By David G. Harnden, A. M. R. Taylor (auth.), Harry Harris, Kurt Hirschhorn (eds.)
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Additional resources for Advances in Human Genetics 9
It is hard to doubt that this is the correct explanation. This sort of notion is supported by the findings of Fialkow (personal communication) that when studying the clonal origin of CML using polymorphic marker systems, it can be shown not only that the clone extends to the myeloid, erythroid, megakaryocytic, and monocytic series, but also that it includes some lymphoid cells with B-cell-like markers. This could suggest that the B cell is closer to the myeloid cells than it is to the T cells in its stem cell of origin.
208 This karyotype can be explained in terms of the translocation t(8;21) (q22;q22) observed to date in banded preparations from 6 patients. 208,240,253,310 Two further patients have been shown to have a more complex rearrangement, but still involving the same breakpoints in chromosomes 8 and 21. 151 These were t(8;17;21) (q22;q23;q22) and t(8;11;21) (q22;pI5;q22). Chapter 1: Chromosomes and Neoplasia 39 Another translocation, between chromosomes 6 and 9, t(6;9) (p23;q34) has been described in two patients by Rowley and Potter,246 but this has not yet been confirmed in other studies.
In patients with AT, there is commonly clone formation in the peripheral lymphocytes that specifically involves breakage of chromosome 14 at 14qI2. 212 These are nonmalignant proliferating clones, but the patients do have a predisposition to malignancy. One can therefore establish a link between spontaneously occurring aberrations and the much higher frequency of the same aberrations in patients sensitive to radiation, but we cannot be certain that these latter are radiation-induced. 201 but this is unusual.
Advances in Human Genetics 9 by David G. Harnden, A. M. R. Taylor (auth.), Harry Harris, Kurt Hirschhorn (eds.)