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1 h chromosomal abnormalities commonly seen in secondary leukemia.
2 rimary importance in determining the risk of secondary leukemia.
3 ment of ovarian cancer increases the risk of secondary leukemia.
4 ed: two of cardiovascular disease and one of secondary leukemia.
5 early step leading to MLL translocations and secondary leukemia.
6 chanism that is linked to the development of secondary leukemias.
7 ntation-related complications, including two secondary leukemias.
8 nd lymphoid lineage and in treatment-induced secondary leukemias.
9 tial proportion progress to myelofibrosis or secondary leukemia, advanced cancers with a poor prognos
10                             The incidence of secondary leukemia after epipodophyllotoxin treatment an
11  to obtain reliable estimates of the risk of secondary leukemia after epipodophyllotoxin treatment.
12 ative disorders, some of which progressed to secondary leukemia after long latency.
13 -induced cytotoxicity and the development of secondary leukemia after nitrosourea treatment.
14 posure, we have likely captured all cases of secondary leukemia and myelodysplastic syndrome (MDS).
15 ent with extensive prior treatment developed secondary leukemia and three became hypothyroid.
16 th respect to progression, survival, risk of secondary leukemia, and impact of genomic risk factors h
17                                              Secondary leukemia appeared linked with antecedent chemo
18 ty and possibly to an increased incidence of secondary leukemias as a result of elevated mutation fre
19  chromosomal translocations in patients with secondary leukemias associated with chemotherapeutic reg
20                                        These secondary leukemias associated with topoisomerase II inh
21                                              Secondary leukemia developed in five patients.
22 as a true recurrence rather than a second or secondary leukemia, DNA extracted from archived marrow s
23                                              Secondary leukemia emerged as a major risk with dose-int
24 tion of cumulative 6-year incidence rates of secondary leukemia for each etoposide dose group.
25 d cumulative 6-year risks for development of secondary leukemia for the low, moderate, and higher cum
26 iduals to blood cancers, often presenting as secondary leukemias, has largely been driven in the last
27  biology (European Leukemia Network risk and secondary leukemia), health care access (insurance and c
28         We conducted a case-control study of secondary leukemia in a population-based cohort of 28,97
29                          New drugs active in secondary leukemias include CPX-351, or venetoclax in co
30                                     Cases of secondary leukemia (including treatment-related myelodys
31 cute myeloid leukemia, with the risk of this secondary leukemia linked to a genetic defect in thiopur
32 ide in adjuvant therapy and that the risk of secondary leukemia may be increased.
33 izure, neurologic impairment, limb ischemia, secondary leukemia, metastasis, or death.
34                    Data obtained by the CTEP secondary leukemia monitoring plan support the relative
35                                              Secondary leukemias occurred in 2 patients.
36                                          The secondary leukemia presented as myelodysplasia with mono
37 sitive leukemia represents an outgrowth of a secondary leukemia that shares a common initiating event
38 ts treated with etoposide eventually develop secondary leukemias that are characterized by translocat
39 Disease transformation into myelofibrosis or secondary leukemia was not reported.
40                                           No secondary leukemia was observed.
41                    No primary CNS relapse or secondary leukemia was seen.
42                                     All four secondary leukemias were fatal.
43 ficantly different from the expected rate of secondary leukemias when patients receive additional cyc