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Ludwig Institute for Cancer Research, Montréal, Québec, Canada H3A 1A1 [P. N. T., H. S., W. K. C.]; Children's Hospital of Los Angeles, Department of Pathology, Los Angeles, California 90027 [H. Sh.]; and Departments of Medicine, Pathology, Biology and Neurology, McGill University, Montréal, Québec, Canada H3A 2B4 [W. K. C.]
Rhabdomyosarcomas (RMS) bear a morphological resemblance to developing striated muscle. It has been reported that two histologically distinct subtypes of RMS, embryonal and alveolar, behave differently in many clinical aspects, such as age distribution, primary site, and prognosis. We have investigated the expression of various genes, which are preferentially expressed in normal muscle tissue or cell culture (actins, myosins, and creatine kinases, and myogenic regulatory genes MyoD, myogenin, MRF4, and Myf5), in embryonal and alveolar subtypes and compared the results to the stages of developing human fetal limb muscle. The data showed that each of the RMS tumors tested, regardless of histological features, expressed MyoD1 and MRF4 transcripts. Expression of the myogenin gene was detectable in all alveolar RMS (n = 8), whereas only 5 of 8 embryonal RMS expressed myogenin transcripts. Trace levels of Myf5 transcripts were visible in all alveolar RMS and 7 of 8 embryonal RMS. The 
-skeletal, -cardiac, and ß- and 
-cytoplasmic actin transcripts were detectable in all alveolar RMS. While the ß- and -cytoplasmic actin transcripts were evident in all embryonal RMS, only 3 of 8 and 6 of 8 embryonal RMS expressed detectable levels of -skeletal and -cardiac actin transcripts, respectively. The embryonic form of myosin heavy chain was detectable in 1 of 8 of each type of tumor. Myosin light chain-1/3 transcripts were detectable in 4 of 8 alveolar RMS and 5 of 8 embryonal RMS. Brain creatine kinase transcripts were detectable in all alveolar RMS and 4 of 8 embryonal RMS, whereas none of the RMS samples contained detectable levels of the muscle form of creatine kinase. A comparison of the expression profiles with those of normal developing human fetal limb muscle (from 7.5 to 24 weeks' gestation) suggested that RMS resembled a relatively restricted segment of fetal muscle development. Furthermore, the data also showed a great deal of overlap in the differentiation state achieved by the embryonal and alveolar subtypes of RMS, suggesting that the clinicopathological difference between these two may not be due to malignant transformation of the cells from different positions in the normal pathway of myogenesis.
1 P. N. T. is a recipient of a Medical Research Council of Canada Postdoctoral Fellowship.
2 Present address: Department of Anatomy and Cell Biology, University of Cincinnati Medical School, 231 Bethesda Avenue, Cincinnati, OH 45267.
3 To whom requests for reprints should be addressed, at Ludwig Institute for Cancer Research, Montréal Branch, 687 Pine Ave. West, Montréal, Québec, Canada H3A 1A1.
Received 5/10/91. Accepted 7/19/91.
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