  Heterogeneity in the size distribution of cancer cell populations has been
recently linked to drug resistance and invasiveness. However, despite many
progresses have been made in understanding how such heterogeneous size
distributions arise in fast-proliferating cell types -like bacteria and yeast-,
comprehensive investigations on cancer cell populations are still lacking
mainly due to the difficulties of monitoring the proliferation of the time
scales typical of mammalian cells. From a reductionist cell dynamics point of
view, the strategies allowing size homeostasis are roughly grouped into three
classes, \emph{i.e.} timer, sizer, or adder. These strategies are empirically
distinguishable given the phenomenological measurable relationship between the
cell size at birth and at division, which requires following the proliferation
at the single-cell level.
  Here, we show how it is possible to infer the growth regime and division
strategy of leukemia cell populations using live cell fluorescence labeling and
flow cytometry in combination with a quantitative analytical model where both
cell growth and division rates depend on powers of the cell size.
  Using our novel approach, we found that the dynamics of the size distribution
of leukemia Jurkat T-cells is quantitatively reproduced by (i) a sizer-like
division strategy, with (ii) division times following an Erlang distribution
given by the sum of at least three independent exponentially-distributed times
and (iii) fluctuations up to 15\% of the inherited fraction of size at division
with respect to the mother cell size. Finally, we note that our experimental
and theoretical apparatus can be easily extended to other cell types and
environmental conditions, allowing for a comprehensive characterization of the
growth and division model different cells can adopt.
