translocation t(11;18)(q21;q21) has been implicated recently in low-grade
marginal-zone B-cell lymphomas of the mucosa associated lymphoid tissue
(MALT).1,2 This translocation has been detected in MALT
lymphomas of low grade only. The genes involved in the translocation
have been cloned,3 showing that the 5' partner gene is a
member of the survivin family API2
( nhibitor of
 poptosis 2) and the 3' partner is a novel
gene of unknown function, designated MLT
( ALT
 ymphoma-associated  ranslocation). This genetic aberration has
been detected in approximately one third of low-grade MALT lymphomas.
The most frequent site in which MALT lymphomas are found is within the
gastric mucosal wall. MALT lymphomas arising in the stomach have been
linked to a chronic infection caused by Helicobacter pylori.4 Early gastric MALT lymphomas have been
reported to respond to cure of the H pylori infection, with
such remissions lasting for up to several years.5,6 We
wanted to investigate whether the response of early gastric low-grade
marginal-zone B-cell lymphomas of the MALT type to H pylori
eradication therapy corresponded to the presence of t(11;18). Biopsies
from 20 cases of low-grade gastric MALT lymphomas, recruited into a
nationwide trial, were analyzed.7 All samples were reviewed
by a central pathologist (M.S.). In 18 biopsy samples, MALT lymphoma
response to H pylori eradication therapy was observed, whereas
in 1 patient no response to H pylori eradication therapy
occurred. In 3 patients the follow-up period has been too short to
evaluate the response as yet.
Reverse transcriptase polymerase chain reaction (RT-PCR) was used to
detect the specific fusion transcript API2-MLT in RNA obtained from the
biopsy samples. The fusion transcript was expressed in none of the 18 samples from which RNA could be successfully extracted (see
Figure).
In contrast, the reference gene,
 -actin, was expressed at a constant level in
all samples (see Figure). Thus in these 18 cases of low-grade gastric
marginal-zone B-cell lymphoma of MALT type, t(11;18) does not seem to
be as frequent as has been reported for extranodal marginal-zone B-cell
lymphomas. We feel that this discrepancy is unlikely to result from
technical problems, because analysis of a further case with known
t(11;18) clearly bore a specific fusion transcript detectable by our
RT-PCR assay (see Figure). We suggest that, instead, t(11;18) plays no
role in the response of gastric MALT lymphomas to cure of H
pylori infection. Low-grade lymphomas harboring t(11;18) may be
more advanced in their progression than those low-grade cases analyzed
in this study. In agreement with this is the report that t(11;18)
occurs predominantly in more progressed low-grade MALT
lymphomas.3 Whether the presence of t(11;18) might predict
nonresponse in MALT lymphomas to eradication of H
pylori infection cannot be stated on the basis of our data, but
this may be likely.
In summary, although t(11;18) is found in more progressed low-grade
gastric MALT lymphomas, it is rare in those early gastric MALT
lymphomas responding to H pylori eradication treatment. Thus t(11;18) may be a clonal marker of lymphoma progression in extranodal marginal-zone B-cell lymphomas.
Birgit Alpen
Andreas Neubauer
Department of Hematology, Oncology, and Immunology
Hospital
of the Philipps-University
Marburg, Germany
Judith Dierlamm
Department of Oncology and Hematology
University Hospital
Eppendorf
Hamburg, Germany
Peter Marynen
Human Genome Laboratory, Center for Human Genetics
University
of Leuven
Leuven, Belgium
Christian Thiede
Ekkehard Bayerdörffer
Department of Internal Medicine I
Carl Gustav Carus
University Hospital
Dresden, Germany
Manfred Stolte
Institute of Pathology
Klinikum Bayreuth
Bayreuth,
Germany
Supported in part by grants from the Deutsche Krebshilfe, Bonn,
Germany
(to A.N. and J.D.).
| |
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Related Article in Blood Online:
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The Apoptosis Inhibitor Gene API2 and a Novel 18q Gene, MLT, Are Recurrently Rearranged in the t(11;18)(q21;q21) Associated With Mucosa-Associated Lymphoid Tissue Lymphomas
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