Solid Tumor Resistance Discovery

Solutions Accelerated by IsoPlexis

  • Tumor Resistance in Melanoma

Make decisions to predict resistance to targeted inhibitor therapeutics in oncology1

Accelerate biomarker discovery of resistance and relapse in targeted therapy for solid tumors.

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Research Area

Development Stage

Discovery

Goal

Discovering improved metrics to predict resistance to targeted inhibitor therapeutics in oncology

How our Award-Winning IsoLight Single-Cell System is Making a Difference

polyfunctional cell

Solution

The SNAI (signaling network activity index) and IsoPlexis’ systems provides insights into how BRAF mutant melanoma cells adapt to MAPK inhibition, that result in drug-tolerant or drug-resistant cell states, which can then be reversed.

polyfunctional cell

Finding

A multiplexed set of functional proteins, analyzed at the single-cell level, pointed to signaling network hubs that drive the initiation of the melanoma cell adaptive transition. Targeting those hubs halted the transition and arrested resistance development.

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Follow Our Data

See the latest published data in Solid Tumor & Oncology

The overall activity of the signaling network in each cancer cell may be quantified by the signaling network activity index (SNAI), which accounts for both the numbers and the strengths of statistically significant correlations.

The SNAI is highest at day 6, with particularly strong signaling participation of p-ERK and p-NFκB p65.1

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SNAI

Solution

Detect Critical Differences

These results suggest a potential gain of function through MEK/ERK and NFκB p65 signaling that might lead to BRAFi drug tolerance by promoting the adaptive transition.

This behavior suggests that combining BRAFi with MEK and NFκB p65 inhibition might arrest the adaptive cell state transition toward drug-resistant phenotypes.1

Signaling Coordination Day 0 and Day 6

[1] Reference: Su et al, PNAS 2017

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