Bio

Current Role at Stanford

Life Science Research Professional -1

Honors & Awards

  • Virtual Travel Award, Society for Basic Urology Research (November, 2020)

Education & Certifications

  • Certificate, University of California Santa Cruz, Biotechnology (2017)
  • MS, Istanbul Technical University, Molecular Bology and Genetics, Biotechnology (2008)
  • BS, Istanbul Technical University, Molecular Biology and Genetics (2006)

Projects

  • A novel oncogene-mediated metabolic gene signature predicts breast cancer outcome, Stanford University

    Location

    Palo Alto, California

Contact

Publications

All Publications

  • Ferroptosis inducers are a novel therapeutic approach for advanced prostate cancer. Cancer research Ghoochani, A. n., Hsu, E. C., Aslan, M. n., Rice, M. A., Nguyen, H. M., Brooks, J. D., Corey, E. n., Paulmurugan, R. n., Stoyanova, T. n. 2021

    Abstract

    Ferroptosis is a type of programmed cell death induced by the accumulation of lipid peroxidation and lipid reactive oxygen species (ROS) in cells. It has been recently demonstrated that cancer cells are vulnerable to ferroptosis inducers (FIN). However, the therapeutic potential of ferroptosis inducers in prostate cancer in pre-clinical settings has not been explored. In this study, we demonstrate that mediators of ferroptosis SLC7A11, SLC3A2 and GPX4 are expressed in treatment-resistant prostate cancer. We further demonstrate that treatment-resistant prostate cancer cells are sensitive to two ferroptosis inducers, erastin and RSL3. Treatment with erastin and RSL3 led to a significant decrease in prostate cancer cell growth and migration in vitro and significantly delayed the tumor growth of treatment-resistant prostate cancer in vivo, with no measurable side effects. Combination of erastin or RSL3 with standard-of-care second-generation anti-androgens for advanced prostate cancer halted prostate cancer cell growth and migration in vitro and tumor growth in vivo. These results demonstrate the potential of erastin or RSL3 independently and in combination with standard-of-care second-generation anti-androgens as novel therapeutic strategies for advanced prostate cancer.

    View details for DOI 10.1158/0008-5472.CAN-20-3477

    View details for PubMedID 33483372

  • Discovery of CASP8 as a potential biomarker for high-risk prostate cancer through a high-multiplex immunoassay. Scientific reports Liu, S. n., Garcia-Marques, F. n., Zhang, C. A., Lee, J. J., Nolley, R. n., Shen, M. n., Hsu, E. C., Aslan, M. n., Koul, K. n., Pitteri, S. J., Brooks, J. D., Stoyanova, T. n. 2021; 11 (1): 7612

    Abstract

    Prostate cancer remains the most common non-cutaneous malignancy among men in the United States. To discover potential serum-based biomarkers for high-risk prostate cancer, we performed a high-multiplex immunoassay utilizing patient-matched pre-operative and post-operative serum samples from ten men with high-grade and high-volume prostate cancer. Our study identified six (CASP8, MSLN, FGFBP1, ICOSLG, TIE2 and S100A4) out of 174 proteins that were significantly decreased after radical prostatectomy. High levels of CASP8 were detected in pre-operative serum samples when compared to post-operative serum samples and serum samples from patients with benign prostate hyperplasia (BPH). By immunohistochemistry, CASP8 protein was expressed at higher levels in prostate cancer tissues compared to non-cancerous and BPH tissues. Likewise, CASP8 mRNA expression was significantly upregulated in prostate cancer when compared to benign prostate tissues in four independent clinical datasets. In addition, mRNA levels of CASP8 were higher in patients with recurrent prostate cancer when compared to patients with non-recurrent prostate cancer and high expression of CASP8 was associated with worse disease-free survival and overall survival in renal cancer. Together, our results suggest that CASP8 may potentially serve as a biomarker for high-risk prostate cancer and possibly renal cancer.

    View details for DOI 10.1038/s41598-021-87155-5

    View details for PubMedID 33828176

  • Trop2 is a driver of metastatic prostate cancer with neuroendocrine phenotype via PARP1. Proceedings of the National Academy of Sciences of the United States of America Hsu, E. C., Rice, M. A., Bermudez, A. n., Marques, F. J., Aslan, M. n., Liu, S. n., Ghoochani, A. n., Zhang, C. A., Chen, Y. S., Zlitni, A. n., Kumar, S. n., Nolley, R. n., Habte, F. n., Shen, M. n., Koul, K. n., Peehl, D. M., Zoubeidi, A. n., Gambhir, S. S., Kunder, C. A., Pitteri, S. J., Brooks, J. D., Stoyanova, T. n. 2020

    Abstract

    Resistance to androgen deprivation therapy, or castration-resistant prostate cancer (CRPC), is often accompanied by metastasis and is currently the ultimate cause of prostate cancer-associated deaths in men. Recently, secondary hormonal therapies have led to an increase of neuroendocrine prostate cancer (NEPC), a highly aggressive variant of CRPC. Here, we identify that high levels of cell surface receptor Trop2 are predictive of recurrence of localized prostate cancer. Moreover, Trop2 is significantly elevated in CRPC and NEPC, drives prostate cancer growth, and induces neuroendocrine phenotype. Overexpression of Trop2 induces tumor growth and metastasis while loss of Trop2 suppresses these abilities in vivo. Trop2-driven NEPC displays a significant up-regulation of PARP1, and PARP inhibitors significantly delay tumor growth and metastatic colonization and reverse neuroendocrine features in Trop2-driven NEPC. Our findings establish Trop2 as a driver and therapeutic target for metastatic prostate cancer with neuroendocrine phenotype and suggest that high Trop2 levels could identify cancers that are sensitive to Trop2-targeting therapies and PARP1 inhibition.

    View details for DOI 10.1073/pnas.1905384117

    View details for PubMedID 31932422

  • Discovery of PTN as a blood-based biomarker of pro-metastatic prostate British Journal of Cancer Liu, S., Shen, M., Hsu, E., Zhang, A., Garcia-Marques, F., Nolley, R., Koul Koul, K., Rice, M., Aslan, M., Pitteri, S., Massie, C., George, A., Brooks, J., Gnanapragasam, V., Stoyanova, T. 2020
  • Plectin is a Regulator of Prostate Cancer Growth and Metastasis Oncogene Buckup, M., Rice, M., Hsu, E., Marques, F., Liu, S., Aslan, M., Bermudez, A., Huang, J., Pitteri, S., Stoyanova, T. 2020
  • Loss of Notch1 activity inhibits prostate cancer growth and metastasis and sensitizes prostate cancer cells to anti-androgen therapies. Molecular cancer therapeutics Rice, M. A., Hsu, E. C., Aslan, M. n., Ghoochani, A. n., Su, A. n., Stoyanova, T. n. 2019

    Abstract

    Prostate cancer remains among the leading causes of cancer-related deaths in men. Patients with aggressive disease typically undergo hormone-deprivation therapy. While treatment is initially very successful, these men commonly progress to lethal, castration resistant prostate cancer in 2-3 years. Standard therapies for castration resistant prostate cancer include second-generation anti-androgens, which prolong patient lifespan by only several months. It is imperative to advance our understanding of the mechanisms leading to resistance to identify new therapies for aggressive prostate cancer. This study identifies Notch1 as a therapeutic target in prostate cancer. Loss of Notch1 in aggressive prostate cancer cells decreases proliferation, invasion and tumorsphere formation. Therapeutic inhibition of Notch1 activity with gamma secretase inhibitors RO4929097 or DAPT in prostate cancer cells further results in decreased proliferative abilities. Loss of Notch1 and treatment of immunocompromised mice bearing prostate cancer xenografts with RO4929097 display significantly impaired tumor growth. Loss of Notch1 additionally decreased metastatic potential of prostate cancer cells in invasion assays in vitro as well as in vivo experiments. Moreover, treatment with gamma secretase inhibitors, or Notch1 gene deletion synergized with anti-androgen therapies, Enzalutamide or Abiraterone, to decrease the growth of prostate cancer cells. Combination of gamma secretase inhibitors with Abiraterone significantly inhibited cell migration and invasion, while combination with Enzalutamide reversed Enzalutamide induced migration and invasion. These collective findings suggest loss of Notch1 delays growth of CRPC, inhibits metastasis, and inhibition of Notch1 activation in conjunction with second-generation anti-androgen therapies could delay growth and progression of prostate cancer.

    View details for PubMedID 31028097

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