Aggressiveness and time of onset of accelerated repopulation |
Intertumour variability that is unknown cannot measure/estimate for individual patients without cell biopsy sample used in in vitro tests which may alter results |
Grouping patients into tumours that are likely to have slow or fast repopulation by some means of genetic/pathologic testing—however methods currently unknown |
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The extent of various mechanisms responsible for tumour repopulation during treatment |
The interplay between recruitment, accelerated stem division, abortive division and loss of asymmetrical division, in stem cells makes it difficult to evaluate their individual effect |
Research stem cell properties for rapidly proliferating tumours.Sensitivity study on each individual and combined parameter when modelling |
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Input of individualised tumour data, for example, intrinsic radiosensitivity, differences in stem/transit or quiescent cell radiosensitivity |
Currently no pretreatment testing due to logistics and time of testing |
Research cell type/proliferative capacity-dependent radiosensitivities for different tumour cell lines, individualised radiosensitivity pre-treatment testing (requires staff/money/time) |
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Tumour oxygenation/reoxygenation |
Different in every tumour, changes in time, access to equipment, for example, daily/weekly PET, invasive nature of in vivo quantitative data gathering, for example, Eppendorf/Oxy Lab probe |
Access and research into to the feasibility and drug development for daily/weekly PET scans, with tracers that can image hypoxic regions with various thresholds, for example, 2.5, 5.0, 10 mm Hg |
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Drug pharmacokinetics |
Lack of quantitative in vivo assays |
Using in vitro data if existent, parameter estimation and sensitivity study. Molecular pharmacological modelling is required |
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Cell survival data for chemotherapy |
Lack of mathematical formalism equivalent to the LQ model used in radiotherapy |
Using in vitro data if existent for that particular agent |