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Intermetastatic and Intrametastatic Heterogeneity Shapes Adaptive Therapy Cycling Dynamics. | LitMetric

AI Article Synopsis

  • Adaptive therapies that alternate drug treatment and drug-free periods can slow cancer progression by leveraging competition between sensitive and resistant cells in metastatic cancer.
  • A framework was proposed to assess the characteristics of metastases using tumor response data, particularly examining prostate-specific antigen (PSA) levels in patients with metastatic castration-resistant prostate cancer.
  • The study revealed that the size and makeup of metastases significantly influence treatment cycles, with larger tumors leading to longer treatment cycles and higher intrametastatic heterogeneity improving responses to adaptive therapy.

Article Abstract

Unlabelled: Adaptive therapies that alternate between drug applications and drug-free vacations can exploit competition between sensitive and resistant cells to maximize the time to progression. However, optimal dosing schedules depend on the properties of metastases, which are often not directly measurable in clinical practice. Here, we proposed a framework for estimating features of metastases through tumor response dynamics during the first adaptive therapy treatment cycle. Longitudinal prostate-specific antigen (PSA) levels in 16 patients with metastatic castration-resistant prostate cancer undergoing adaptive androgen deprivation treatment were analyzed to investigate relationships between cycle dynamics and clinical variables such as Gleason score, the change in the number of metastases over a cycle, and the total number of cycles over the course of treatment. The first cycle of adaptive therapy, which consists of a response period (applying therapy until 50% PSA reduction), and a regrowth period (removing treatment until reaching initial PSA levels), delineated several features of the computational metastatic system: larger metastases had longer cycles; a higher proportion of drug-resistant cells slowed the cycles; and a faster cell turnover rate sped up drug response time and slowed regrowth time. The number of metastases did not affect cycle times, as response dynamics were dominated by the largest tumors rather than the aggregate. In addition, systems with higher intermetastasis heterogeneity responded better to continuous therapy and correlated with dynamics from patients with high or low Gleason scores. Conversely, systems with higher intrametastasis heterogeneity responded better to adaptive therapy and correlated with dynamics from patients with intermediate Gleason scores.

Significance: Multiscale mathematical modeling combined with biomarker dynamics during adaptive therapy helps identify underlying features of metastatic cancer to inform treatment decisions.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10425736PMC
http://dx.doi.org/10.1158/0008-5472.CAN-22-2558DOI Listing

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