About

Tanya Stoyanova is an Associate Professor in the Department of Molecular and Medical Pharmacology and has a secondary appointment in the Department of Urology at the University of California, Los Angeles. Her educational background includes a B.S. in Ecology and Protection of the Environment from the Technical University of Varna, Bulgaria, a B.S. in Biology from the University of Kansas, and a Ph.D. in Biochemistry and Molecular Genetics from the University of Illinois, Chicago. She completed postdoctoral fellowships in Stem Cell and Cancer Biology at UCLA. Her research focuses on developing new cancer early detection approaches and therapeutic strategies for late-stage cancers. Her lab's current areas of interest include targeted cancer therapies, antibody-based therapies for advanced prostate and other metastatic epithelial cancers, combination therapies to enhance therapeutic responses, and the discovery of protein-based biomarkers for cancer early detection. Additionally, her team works on developing new imaging modalities, such as positron emission tomography (PET), to improve early detection and monitor treatment responses. The ultimate goal of her research is to improve early diagnosis and prognosis of significant cancers and to guide the development of effective therapeutic strategies for metastatic cancers.

Research topics

• Political Science
• Computer Science
• Medicine
• Engineering ethics
• Biology
• Medical education
• Physics
• Cancer research
• Materials science
• Telecommunications
• Nanotechnology
• Business
• Internal medicine
• Acoustics
• Engineering
• Pathology

Selected publications

• Overcoming T cell tolerance to tumor self-antigens through catch-bond engineering

  Science · 2026-03-19 · 1 citations

  articleOpen access

  T cells are often weakly responsive to tumor self-antigens because of central tolerance, constraining their ability to eliminate tumors. We exploited mechanical force to engineer a weakly reactive T cell receptor (TCR) specific for a nonmutated tumor-associated antigen (TAA), prostatic acid phosphatase (PAP). We identified a catch-bonding "hotspot" whose mutation enhanced T cell activity by increasing TCR-pMHC (peptide-major histocompatibility complex) bond lifetime while preserving physiological affinities and antigen fine specificities. T cells expressing these engineered TCRs showed vastly superior expansion in the tumor, effector phenotypes, and tumor elimination. Crystal structures and molecular dynamics simulations revealed a single amino acid mutation at the catch-bond hotspot primes the TCR for peptide interaction through water reorganization at the TCR-pMHC interface. Catch-bond engineering is a viable biophysically based strategy for transforming tolerized antitumor T cells into potent TCR-T cell therapy killers.

  PublisherOA PDFDOI

• Abstract 3917: Developing new anti-Trop2-antibody-based therapies and optical imaging modalities for epithelial cancers.

  Cancer Research · 2026-04-03

  article1st authorCorresponding

  Abstract Carcinomas, which arise from epithelial tissues, account for 80 to 90 percent of all cancer cases and remain a major clinical challenge. Trophoblastic cell surface antigen-2 (Trop-2) is a transmembrane glycoprotein widely overexpressed in nearly all epithelial cancers. The strong association of elevated Trop-2 with metastasis and poor patient outcomes highlights Trop-2 as a compelling therapeutic and diagnostic target. Here, we report the development of a new class of highly specific human antibodies targeting Trop-2 that represents a promising approach for the development of novel therapeutic and imaging strategies in Trop-2-positive carcinomas. Our lead anti-Trop-2antibodies exhibit high binding affinity and specificity. The anti-Trop-2 antibodies demonstrate potent antitumor activity in vivo, significantly delaying tumor progression and suppressing metastasis in pre-clinical models of breast and lung cancers. Importantly, no detectable toxicity was observed in animals receiving anti-Trop-2 antibodies. To enable real-time detection of Trop-2-expressing tumors, we engineered an optical imaging agent by conjugating our lead anti-Trop-2 antibody to ICG. These antibody-ICG-conjugates robustly visualized Trop-2-positive lesions with a high positive-to-negative tumor contrast ratio and enabled precise surgical guidance during lymph node resection. Collectively, we have developed a new series of anti-Trop-2 antibodies that can be utilized as therapeutic and optical imaging agents, establishing a strong foundation for the translational development of targeted interventions for Trop-2-positive carcinomas. Citation Format: Tanya Stoyanova.. Developing new anti-Trop2-antibody-based therapies and optical imaging modalities for epithelial cancers [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 3917.

  PublisherDOI

• Supplementary Figure S2 from Extracellular Domain Shedding of TROP2 Activates EGFR Signaling to Drive Prostate Cancer Metastasis

  2025-12-01

  articleOpen accessSenior author

  <p>Supplementary Figure S2 shows that treatment with recombinant TECD enhances migration ability of prostate cancer cells.</p>

  PublisherOA PDFDOI

• Circulating extracellular vesicles in serum carry Trop2 marker for prostate cancer liquid biopsy and clinical care

  medRxiv · 2025-04-04

  preprintOpen accessCorresponding

  ABSTRACT Extracellular vesicles (EVs) are lipid nano-to-micro-sized vesicles increasingly identified as valuable liquid biopsy tools for medical applications. However, the heterogeneity of cargo and the lack of convenient quantification methods to characterize EVs pose challenges in identifying vesicles with specific markers. In this study, we show the isolation, characterization, detection, and quantification of a cancer-specific marker, Trop2, on circulating extracellular vesicles in serum (EV-Trop2). This work combines the unique advantages of our user-friendly isolation method with serum diagnostics to identify high-risk prostate cancer cases and predict recurrence after prostate surgery. To our knowledge, this is the first demonstration to isolate and quantify EV-Trop2 from prostate cancer patient serum to study its analytical validity and potential clinical utility as an EV-based liquid biopsy. Initial study with patient serum samples from three clinical groups: high- risk prostate cancer (n = 22), low-risk prostate cancer (n = 23), and cancer-free groups (n = 21), demonstrates the potential of this approach in distinguishing prostate cancer aggressiveness. We observed significantly different levels of EV-Trop2 expression between the high-risk and low-risk patient groups (p = 0.0015), and between high-risk patient and cancer-free groups (p < 0.0001). Furthermore, employing machine learning algorithms, EV-Trop2 was shown to enhance classifier metrics across the three sample groups, aiding both in risk stratification and predicting recurrence post-prostatectomy. The availability of such tool could have a broad impact across multiple cancers by enabling minimally invasive liquid biopsy sampling. Abstract Figure

  PublisherOA PDFDOI

• Extracellular Domain Shedding of TROP2 Activates EGFR Signaling to Drive Prostate Cancer Metastasis

  Cancer Research · 2025-09-05 · 2 citations

  articleSenior author

  Metastasis is the main cause of prostate cancer-associated deaths, highlighting the urgent need to determine the mechanisms underlying prostate cancer progression. TROP2 (also known as tumor-associated calcium signal transducer 2) is an oncogenic transmembrane surface protein that is highly expressed in metastatic prostate cancer. Naturally occurring cleavage of TROP2 leads to a release of the TROP2 extracellular domain (TECD) into the extracellular environment. In this study, we identified an important functional role of TECD in prostate cancer metastasis. TECD was detectable in media from prostate cancer cells and serum from patients with clinically significant prostate cancer. Although shed TECD did not affect prostate cancer cell proliferation and tumor growth, it increased cell migration and invasion in vitro and promoted metastatic colonization and spontaneous metastasis in vivo. TECD interactome and proteomic studies revealed that TECD binds to EGFR and shed TECD modulates a set of proteins associated with invasion, migration, mTOR signaling, and epithelial-to-mesenchymal transition. Furthermore, elevated shed TECD increased EGFR phosphorylation, resulting in the activation of the EGFR-PI3K-AKT-mTOR pathway in prostate cancer. EGFR inhibitors suppressed the invasive ability of prostate cancer cells driven by TECD overexpression, further supporting the key role of EGFR in TECD-mediated prostate cancer progression. This study uncovers a function of TECD in driving prostate cancer progression and provides mechanistic insights into TECD signaling through EGFR. SIGNIFICANCE: Shed extracellular domain of TROP2 binds to and activates EGFR and stimulates the PI3K-AKT-mTOR signaling cascade to promote prostate cancer metastasis, providing potential biomarkers and therapeutic targets.

  PublisherDOI

• Abstract 2378: Developing new potent therapeutic strategies for neuroendocrine carcinomas

  Cancer Research · 2025-04-21

  article1st authorCorresponding

  Abstract Neuroendocrine carcinomas, such as neuroendocrine prostate cancer (NEPC), small cell lung cancer (SCLC), and neuroblastoma, share common histological features, including expression of neuroendocrine markers, rapid relapse after treatment, and poor prognosis. Due to the poor clinical outcome of patients with neuroendocrine carcinomas, there is a critical need to identify new drivers, therapeutic targets, and effective therapeutic strategies for these malignancies. Ubiquitin carboxy-terminal hydrolase L1 (UCHL1) is a protease that has a dual function in regulating protein stability. We demonstrated that UCHL1 is significantly elevated in tissues from patients with NEPC, SCLC, and neuroblastoma. Loss of UCHL1 decreases tumor growth and inhibits metastasis of these malignancies. UCHL1 maintains neuroendocrine differentiation and promotes cancer progression by regulating nucleoporin, POM121, and p53. UCHL1 stabilizes POM121 to regulate POM121-associated nuclear transport of key transcriptional factors, E2F1 and c-MYC. Here, we developed novel and more potent UCHL1 small molecule inhibitors as a new therapeutic strategy to target neuroendocrine carcinomas. Our new compounds demonstrate high potency with safety profile in vivo for neuroendocrine carcinomas. Importantly, treatment with UCHL1 inhibitors significantly reduces tumor growth of neuroendocrine carcinomas in pre-clinical settings. Our study reveals new mechanisms of UCHL1 function in neuroendocrine carcinomas tumorigenesis, identifies UCHL1 as a therapeutic target and potential molecular indicator for diagnosis and monitoring treatment responses in neuroendocrine carcinomas and develops new inhibitors to target UCHL1. Citation Format: Tanya Ivanova Stoyanova. Developing new potent therapeutic strategies for neuroendocrine carcinomas [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 2378.

  PublisherDOI

• Supplementary Figure S5 from Extracellular Domain Shedding of TROP2 Activates EGFR Signaling to Drive Prostate Cancer Metastasis

  2025-12-01

  articleOpen accessSenior author

  <p>Supplementary Figure S5 shows that TECD regulates pathways involved in metastasis.</p>

  PublisherOA PDFDOI

• Deciphering Resistance: Beyond the Androgen Paradigm; Report From the 2025 Coffey‐Holden Prostate Cancer Academy Meeting

  The Prostate · 2025-12-07

  articleOpen access1st author

  INTRODUCTION: The 12th Annual 2025 Coffey-Holden Prostate Cancer Academy (CHPCA) Meeting, "Deciphering Resistance: Beyond the Androgen Paradigm," was held at the University of California, Los Angeles (UCLA), Luskin Conference Center, in Los Angeles, CA, from June 19 to 22, 2025. METHODS: The CHPCA Meeting is a discussion-focused conference held annually by the Prostate Cancer Foundation (PCF), for in-depth academic analysis of emerging research with the greatest potential to drive new understandings and treatments for prostate cancer. The 2025 CHPCA Meeting included attendance by 79 academic investigators and 39 talks over 8 sessions. RESULTS: The session topics included: drug discovery in academia, non-apoptotic cell death mechanisms, understanding and overcoming treatment resistance, chromosomal instability (CIN) as a driver of metastasis and treatment resistance, targeting metastatic sites, immunotherapy sensitizers, and optimizing therapy delivery and biomedical engineering. DISCUSSION: This meeting report summarizes the presentations from the 2025 CHPCA Meeting. We hope that disseminating this information will directly contribute to novel research efforts and improved treatment strategies for patients with prostate cancer.

  PublisherOA PDFDOI

• CDC7 is a targetable regulator of advanced prostate cancer

  Scientific Reports · 2025-12-18 · 1 citations

  articleOpen accessSenior author

  Prostate cancer is estimated to contribute to over 35,000 deaths of men residing in the United States, with the majority fatality due to metastatic disease. CDC7 is a kinase that regulates DNA replication and is found elevated during neuroendocrine transdifferentiation in lung and prostate cancer. In this study, we demonstrate that CDC7 is highly expressed in treatment-resistant prostate cancer, with even higher levels observed in treatment-resistant prostate cancer with neuroendocrine phenotype (NEPC). We further identify CDC7 as a critical regulator of prostate tumorigenesis. Downregulation of CDC7 significantly reduces prostate cancer cells growth and invasion in vitro and silencing CDC7 suppresses prostate tumor growth in vivo. Furthermore, we demonstrate that the inhibition of CDC7 using TAK-931, a selective CDC7 inhibitor, significantly reduces the proliferation, migration, and invasion of aggressive prostate cancer cells. TAK-931 treated prostate cancer cells exhibit an abnormal cell cycle profile, suggesting that CDC7 inhibition induces replication stress and promotes apoptosis. Collectively, our findings demonstrate that CDC7 is a regulator of tumor progression in prostate cancer and represents new therapeutic target in advanced prostate cancer.

  PublisherOA PDFDOI

• Supplementary Figure S1 from Extracellular Domain Shedding of TROP2 Activates EGFR Signaling to Drive Prostate Cancer Metastasis

  2025-12-01

  articleOpen accessSenior author

  <p>Supplementary Figure S1 shows that Shed TECD is detected in the serum of patients with advanced and clinically significant prostate cancer.</p>

  PublisherOA PDFDOI

Recent grants

• Elucidating Novel Mechanisms Underlying Prostate Cancer Development

  NIH · $160k · 2018–2020

• Proteolytically Cleaved Receptors as Oncogenes and Therapeutic Targets

  NIH · $278k · 2014–2016

• Elucidating the Role of UCHL1 in Aggressive Prostate Cancer

  NIH · $1.8M · 2020–2025

• Proteolytically Cleaved Receptors as Oncogenes and Therapeutic Targets

  NIH · $729k · 2015–2018

• Elucidating the Role of Trop2 in Prostate Cancer

  NIH · $2.5M · 2025–2027

Frequent coauthors

• En‐Chi Hsu

  Palo Alto University

  65 shared

• Owen N. Witte

  61 shared

• Houjian Cai

  University of Georgia

  55 shared

• Jiaoti Huang

  Duke University

  50 shared

• Sanaz Memarzadeh

  University of California, Los Angeles

  43 shared

• Zanna Beharry

  43 shared

• Meghan A. Rice

  Stanford University

  43 shared

• Andrew S. Kraft

  43 shared

Labs

• Stoyanova LabPI