germline origin of reported changes in T-PLL tumors, although they ultimately cannot exclude it. In their response to the letter of Stoppa-Lyonnet et al, 5 Vanasse and colleagues 17 argue that the recurrence of ATM mutations previously found in T-PLL 1,2 does not fit well with their strictly somatic origin. Our present data illustrate that recurrent mutations in tumor DNA are compatible with their somatic origin. At present, we believe that there are no data to support a tacit acceptance of the hypothesis of the germline origin of ATM mutations in sporadic T-PLL. This, of course, can now be tested prospectively using matched normal and tumor DNA from a larger number of T-PLL cases with ATM mutations.
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Gobin et al. (2001) studied this question.
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