Instructional Insights: Learnings from a Case Study of Collaborating with an Individual with Lived Experience in Occupational Therapy Education.

This case study shares the knowledge gained from working with an individual having lived experience of a health condition contributing toward an occupational therapy education module through the reflections of an occupational therapy academic and an individual with lived experience working in a university. The primary goal is to establish an empirical evidence base for involvement of people with lived experience in occupational therapy education and to encourage other educators and individuals with lived experience to follow this model of teaching and learning in their curricula. Based on the belief that teaching and learning through co-production creates a 'triangle' of benefit for individuals with lived experience, students and academics.

Intratumor heterogeneity of EGFR expression mediates targeted therapy resistance and formation of drug tolerant microenvironment.

Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors are commonly used to treat non-small cell lung cancers with EGFR mutations, but drug resistance often emerges. Intratumor heterogeneity is a known cause of targeted therapy resistance and is considered a major factor in treatment failure. This study identifies clones of EGFR-mutant non-small cell lung tumors expressing low levels of both wild-type and mutant EGFR protein.

Cyclin A/B RxL Macrocyclic Inhibitors to Treat Cancers with High E2F Activity.

Cancer cell proliferation requires precise control of E2F1 activity; excess activity promotes apoptosis. Here, we developed cell-permeable and bioavailable macrocycles that selectively kill small cell lung cancer (SCLC) cells with inherent high E2F1 activity by blocking RxL-mediated interactions of cyclin A and cyclin B with select substrates. Genome-wide CRISPR/Cas9 knockout and random mutagenesis screens found that cyclin A/B RxL macrocyclic inhibitors (cyclin A/Bi) induced apoptosis paradoxically by cyclin B- and Cdk2-dependent spindle assembly checkpoint activation (SAC).