# Predictive Modeling of the EGFR-MAPK pathway for Triple Negative Breast Cancer Patients

> **NIH NIH U01** · UNIV OF NORTH CAROLINA CHAPEL HILL · 2021 · $572,275

## Abstract

The EGFR-MAPK pathway is a key signaling pathway in human Triple Negative Beast Cancers (TNBC). We
propose to leverage genomic and proteomic data from a rich animal model system, and 2 human clinical trials,
to build predictive models of the EGFR-MAPK signaling pathway activity for TNBC patients. The heterogeneity
of TNBC has hindered previous development of predictive pathway-based computational models because
most approaches are based on experimental data from a single cell line or animal model that is then
extrapolated to fit multiple tumor subtypes. Our approach is to use a diverse experimental model system that
reflects the heterogeneous disease subtypes, and then use two distinct and complementary methods to build
the computational model. We will simultaneously use mechanistic and statistical modeling approaches, at a
variety of scales, that incorporate data from drug treated tumors and cell lines, assayed for gene expression,
DNA copy number, DNA mutations, and protein kinome activity. Lastly, we will test these computational
models on human tumors to evaluate their predictive performance.

## Key facts

- **NIH application ID:** 10140308
- **Project number:** 5U01CA238475-03
- **Recipient organization:** UNIV OF NORTH CAROLINA CHAPEL HILL
- **Principal Investigator:** Timothy C Elston
- **Activity code:** U01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $572,275
- **Award type:** 5
- **Project period:** 2019-06-01 → 2024-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10140308

## Citation

> US National Institutes of Health, RePORTER application 10140308, Predictive Modeling of the EGFR-MAPK pathway for Triple Negative Breast Cancer Patients (5U01CA238475-03). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10140308. Licensed CC0.

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