# The Role of Akt in Cell Survival and Cell Growth

> **NIH NIH R01** · UNIVERSITY OF ILLINOIS AT CHICAGO · 2023 · $456,744

## Abstract

During the last 20 years, we have been characterizing mice with different Akt isoforms deficiencies for
survival, lifespan, and susceptibility to cancer at the cellular and organismal levels. The current renewal
application is focused on the systemic effect of Akt isoforms deletion in adult mice. First, the systemic
deletion of Akt1 and Akt2 as well as moderate to high doses of pan-Akt inhibitor in adult mice induces
intestinal damage, loss of body weight, and eventually mortality. Thus, in the first part of this grant
application we will delineate the mechanism of the intestinal damage and will employ approaches to alleviate
it. Second, we found a marked discrepancy between the systemic effect and cell autonomous effect of Akt1
or Akt2 deletion on tumor initiation, progression, and metastasis. These results underscore the importance
of determining the systemic effect of gene targeting for cancer therapy. We will delineate the mechanisms by
which the systemic deletions of Akt1 or Akt2 in adult mice exert their effects on tumor progression and
metastasis in mouse models of breast cancer.

## Key facts

- **NIH application ID:** 10589753
- **Project number:** 5R01AG016927-25
- **Recipient organization:** UNIVERSITY OF ILLINOIS AT CHICAGO
- **Principal Investigator:** Nissim Hay
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2023
- **Award amount:** $456,744
- **Award type:** 5
- **Project period:** 1998-09-01 → 2025-02-28

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10589753

## Citation

> US National Institutes of Health, RePORTER application 10589753, The Role of Akt in Cell Survival and Cell Growth (5R01AG016927-25). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10589753. Licensed CC0.

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