Clinical Focus


  • Oncology Hospital Medicine
  • Internal Medicine

Academic Appointments


  • Clinical Assistant Professor, Medicine

Professional Education


  • Chief Residency, UCSD Internal Medicine Residency (2023)
  • Board Certification: American Board of Internal Medicine, Internal Medicine (2022)
  • Residency: UCSD Internal Medicine Residency (2022) CA
  • Medical Education, Case Western Reserve University School of Medicine (2019)

All Publications


  • Bipolar androgen therapy for treatment of metastatic castration-resistant prostate cancer: A case series. The Prostate Tran, E. U., Royz, E., Yamamoto, K., Marley, S., Song, A., Pan, E., Lee, A. M., Herchenhorn, D., Denmeade, S., Antonarakis, E. S., Markowski, M., McKay, R. R. 2025; 85 (1): 40-47

    Abstract

    Advanced prostate cancer treatment has improved with androgen receptor signaling inhibitors (ARPI), yet many patients develop metastatic castration-resistant prostate cancer (mCRPC), characterized by sustained androgen receptor (AR) signaling. Bipolar androgen therapy (BAT) introduces supraphysiologic testosterone levels to inhibit tumor growth, offering novel treatment for mCRPC by exploiting AR-dependent mechanisms.Case 1: A 53-year-old man with mCRPC, post multiple systemic therapies, initiated BAT and pembrolizumab, achieving PSA reduction and improved quality of life before progression. The patient exhibited AR amplification, which may have contributed to favorable response to BAT. Case 2: A 73-year-old man with recurrent prostate cancer, stable on ADT and abiraterone, experienced PSA decline with BAT to an undetectable level, maintaining stability post-therapy discontinuation. Case 3: A 73-year-old man with metastatic prostate cancer, initially resistant to enzalutamide, achieved clinical benefit and disease control with BAT, although he did not meet PSA response criteria, patient had remarkable response upon enzalutamide rechallenge. Case 4: A 90-year-old man with localized prostate cancer, refractory to multiple treatments, experienced symptom relief and PSA reduction with BAT before progression.BAT represents a promising treatment strategy for mCRPC. This case series underscores BAT's potential to induce significant clinical and biochemical responses, resensitize tumors to ARPIs, and improve patients' quality of life. Despite eventual progression in some cases, BAT offers a period of disease control. Further research is needed to optimize patient selection and understand the molecular determinants of BAT responsiveness.

    View details for DOI 10.1002/pros.24798

    View details for PubMedID 39308006

  • Clearance of Plasma Free Hemoglobin by Therapeutic Plasma Exchange for Mechanical Hemolysis-Related Pigment-Induced AKI Crane, C., Song, A., Cruz, D. AMER SOC NEPHROLOGY. 2024
  • Targeted gene addition in human CD34(+) hematopoietic cells for correction of X-linked chronic granulomatous disease. Nature biotechnology De Ravin, S. S., Reik, A., Liu, P. Q., Li, L., Wu, X., Su, L., Raley, C., Theobald, N., Choi, U., Song, A. H., Chan, A., Pearl, J. R., Paschon, D. E., Lee, J., Newcombe, H., Koontz, S., Sweeney, C., Shivak, D. A., Zarember, K. A., Peshwa, M. V., Gregory, P. D., Urnov, F. D., Malech, H. L. 2016; 34 (4): 424-9

    Abstract

    Gene therapy with genetically modified human CD34(+) hematopoietic stem and progenitor cells (HSPCs) may be safer using targeted integration (TI) of transgenes into a genomic 'safe harbor' site rather than random viral integration. We demonstrate that temporally optimized delivery of zinc finger nuclease mRNA via electroporation and adeno-associated virus (AAV) 6 delivery of donor constructs in human HSPCs approaches clinically relevant levels of TI into the AAVS1 safe harbor locus. Up to 58% Venus(+) HSPCs with 6-16% human cell marking were observed following engraftment into mice. In HSPCs from patients with X-linked chronic granulomatous disease (X-CGD), caused by mutations in the gp91phox subunit of the NADPH oxidase, TI of a gp91phox transgene into AAVS1 resulted in ∼15% gp91phox expression and increased NADPH oxidase activity in ex vivo-derived neutrophils. In mice transplanted with corrected HSPCs, 4-11% of human cells in the bone marrow expressed gp91phox. This method for TI into AAVS1 may be broadly applicable to correction of other monogenic diseases.

    View details for DOI 10.1038/nbt.3513

    View details for PubMedID 26950749

    View details for PubMedCentralID PMC4824656

  • Functional footprinting of regulatory DNA. Nature methods Vierstra, J., Reik, A., Chang, K. H., Stehling-Sun, S., Zhou, Y., Hinkley, S. J., Paschon, D. E., Zhang, L., Psatha, N., Bendana, Y. R., O'Neil, C. M., Song, A. H., Mich, A. K., Liu, P. Q., Lee, G., Bauer, D. E., Holmes, M. C., Orkin, S. H., Papayannopoulou, T., Stamatoyannopoulos, G., Rebar, E. J., Gregory, P. D., Urnov, F. D., Stamatoyannopoulos, J. A. 2015; 12 (10): 927-30

    Abstract

    Regulatory regions harbor multiple transcription factor (TF) recognition sites; however, the contribution of individual sites to regulatory function remains challenging to define. We describe an approach that exploits the error-prone nature of genome editing-induced double-strand break repair to map functional elements within regulatory DNA at nucleotide resolution. We demonstrate the approach on a human erythroid enhancer, revealing single TF recognition sites that gate the majority of downstream regulatory function.

    View details for DOI 10.1038/nmeth.3554

    View details for PubMedID 26322838

    View details for PubMedCentralID PMC5381659