IN 1960, Nowell and Hungerford demonstrated an abnormal chromosomal marker in chronic myelocytic leukemia (CML).¹This observation has been confirmed²⁻⁸and the abnormal chromosome has been named Philadelphia or Ph¹chromosome.³The mechanism of its production may be analogous to the production of a smaller G choromosome found in patients accidentally exposed to total-body irradiation.⁹If so, it would indicate that the Ph¹chromosome is an acquired abnormality rather than a prezygotic abnormality. This postulation was supported by our finding that there was no Ph¹chromosome in a normal identical twin whose leukemic twin showed typical Ph¹chromosome.¹⁰This communication reports the clinical and cytogenetic findings in another set of identical twins, one having CML; it also reports follow-up studies of the surviving normal identical twin of our first reported set¹⁰7½ years after the diagnosis of CML in his
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Kong-Oo Goh (1967) studied this question.
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