Setsuko K. Chambers
· Bobbi Olson Endowed Chair of Ovarian Cancer Research, Director of Women's Cancers, University of Arizona Cancer Center, Professor and Division Director of Gynecology Oncology, University of ArizonaUniversity of Arizona · Obstetrics and Gynecology
Active 1986–2026
About
Setsuko K. Chambers, MD, is a nationally recognized Gynecologic Oncologist and the Bobbi Olson Endowed Chair of Ovarian Cancer Research at the University of Arizona. She serves as the Director of Women’s Cancers at the University of Arizona Cancer Center and is the Division Director of Gynecology Oncology. Dr. Chambers has over 30 years of experience specializing in the management, surgery, and chemotherapy of gynecologic cancers. Her expertise spans basic through translational research, clinical trials—including investigator-initiated trials—and active clinical care. She performs open and laparoscopic surgeries for cancers, pelvic masses, and high-risk women requiring risk-reducing surgeries, and runs several innovative chemotherapy trials in ovarian cancer. As the team leader for gynecologic oncology trials at the Cancer Center, she oversees cooperative group, industry-sponsored, and investigator-initiated trials, and is one of the top accruers to clinical trials at the center. Her research laboratory focuses on understanding the molecular basis of breast and ovarian cancer metastasis and initiation, with an increasing focus on the tumor micro-environmental influence on tumor initiation in the fallopian tube and ovary. Dr. Chambers is also involved in genetic counseling and management of women at risk for breast, ovarian, and uterine cancers, and she developed and directs the only clinic for individuals at high risk for hereditary cancers in Arizona. She received her BS and MD degrees from Brown University, completed her residency and fellowship at Yale University, and was the first female tenured professor in Obstetrics and Gynecology at Yale. Since joining the University of Arizona in 2004, she has held various leadership roles, including Vice Chair and Section Head of Gynecologic Oncology, and has contributed significantly to the university’s cancer research infrastructure. She is a co-founding Editor-in-Chief of the American Journal of Clinical and Experimental Obstetrics and Gynecology and has served on numerous national committees and grant review panels. Dr. Chambers is certified in Gynecologic Oncology by the American Board of Obstetrics & Gynecology and has authored over 145 peer-reviewed publications and chapters.
Research topics
- Oncology
- Cancer research
- Biology
- Medicine
- Internal medicine
- Genetics
- Gastroenterology
- Cell biology
- Bioinformatics
- Surgery
Selected publications
International Journal of Gynecological Cancer · 2026-02-01
articleScientific Reports · 2024-12-02 · 4 citations
articleOpen accessSenior authorThe involvement of the androgen receptor (AR) pathway in developing epithelial ovarian cancer is increasingly acknowledged. However, the specific mechanisms by which anti-androgen agents, such as flutamide, may prevent ovarian cancer and their efficacy remain unknown. This study was initiated by investigating the impact of flutamide on miRNA expression in women at high risk (HR) for ovarian cancer. Ovarian and tubal tissues, free from ovarian, tubal, peritoneal cancers, and serous tubal intraepithelial carcinoma (STIC), were collected from untreated and flutamide-treated HR women as well as low-risk (LR) women controls. We performed miRNA sequencing on these 3 sample cohorts and observed that flutamide normalized miRNA levels in HR tissues, notably upregulating the miR-449 family to levels seen in LR tissues. In subsequent tests in primary ovarian epithelial cells and ovarian cancer cell lines (SKOV3 and Hey), flutamide also increased miR-449a and miR-449b-5p levels. Introducing mimics of these miRNAs reduced the mRNA and protein levels of AR and colony-stimulating factor 1 receptor (CSF1R, also known as c-fms), both of which are known contributors to ovarian cancer progression, with emerging evidence also supporting their roles in ovarian cancer initiation. Ovarian cancer cell migration was inhibited upon introducing miR-449a and miR-449b-5p mimics. Together, our study suggests a novel dual-inhibitory mechanism of flutamide on the AR pathway (AR expression suppression in addition to direct androgen antagonism) and supports its chemopreventive potential in ovarian cancer, especially for HR patients with low miR-449 expression.
European Journal of Cancer · 2024-06-12 · 7 citations
articleOpen accessPURPOSE: To explore safety and tolerability parameters for the niraparib individualized starting dose (ISD) in patients with newly diagnosed advanced ovarian cancer that responded to platinum-based chemotherapy who participated in the phase 3 PRIMA/ENGOT-OV26/GOG-3012 trial (NCT02655016). METHODS: The PRIMA protocol was amended so newly enrolled patients received an ISD based on baseline body weight/platelet count. In this ad hoc analysis, the timing, duration, and resolution of the first occurrence of common any-grade hematologic (thrombocytopenia, anemia, neutropenia) and nonhematologic (nausea, asthenia/fatigue, constipation, insomnia, hypertension) treatment-emergent adverse events (TEAEs) were evaluated by treatment arm in the ISD safety population (data cutoff, November 17, 2021; median follow-up, 3.5 years). RESULTS: Of 733 randomized patients, 255 were enrolled after the ISD protocol amendment and received ≥ 1 dose of study treatment (niraparib, 169; placebo, 86). In the niraparib arm, median times to first events were 22.0-35.0 days for hematologic TEAEs and 7.0-56.0 days for nonhematologic TEAEs. First events resolved in ≥ 89.8% of patients for hematologic TEAEs; for nonhematologic TEAEs, resolution rates ranged from 55.3% (insomnia) to 86.0% (nausea). Median durations of first hematologic TEAEs were ≤ 16.0 days, but for first nonhematologic TEAEs ranged from 18.0 days (nausea) to 134.0 days (insomnia). CONCLUSION: The niraparib ISD was generally well tolerated and TEAEs were manageable. Common hematologic and nonhematologic TEAEs occurred early and first events of hematologic TEAEs had a short duration (≈ 2 weeks) and a high resolution rate. These findings support close monitoring immediately following niraparib initiation and may help inform patient expectations for niraparib safety.
medRxiv (Cold Spring Harbor Laboratory) · 2024
Senior authorCorresponding- Oncology
- Cancer research
- Medicine
Background: The involvement of the androgen and androgen receptor (AR) pathway in the development of epithelial ovarian cancer is increasingly recognized. However, the specific mechanisms by which anti-androgen agents, such as flutamide, may prevent ovarian cancer and their efficacy remain unknown. We examined the effects of flutamide on the miRNA expression profile found in women at high risk (HR) for ovarian cancer. Methods: Ovarian and tubal tissues, free from ovarian, tubal, peritoneal cancers, and serous tubal intraepithelial carcinoma (STIC), were collected from untreated and flutamide-treated HR women. Low-risk (LR) women served as controls. Transcriptomic miRNA sequencing was performed on these 3 sample cohorts. The miRNAs that showed the most notable differential expression were subjected to functional assays in primary ovarian epithelial cells and ovarian cancer cells. Results: ), both of which are known contributors to ovarian cancer progression, with emerging evidence also supporting their roles in ovarian cancer initiation. These findings were experimentally validated in primary ovarian epithelial cells and ovarian cancer cell lines (SKOV3 and Hey): flutamide treatment resulted in elevated levels of miR-449a and miR-449b-5p, and introducing mimics of these miRNAs reduced the mRNA and protein levels of CSF1R and AR. Furthermore, introducing miR-449a and miR-449b-5p mimics showed inhibitory effects on the migration and proliferation of ovarian cancer cells. Conclusion: Flutamide treatment restored the reduced expression of miR-449a and miR-449b-5p in HR tissues, thereby decreasing the expression of CSF1R and AR, functional biomarkers associated with an increased risk of ovarian cancer. In addition to the known direct binding of flutamide to the AR, we found that flutamide also suppresses AR expression via miR-449a and miR-449b-5p upregulation, revealing a novel dual-inhibitory mechanism on the AR pathway. Taken together, our study highlights mechanisms supporting the chemopreventive potential of flutamide in ovarian cancer, particularly in HR patients with reduced miR-449 expression.
Gynecologic Oncology · 2024-10-09
articleInternational Journal of Gynecological Cancer · 2024-10-01
articleInternational Journal of Gynecological Cancer · 2024-03-01
article2023-03-31
preprintOpen access<div>AbstractPurpose:<p>This study assessed the efficacy, safety, and pharmacokinetics of adavosertib in combination with four chemotherapy agents commonly used in patients with primary platinum-resistant ovarian cancer.</p>Patients and Methods:<p>Women with histologically or cytologically confirmed epithelial ovarian, fallopian tube, or peritoneal cancer with measurable disease were enrolled between January 2015 and January 2018 in this open-label, four-arm, multicenter, phase II study. Patients received adavosertib (oral capsules, 2 days on/5 days off or 3 days on/4 days off) in six cohorts from 175 mg once daily to 225 mg twice daily combined with gemcitabine, paclitaxel, carboplatin, or pegylated liposomal doxorubicin. The primary outcome measurement was overall response rate.</p>Results:<p>Three percent of patients (3/94) had confirmed complete response and 29% (27/94) had confirmed partial response. The response rate was highest with carboplatin plus weekly adavosertib, at 66.7%, with 100% disease control rate, and median progression-free survival of 12.0 months. The longest median duration of response was in the paclitaxel cohort (12.0 months). The most common grade ≥3 adverse events across all cohorts were neutropenia [45/94 (47.9%) patients], anemia [31/94 (33.0%)], thrombocytopenia [30/94 (31.9%)], and diarrhea and vomiting [10/94 (10.6%) each].</p>Conclusions:<p>Adavosertib showed preliminary efficacy when combined with chemotherapy. The most promising treatment combination was adavosertib 225 mg twice daily on days 1–3, 8–10, and 15–17 plus carboplatin every 21 days. However, hematologic toxicity was more frequent than would be expected for carboplatin monotherapy, and the combination requires further study to optimize the dose, schedule, and supportive medications.</p></div>
2023-04-03
preprintOpen access<p>Figure S1 shows a consort diagram of patients with pretreatment and postprogression circulating cell-free DNA samples sequenced; Figure S2 shows a bar graph showing that a significantly lower level of the serum marker CA-125 was found at study enrollment in patients with no TP53 or BRCA mutations detected in the pretreatment circulating cell-free DNA; Figure S3 shows a scatter plot showing significant correlation between mutant allele frequency of primary somatic BRCA and TP53 mutations detected in pretreatment circulating cell-free DNA; Figure S4 shows a graph indicating the location of deleterious BRCA mutations where reversion mutations were detected in pretreatment and postprogression circulating cell-free DNA; Figure S5 shows a scatter plot showing a significant correlation of mutation allele frequency for the detected primary deleterious BRCA mutations between two independent next-generation sequencing-based circulating cell-free DNA assays; Figure S6 shows a swimlane graph showing the duration on rucaparib treatment of patients with or without BRCA reversion mutations detected in pretreatment circulating cell-free DNA; Figure S7 shows a graph from a linear regression analysis between the sum of mutation allele frequency of BRCA reversion mutations from pretreatment plasma and rucaparib progression-free survival; Figure S8 shows a bar graph of changes in BRCA reversion allele frequencies detected in pretreatment and postprogression circulating cell-free DNA from one patient.</p>
2023-04-03 · 1 citations
preprintOpen access<p>Table S3 shows a summary of BRCA reversion mutations detected in postprogression circulating cell-free DNA</p>
Recent grants
NIH · $577k · 2002
NIH · $1.4M · 2009
NIH · $246k · 1996
NIH · $100k · 1995
NIH · $63k · 1993
Frequent coauthors
- 216 shared
Yan Wang
Hunan Agricultural University
- 157 shared
Hye Sook Chon
Cancer Institute (WIA)
- 155 shared
Robert M. Wenham
- 153 shared
Kristina Butler
- 153 shared
János L. Tanyi
Cancer Research Center
- 153 shared
Carrie Langstraat
- 152 shared
Mark A. Morgan
- 151 shared
Ira Winer
Wayne State University
Awards & honors
- Bobbi Olson Endowed Chair in Ovarian Cancer Research
- Member of the National Academy of Medicine (2009)
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