rates have risen from less than 10% in the 1960s to around 90%
today primarily due to the drug development as well as risk-adapted
personalized therapy [9–12]. However, ~10–20% of the pediatric
patients and more than 50% of the adults suffer relapse, which is
associated with a high rate treatment failure and death
[13–16]. Unfortunately, little progress has been made in the treat-
ment of relapsed ALL in either the older (1988–1994) or recent
(1995–2002) eras [13]. Therefore, multiple diagnostic or prognos-
tic factors have been taken into consideration for risk classification
and used for individualized treatment, including well-known non--
genomic (e.g., age and leukocyte count at diagnosis) as well as
genomic signatures of ALL (e.g., leukemia cells with structural
rearrangements or aneuploidy) [10]. Actually, multiple genomic
alterations have also been noticed to be associated with
non-genomic factors and have already been considered as strong
prognostic factors to guide the clinical regimen determination and
predict the treatment outcomes more sensitively [4, 9, 17]. To
balance the treatment efficacy and adverse drug reactions risk,
patients at high risk for a relapse are treated aggressively, with less
toxic treatments for patients with a lower risk. On the other hand,
recurrent genomic alterations can also be considered as potential
targets for drug development, which already have multiple success-
ful examples including imatinib for patient with BCR-ABL fusion
[8, 10]. No doubt current and future genomic profiling investiga-
tion identified by the new technologies and in-depth mechanism
studies, together with advanced understandings of the
non-genomic clinical features, will guild more precious ALL classi-
fication, which is helpful to determine the individualized treatment
therapy and further improve the survival rate as well as life quality of
ALL patients [11]. In addition to the clinical treatment, prevention
of ALL has also been drawn attention, especially for those indivi-
duals with family history or inherited predisposition. With the
development of inherited genetic investigations of ALL susceptibil-
ity, many rare and common germline variants have been determined
as risk indicators with varied odds ratio [18]. Therefore, preven-
tions or interventions can be taken into consideration for indivi-
duals with high risk to develop ALL, including getting away from
the risk environment (e.g., formaldehyde-based home decoration,
ionizing radiation, and infections), routine physical examinations,
early diagnosis, and treatments [4].
On the other hand, genetic analysis is a powerful and obliga-
tory tool to discover and identify the important genomic alterations
for leukemogenesis, diagnosis, and treatment outcomes. Lots of
genomic technologies have been developed in the past decades, and
some old methods have been replaced by more effective techniques,
especially for genome-wide screening. Multiple frequently used
techniques for genetic investigation include chromosome banding
analysis, fluorescence in situ hybridization (FISH), polymerase388 Heng Xu and Yang Shu