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Frame et al. Investigating models for prostate cancer research

would benefit from a new combination treatment . act as cell cycle inhibitors since it appears that the
[37]
We carried out a preliminary analysis to measure gene reduced proliferation rate of the stem cells is acting
expression, using “DNA damage signaling pathway” as a resistance mechanism. This result also highlights
polymerase chain reaction arrays, in primary cultures. the need to enrich and/or sort for subpopulations of
Cell subpopulations (SC/TA/CB) selected and cells within the patient cell cultures to observe the
[22]
enriched from primary cultures derived from different response of rare populations of cells, since they can be
disease states (benign prostatic hyperplasia, Gleason masked when looking at the whole population.
7 prostate cancers and high Gleason prostate cancers)
were used, both untreated and treated with radiation The use of QPI illustrates behavioral differences
(2 Gy). The results illustrated variation between between cell lines and primary cells. By making
patients, between disease state, and between each measurements encompassing morphological, kinetic
cell type (SC, TA, CB). Exploring the heterogeneity of and population data a cell signature for each cell type
gene expression between disease states and between can be established. One significant observation is the
cell types with and without treatment may ultimately larger size of primary cells. Also, the different growth
lead to novel drug targets being exploited [38,39] . and proliferation rates of the cell lines and primary
cells will impact the length of time for drugs to take
This is the first report of chemotherapy resistance of effect. In addition, it will be of interest to explore the
cancer stem-like cells from primary prostate epithelial meaning behind the increased cell motility of the
cultures. This study only shows the resistance to primary cultures. Since, ptychography is able to identify
etoposide, however we anticipate that this would heterogeneous populations within a culture, the hope
also be true for other chemotherapeutic drugs that for this technique is to use analysis post-treatment to

Figure 6: Consequences of treatment; paths to resistance or death. Inducing cell death in cancer cells is not a single pathway and initial
treatments may push cells to many different outcomes. To overcome cell thresholds and safeguards and push cells towards cell death,
other stimuli may be required. This could involve sensitisers to make the initial treatment more effective or it could include inhibitors to
prevent activation of cell survival mechanisms. Heterogeneity of response dictates that combination treatments are likely to be more
effective
Journal of Cancer Metastasis and Treatment ¦ Volume 3 ¦ December 6, 2017 311