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Biology subjects

Whiting, F. J. H.

Publications and source records attributed to Whiting, F. J. H..

2 recordsLinked to original sources

Inference of Cancer Drug Cross Resistance Using Only Single-Drug Exposure Data

Combining drugs may prevent resistance in cancer treatment. However, the evolution of resistance to more than one drug simultaneously - cross resistance - remains a major obstacle to durable clinical response. Here, we show that we can identify the presence and strength of cross resistance using lineage tracing data from cell populations exposed only to each drug independently, removing the need for complex combinatorial treatment experiments. Simulations where the ground truth was known showed that the method accurately recovered the true underlying resistance dynamics. We applied the framework to breast cancer, lung cancer and lymphoma datasets, quantifying cross resistance across diverse therapy types. Our predictions align with biological expectations and reveal that even drugs with shared putative targets can exhibit variable cross resistance across pre-clinical models. Finally, we used inferred cross resistance strengths to evaluate treatment strategies, predicting that high cross resistance contributes to the limited efficacy of switching between CDK4/6 inhibitors. By enabling the identification of cross resistance without requiring multi-drug exposure experiments, our framework provides a method for prioritising drug combinations and screening for novel resistance-minimising drug targets.

cancer biology↗

Quantitative measurement of phenotype dynamics during cancer drug resistance evolution using genetic barcoding

Cancer treatment frequently fails due to the evolution of drug-resistant cell phenotypes driven by genetic or non-genetic changes. The origin, timing, and rate of spread of these adaptations are critical for understanding drug resistance mechanisms but remain challenging to observe directly. We present a mathematical framework to infer drug resistance dynamics from genetic lineage tracing and population size data without direct measurement of resistance phenotypes. Simulation experiments demonstrate that the framework accurately recovers ground-truth evolutionary dynamics. Experimental evolution to 5-Fu chemotherapy in colorectal cancer cell lines SW620 and HCT116 validates the framework. In SW620 cells, a stable pre-existing resistant subpopulation was inferred, whereas in HCT116 cells, resistance emerged through phenotypic switching into a slow-growing resistant state with stochastic progression to full resistance. Functional assays, including scRNA-seq and scDNA-seq, validate these distinct evolutionary routes. This framework facilitates rapid characterisation of resistance mechanisms across diverse experimental settings.

cancer biology↗