Overview

Dr. So-Youn Kim is an Associate Professor in the Department of Obstetrics and Gynecology at
Rutgers New Jersey Medical School. She received her Ph.D. and M.S. in Biochemistry and Molecular
Biology from Yonsei University College of Medicine in Seoul, Korea.

Dr. Kim completed postdoctoral training at Northwestern University Feinberg School of Medicine in
the laboratories of J. Larry Jameson, M.D., Ph.D., and Teresa K. Woodruff, Ph.D. She subsequently
served as a Research Assistant Professor at Northwestern University before joining the University of
Nebraska Medical Center in 2018 as a tenure-track Assistant Professor in Obstetrics and
Gynecology, where she was later promoted to Associate Professor. In January 2026, she joined
Rutgers New Jersey Medical School as a tenure-track Associate Professor.

Dr. Kim's research program focuses on reproductive endocrinology, ovarian biology, and fertility
preservation, with a particular emphasis on the molecular mechanisms regulating primordial follicle
dynamics in the ovary. Her work has contributed to understanding the roles of the c-KIT/PI3K and
CHK2 TAp63 signaling pathways in the activation and demise of primordial follicle oocytes. Using
knockout mouse models, her laboratory has elucidated the pivotal role of TAp63 in mediating oocyte
death triggered by chemotherapy or radiation therapy. Her group has also identified a novel
mechanism by which TAp63 regulates oocyte death induced by cisplatin and cyclophosphamide,
providing important insights into chemotherapy-related ovarian damage. In addition, her studies have
demonstrated that PI3K and c-KIT signaling are essential for oocyte survival and the maintenance of
reproductive lifespan.

More recently, Dr. Kim's laboratory has investigated the direct impact of leukemia on ovarian function,
revealing how leukemic infiltration compromises ovarian tissue. Her ongoing work aims to develop
strategies to preserve ovarian function in the context of disease-related damage, with the ultimate
goal of improving fertility preservation approaches for female patients.

Education

D.Phil, 2005, Yonsei University College of Medicine

Relevant Publications

1. Abazarikia A, So W, Xiao S, Kim SY. Oocyte death is triggered by the stabilization of TAp63a dimers in response to cisplatin. Cell Death Dis. 2024 Nov 7;15(11):799 (PMCID:PMC11544165)

2. Luan Y, So W, Dong R, Abazarikia A, Kim SY. KIT in oocytes: a key factor for oocyte survival and reproductive lifespan. EBioMedicine. 2024 Aug;106:105263 (PMCID: PMC11338130)

3. Luan Y, Yu SY, Abazarikia A, Dong R, Kim SY. TAp63 determines the fate of oocytes against DNA damage. Sci Adv. 2022 Dec 21;8(51):eade1846. (PMCID: PMC9770984)

4. Kim SY, Nair DM, Romero M, Serna VA, Koleske AJ, Woodruff TK, Kurita T. Transient inhibition of p53 homologs protects ovarian function from two distinct apoptotic pathways triggered by anticancer therapies. Cell Death Differ 2019 Mar;26(3):502-515 (Corresponding author) (PMCID: PMC6370889)

5. Kim SY, Cordeiro MH, Serna VA, Ebbert K, Butler LM, Sinha S, Mills AA, Woodruff TK, and Kurita T. Rescue of platinum-damaged oocytes from programmed cell death through inactivation of the p53 family signaling network. Cell Death Differ 2013 Aug;20(8):987-97 (PMCID: PMC3705595)

Areas Of Interest

DNA repair in oocytes

Oncofertility

Primordial follicles

Systemic Lupus Erythematosus

TAp63

Fertilty Preservation

Dr. Kim focuses on understanding how cancer treatments affect reproductive function in
cancer patients, a field known as Oncofertility. Over the past thirty years, the survival rate for young
cancer patients has significantly improved, allowing many young cancer survivors to lead relatively
normal lives.

However, cancer therapies can have long-term negative effects on various organ systems, including
the reproductive system. One of the most serious side effects for young women undergoing cancer
treatment is the loss of ovarian follicles. This loss reduces the number of ova (female germ cells or
eggs) available for future fertility and affects the production of essential steroid hormones such as
estrogen and progesterone.

These hormones are vital for normal menstrual cycles, pregnancy, and overall hormonal balance.
Young women receiving cancer treatment may experience primary ovarian insufficiency, which
clinically presents as endocrine dysfunction and infertility. For instance, prepubertal girls may fail to
initiate puberty and require medical therapies to support their normal development. Reproductive-age
women may experience disrupted menstrual cycles, endocrine issues, and the inability to conceive.
Developing effective interventions to prevent the loss of ovarian follicles could greatly enhance the
quality of life for young cancer patients. Current research indicates that certain fertility-preserving
interventions, known as "fertoprotective" therapies, may help protect ovarian follicles from the
damaging effects of cancer treatments. However, the mechanisms by which these
fertoprotective therapies work are not yet fully understood. Dr. Kim aims to clarify how cancer
treatments deplete ovarian follicles, create new therapeutic agents based on the mechanisms of
follicle depletion, and align fertoprotective strategies with specific cancer treatments to preserve
ovarian follicles and maintain fertility.