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From the Institute of Pathology,
*
University of Würzburg, Würzburg, Germany; the Gerhard Domagk Institut für Pathologie,
University of Münster, Münster, Germany; the Institute of Pathology,
University of Kiel, Kiel, Germany; and the Institute of Molecular Medicine,
§
University of Oxford, Oxford, United Kingdom
Detection of minimal residual disease or micrometastases in
rhabdomyosarcoma (RMS) has been an unresolved problem in 70 to 80% of
RMS patients. In patients with alveolar type RMS, which harbors
chromosomal translocations and produces tumor-specific fusion
products, polymerase chain reaction (PCR)-based diagnosis is
clear-cut. In the more frequent embryonal RMS, however,
no such PCR-based marker has been described. Recently it has been
suggested that the PCR-based detection of MyoD1 may be a valuable
adjunct in the diagnosis of minimal disease in embryonal RMS. We report
here that MyoD1 mRNA is not specific for RMS, but can be
amplified from ex vivo samples of many other childhood
tumors and some normal tissues. By contrast, simultaneous
amplification of 
and 
subunit message of the fetal type
acetylcholine receptor (AChR), by a novel duplex PCR,
and the quantification of both transcripts resulting in a /AChR
ratio <1 was 100% sensitive in alveolar (n = 8) and
embryonal (n = 10) RMS. Moreover, AChR was
not detected in other childhood (n = 27) or adult
tumors (n = 12), or normal tissues,
except thymus. The high sensitivity and specificity of the method were
confirmed by the successful detection of five cases of cytologically or
molecularly verified RMS bone marrow micrometastases among 47 bone
marrow samples from childhood tumor patients. By contrast,
MyoD1 showed no amplification because of its low level of
transcription. We conclude that mRNA of the fetal type AChR is a more
specific and (about 100 times) more sensitive marker for the molecular
detection of RMS than MyoD1, and thus appears to be a promising
candidate for the detection of minimal disease in RMS lacking
tumor-specific translocations.
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