# Exploiting metabolism to alter the epigenome of Cyclin E-altered ovarian cancer

> **NIH NIH F31** · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · 2020 · $24,533

## Abstract

Project Summary
The goals of this F31 NRSA are to request support for training to develop expertise in the progression of high-
grad serous epithelial ovarian cancer while addressing a fundamental gap in knowledge that has the potential to
significantly impact healthcare options for ovarian cancer patients. F31 Ruth L. Kirschstein NRSA support will
highly impact this integral phase of my current scientific career and my future aspirations of becoming an
independent academic researcher. The training plan described will utilize all relevant resources available at
Penn State College of Medicine; as well as resources provided by my dynamic mentoring committee at Drexel
University and University of Pennsylvania.
The scientific portion of this proposal focuses on experimentally and mechanistically determining the role of
metabolism and epigenetic modulation in cyclin E-altered high-grade serous carcinoma (HGSC) and whether
this pathway can be targeted as a pro-senescent therapy in the clinic. The proposed studies are based on my
robust preliminary data suggesting that TCA cycle enzyme, IDH1, is upregulated in epithelial ovarian cancer
when compared to the fallopian tube, the potential site of HGSC origin. Additional preliminary data suggests that
IDH1 is upregulated in order to increase transcription of DNA damage response gene, ataxia telangiectasia
mutated (ATM) through histone methylation status, a topic of which I have previously published a review.
Interestingly, my strong preliminary data also indicates that knockdown of IDH1 induces senescence.
Therefore, in continuation of these robust preliminary data I will explore three scientific aims: 1) to determine the
mechanism by which cyclin E upregulates IDH1 expression; 2) to investigate the role of IDH1 in the DNA damage
response; and 3) to develop inhibition of IDH1 as a novel therapeutic strategy in cyclin E-altered HGSC. The
completion of the proposed scientific aims will develop my research skills utilizing HGSC as a model in addition
to increasing my independence as a scientific researcher. Conclusions drawn from the proposed studies may
develop rationale for targeting IDH1 in cyclin E-altered HGSC clinically.

## Key facts

- **NIH application ID:** 9880275
- **Project number:** 5F31CA236372-02
- **Recipient organization:** PENNSYLVANIA STATE UNIV HERSHEY MED CTR
- **Principal Investigator:** Erika S Dahl
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $24,533
- **Award type:** 5
- **Project period:** 2019-03-01 → 2020-11-13

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9880275

## Citation

> US National Institutes of Health, RePORTER application 9880275, Exploiting metabolism to alter the epigenome of Cyclin E-altered ovarian cancer (5F31CA236372-02). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/9880275. Licensed CC0.

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