Supplementary Materials

The PDF file includes:

  • Methods
  • Fig. S1. KP model genetically and histologically recapitulates human lung adenocarcinoma.
  • Fig. S2. Human LUAD-associated proteases are not overexpressed in benign lung diseases.
  • Fig. S3. LUAD protease panel genes are enriched across genetic and histological lung cancer subtypes.
  • Fig. S4. Peptide substrates are cleaved by one or a combination of metallo, serine, and aspartic proteases.
  • Fig. S5. Clearance of PEG-840kDa nanoparticles from lungs follows single phase exponential decay kinetics.
  • Fig. S6. No toxicity is observed in mice treated with intrapulmonary activity-based nanosensors.
  • Fig. S7. Activity-based nanosensors are stable to aerosolization.
  • Fig. S8. Aerosolized nanoparticles penetrate deep within the lung and avoid distribution to off-target organs.
  • Fig. S9. Free reporters enter the bloodstream after pulmonary delivery and are detectable in the urine by mass spectrometry.
  • Fig. S10. Multiple reporters are differentially enriched in the urine of healthy mice and KP mice at 7.5 and 10.5 weeks.
  • Fig. S11. Extrapulmonary disease is undetectable by intrapulmonary activity-based nanosensors.
  • Fig. S12. Intrapulmonary activity-based nanosensors differentiate mice bearing Alk-driven lung cancer from healthy controls.
  • Fig. S13. Pulmonary activity-based nanosensor cleavage profile is distinct in lung cancer and benign lung inflammation.
  • Table S1. Reporter and substrate sequences for in vitro recombinant protease screen.
  • Table S2. Quantification of tumor burden in KP mice by microCT.
  • Table S3. Composition of training and test cohorts for random forest classification.
  • Legend for data file S1

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Other Supplementary Material for this manuscript includes the following:

  • Data file S1 (Microsoft Excel format). Raw data from figures.