Sarah B Gitto
VerifiedUniversity of Pennsylvania · Rehabilitation Medicine
Active 2011–2025
About
Sarah B Gitto, PhD, is a Research Assistant Professor of Radiology at the University of Pennsylvania's Perelman School of Medicine. She is an associate member of the Institute for Translational Medicine and Therapeutics, the Abramson Cancer Center, the Center for Women's Health and Reproductive Medicine, the Ovarian Cancer Research Center, and the Center for Cellular Immunotherapies. Her research focuses on cancer therapy, particularly in ovarian cancer, with an emphasis on targeted therapies such as PARP inhibitors and alpha therapy. Dr. Gitto has contributed to preclinical and translational research exploring bispecific antibodies, immune checkpoint blockade, and radiolabeled compounds for cancer treatment. She has authored multiple publications in the field of molecular cancer therapeutics and nuclear medicine, advancing the understanding of targeted cancer therapies and imaging biomarkers.
Research topics
- Cancer research
- Medicine
- Biology
- Chemistry
- Pharmacology
Selected publications
2025-11-25
articleOpen access<p>PARPi treatment and response.</p>
PARP1-targeted alpha therapy enhances target expression
EJNMMI Research · 2025-06-01
articleOpen accessAbstract Graphical abstract
2025-11-25
articleOpen access<p>Baseline [18F]FTT imaging correlates.</p>
Cancer Research · 2025-09-19
articleSenior authorAbstract Epithelial ovarian cancer (EOC) is generally sensitive to radiation. However, the widespread peritoneal dissemination of advanced EOC renders external beam radiotherapy limited as the required dose has substantial off-target toxicities. Targeted radionuclide therapy can deliver ionizing radiation directly to tumor cells while sparing healthy tissues, offering an alternative strategy to safely exploit the radiosensitivity of these tumors. Our platform is based on the FDA-approved small molecule PARP inhibitor, rucaparib, labeled with 211At for targeted alpha therapy ([211At]Parthanatrace, [211At]PTT). Our prior and ongoing studies support significant anti-tumor efficacy in preclinical neuroblastoma and ovarian cancer models. Here, in vivo studies were performed to evaluate the tolerability of [211At]PTT. C57BL/6 mice (n = 10) were treated intravenously with four fractionated doses of [211At]PTT at the MTD (48 MBq/kg/fraction) over 2 weeks. Generally, mice tolerated the treatment well, with statistically similar weight compared to untreated control mice (n = 6) up to 30 days following treatment, supporting a favorable safety profile. Peripheral blood was collected 5, 13, and 20 days following the last treatment and a subset of mice were euthanized after 30 days for full pathological assessment and additional blood analysis. The data indicated a significant decline in red blood cells (RBCs), white blood cells (WBCs), and hemoglobin in the peripheral blood following treatment. Levels were fully restored by 20 days post treatment. Lymphocyte and platelet counts were similar to untreated mice after 30 days. Additional blood analyses showed statistically similar levels for aspartate aminotransferase (AST), alanine transferase (ALT), bilirubin (BUN), and creatine in mice treated with [211At]PTT compared to untreated controls. Full histological and pathological assessment is ongoing. Subsequent biodistribution studies demonstrated selective tissue uptake of [211At]PTT following a single infusion of 48 MBq/kg, with limited off-target accumulation and rapid clearance from non-target organs. Overall, these findings support the safety of [211At]PTT as a promising candidate for targeted alpha therapy in oncology. Citation Format: Aladdin Riad, Alastair McArthur, Hasan Babazda, David Mankoff, Robert H. Mach, Michael D. Farwell, Sarah B. Gitto. Preclinical evaluation of PTT, an At-211-Labeled rucaparib analogue, as a theranostic agent for cancer therapy [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Advances in Ovarian Cancer Research; 2025 Sep 19-21; Denver, CO. Philadelphia (PA): AACR; Cancer Res 2025;85(18_Suppl):Abstract nr A043.
2025-11-25
articleOpen access<p>Clinical response correlates.</p>
Molecular Cancer Therapeutics · 2025-10-22
articleAbstract Background: Clear cell ovarian cancer (CCOC) is often resistant to standard chemotherapy and has limited treatment options in the advanced or recurrent setting. ARID1A is the most prevalent mutation, with approximately 50% of all CCOC harboring this mutation. ARID1A, a member of the SWI/SNF family, regulates transcription and has a major role in the repair of DNA lesions, directly facilitating DNA accessibility on the chromatin or indirectly by facilitating the functions of DNA repair proteins. We propose that CCOCs unique genomic alterations (e.g., ARID1A frameshift or nonsense mutations) will increase dependency on chromatin remodeling and DNA repair (e.g., ATR/CHK1/WEE1) pathways for survival. We hypothesize that combination of low-dose small-molecule inhibitors of the BET family (BRD4i) and the DNA damage repair pathway (ATR/CHK1/WEE1), will especially target ARID1A mutant cancer cells promoting mitotic catastrophe, apoptosis, and tumor regression, sparing normal cells. Method: Use a small size drug screen, we tested and compared drugs’ efficacy in ARID1A mutant cells with wildtype lines. The efficacy of BRD4i combination with either ATRi or WEE1i were evaluated in ARID1A mutant/wildtype lines, and also knockdown or knockout cells compared with isogenic parental lines. The drugs combination affecting the transcription regulation, cell cycle, homologous recombination, apoptosis, and DNA damage were investigated. A CCOC preclinical drug development patient-derived xenograft (PDX) platform was established and drugs’ combinations were evaluated in ARID1A mutant and ARID1A wild-type (ARID1A MUT and ARID1A WT) PDX models. Results: Through the small size of drug screen, we identified that BRD4i, ATRi and WEE1i are more effective in ARID1A mutant cells comparing to that in wildtype lines. Low-dose combination of BRD4i with DNA damage repair inhibitors, ATRi/WEE1i (BDR4i-ATRi or BRD4i-WEE1i), were synergistic in decreasing survival and colony formation in ARID1A MUT cells compared to ARID1A WT. Both combinations showed significant tumor regression and increased overall survival compared to standard chemotherapy or monotherapy in several ARID1A MUT PDX models but minimal in an ARID1A WT PDXs. Among BRD4i-DDRi combinations, BRD4i-ATRi is superior to BRD4i-WEE1i in terms of antitumor effect and drug tolerability. BRD4i-ATRi caused a robust G1 arrest. The BRD4i-ATRi treatment defects homologous recombination and leads to an increase in DNA double-strand breaks and cell apoptosis in the ARID1A MUT or knockout cells. Conclusion: Our studies identify a novel drug combination targeting a genetic alteration (e.g., ARID1A) common in CCOC that is highly effective and tolerable. BRD4i in combination with ATRi or WEE1i was synergistic in vitro in ARID1A MUT models. Using our novel CCOC drug development PDX platform, we demonstrated that BRD4i-ATRi combination therapy is more effective than standard chemotherapy or monotherapy alone with acceptable toxicity in ARID1A MUTPDXs. Citation Format: Yasuto Kinose, Haineng Xu, Hyoung Kim, Xiaolei Wang, Sushil Kumar, Xiaoyin Shan, Erin George, Sergey Medvedev, Amaryllis Ortiz, Sarah Gitto, Margaret Whicker, Kurt D'Andrea, Bradley Wubbenhorst, Dorothy Hallberg, Mark O'Connor, Lauren Schwartz, Wei-Ting Hwang, Katherine L. Nathanson, Gordon Mills, Victor E. Velculescu, Tian-Li Wang, Eric Brown, Ronny Drapkin, Fiona Simpkins. Target clear cell ovarian cancers with ARID1A loss by combination inhibition of BRD4 and ATR [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics; 2025 Oct 22-26; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2025;24(10 Suppl):Abstract nr A133.
2025-11-25
articleOpen access<p>18F]FTT-PET on subject previously treated with PARPi.</p>
Frontiers in Immunology · 2025-07-04
erratumOpen access[This corrects the article DOI: 10.3389/fimmu.2024.1383281.].
International Journal of Radiation Oncology*Biology*Physics · 2025-06-21
articleOpen access2025-11-25
articleOpen access<p>PDX models treated with PARPi therapies.</p>
Frequent coauthors
- 110 shared
Fiona Simpkins
University of Pennsylvania Health System
- 96 shared
Hyoung Kim
- 84 shared
Benjamin Ferman
- 60 shared
Haineng Xu
- 59 shared
Daniel J. Powell
University of Pennsylvania
- 53 shared
Margaret Whicker
- 49 shared
Sushil Kumar
- 49 shared
Eric J. Brown
Education
- 2022
Masters in Translational Science, Institute for Translational Medicine and Therapeutics
University of Pennsylvania
- 2017
Ph.D, Burnett School of Biomedical Sciences
University of Central Florida
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