About 60% of both Duchenne's muscular dystrophy (DMD) and Becker's muscular 
dystrophy (BMD) is due to deletions of dystrophin gene. For cases with deletion 
mutations the "reading frame" hypothesis predicts that deletions which result in 
disruption of the translation reading frame prevent production of stable protein 
and are associated with DMD. In contrast, intragenic deletions that involve 
exons encoding an integral number of triplet codons maintain proper reading 
frame. The resulting abnormal proteins are stable and partially functional, 
resulting in a milder and more variable BMD phenotype. To test the validity of 
this theory,we analyzed 40 patients-19 independent deletions at the DMD/BMD 
locus. Clinical/molecular correlations based on the altera-tions of the reading 
frame were valid in 69.2% of cases. After exclusion of: --2 patients with del 
3-6 (with no consistent clinical expression); --1 DMD patient with large 
in-frame deletion; --2 patients that were too young to be classified; --4 
patients in whom it was impossible to identify the extent of deletion (del 47 
and del 44-45), the correlation between deletion and clinical severity was as 
predicted in 92.4% of cases. The present data should be useful in establishing 
the prognosis in individual patients even in sporadic cases with no affected 
relatives.