Table 2

Imatinib-naive and imatinib-treated CML-CP–like mice accumulate genetic aberrations in leukemia cells

Mice*CNsCNGs, countsCNGs, bp rangeCNLs, countsCNLs, bp rangeCNG/L§, medianAltered in CML-AP/BP– and TKI-resistant patients
Untreated 2.6 ± 1.8 1-410 3-448908 7-343 3-271869 659 (104-2377) Abcc3, Akt3, Arhgef2, Atn2, Cabin1, Ccdc91, Cep170, Csf3r, Idh1, Ift74, Ikzf1, Mapk1, Nup85, Pax6, Pi4ka, Prkca, Psmd1, Ptbp2, Spire, Tesk1, Trp53, Ush2a, Usp37, Zfp423 
Imatinib 2.7 ± 1.6 113 3-63658 84 3-288609 527 (64-2688) Atf6, Asf1a, Ddx11, Elmo3, Eng, Map3k7, Mcm9, mir-103, Nup85, Pax6, Pdgfrb, Pdss2, Pik3c2g, Ptk2, Ptpn14, Rars2, Rb1, Recql, Sox6, Tssc4, Wdr26 
Mice*CNsCNGs, countsCNGs, bp rangeCNLs, countsCNLs, bp rangeCNG/L§, medianAltered in CML-AP/BP– and TKI-resistant patients
Untreated 2.6 ± 1.8 1-410 3-448908 7-343 3-271869 659 (104-2377) Abcc3, Akt3, Arhgef2, Atn2, Cabin1, Ccdc91, Cep170, Csf3r, Idh1, Ift74, Ikzf1, Mapk1, Nup85, Pax6, Pi4ka, Prkca, Psmd1, Ptbp2, Spire, Tesk1, Trp53, Ush2a, Usp37, Zfp423 
Imatinib 2.7 ± 1.6 113 3-63658 84 3-288609 527 (64-2688) Atf6, Asf1a, Ddx11, Elmo3, Eng, Map3k7, Mcm9, mir-103, Nup85, Pax6, Pdgfrb, Pdss2, Pik3c2g, Ptk2, Ptpn14, Rars2, Rb1, Recql, Sox6, Tssc4, Wdr26 

CN, copy number.

*

Leukemic mice were untreated (n = 8) or treated (n = 3) with imatinib as described in “Methods” and compared with healthy untreated mice (n = 4 and n = 3, respectively).

Median ± SD of gene CNs calculated by the Student t test (P = .383).

The lowest and highest counts of CNGs and CNLs per untreated CML-CP–like mouse; imatinib-treated mice are represented by average number of CNGs and CNLs per mouse. The shortest and longest base pair loss/gain (bp range) is shown. Segments displaying CN > 0.5 and CN < −0.5 and a minimal segment size of 5 probes were selected for investigation. CN = log2 (sample/reference).

§

Results are expressed as median 25 to 75 percentile (range) calculated from CNG and CNL bp range values with the Mann-Whitney rank sum test (P = .074).

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