This article discusses my (recursive) process of theory building and the relationship between research, teaching, and theory development for graduate students. It shows how graduate students can reshape their conceptual frameworks not only through course work, but also through researching classes they teach. Specifically, while analyzing the intersection of modality, evidence, and argument in my students’ writing, I began to adopt Bakhtinian (1981) theory of dialogic voicing and appropriation as a framework through which to approach writing development. I examine the influences of curriculum, policy, citation, and plagiarism on student writing and conclude with discussing the changes in my teaching practices.

Phosphorylation networks intimately regulate mechanisms of response to therapies. Mapping the phospho-catalytic profile of kinases in cells or tissues remains a challenge. Here, we introduce a practical high-throughput system to measure the enzymatic activity of kinases using biological peptide targets as phospho-sensors to reveal kinase dependencies in tumour biopsies and cell lines. A 228-peptide screen was developed to detect the activity of >60 kinases, including ABLs, AKTs, CDKs and MAPKs. Focusing on BRAF^V600E tumours, we found mechanisms of intrinsic resistance to BRAF^V600E-targeted therapy in colorectal cancer, including targetable parallel activation of PDPK1 and PRKCA. Furthermore, mapping the phospho-catalytic signatures of melanoma specimens identifies RPS6KB1 and PIM1 as emerging druggable vulnerabilities predictive of poor outcome in BRAF^V600E patients. The results show that therapeutic resistance can be caused by the concerted upregulation of interdependent pathways. Our kinase activity-mapping system is a versatile strategy that innovates the exploration of actionable kinases for precision medicine.