Clinical Focus

  • Pediatric Hematology-Oncology

Academic Appointments

Boards, Advisory Committees, Professional Organizations

  • Member, American Society of Pediatric Hematology Oncology (2022 - Present)

Professional Education

  • MS, Medical College of Wisconsin, Clinical and Translational Science (2022)
  • Fellowship: Medical College of Wisconsin Hematology/Oncology Fellowship Program (2022) WI
  • Board Certification: American Board of Pediatrics, Pediatrics (2019)
  • Residency: Medical College of Wisconsin Dept of Pediatrics (2019) WI
  • Medical Education: University of Cincinnati College of Medicine (2012) OH

Contact

  • Academic
    kchaomd@stanford.edu
    University - Academic staff Department: Pediatrics - Hematology/Oncology Position: Clinical Assistant Professor
    • 1100 VAN NESS
    • SAN FRANCISCO,  California  94109 
    (650) 723-5231 (fax)
  • Clinical (Primary)  Stanford Children's Health 1100 Van Ness Ave 7th Fl San Francisco, CA 94109 (650) 628-2270 (fax)

Additional Clinical Info

Additional Info

All Publications

  • Potential clinical use of azacitidine and MEK inhibitor combination therapy in PTPN11-mutated juvenile myelomonocytic leukemia. Molecular therapy : the journal of the American Society of Gene Therapy Pasupuleti, S. K., Chao, K., Ramdas, B., Kanumuri, R., Palam, L. R., Liu, S., Wan, J., Annesley, C., Loh, M. L., Stieglitz, E., Burke, M. J., Kapur, R. 2023

    Abstract

    Juvenile myelomonocytic leukemia (JMML) is a rare myeloproliferative neoplasm of childhood. The molecular hallmark of JMML is hyperactivation of the Ras/MAPK pathway with the most common cause being mutations in the gene PTPN11, encoding the protein tyrosine phosphatase SHP2. Current strategies for treating JMML include using the hypomethylating agent, 5-azacitidine (5-Aza) or MEK inhibitors trametinib and PD0325901 (PD-901), but none of these are curative as monotherapy. Utilizing an Shp2E76K/+ murine model of JMML, we show that the combination of 5-Aza and PD-901 modulates several hematologic abnormalities often seen in JMML patients, in part by reducing the burden of leukemic hematopoietic stem and progenitor cells (HSC/Ps). The reduced JMML features in drug-treated mice were associated with a decrease in p-MEK and p-ERK levels in Shp2E76K/+ mice treated with the combination of 5-Aza and PD-901. RNA-sequencing analysis revealed a reduction in several RAS and MAPK signaling-related genes. Additionally, a decrease in the expression of genes associated with inflammation and myeloid leukemia was also observed in Shp2E76K/+ mice treated with the combination of the two drugs. Finally, we report two patients with JMML and PTPN11 mutations treated with 5-Aza, trametinib, and chemotherapy who experienced a clinical response because of the combination treatment.

    View details for DOI 10.1016/j.ymthe.2023.01.030

    View details for PubMedID 36739480

  • Real-world experience in treating pediatric relapsed/refractory or therapy-related myeloid malignancies with decitabine, vorinostat, and FLAG therapy based on a phase 1 study run by the TACL consortium PEDIATRIC BLOOD & CANCER Schafer, E. S., Chao, K., Stevens, A. M., Jo, E., Hilsenbeck, S. G., Gossai, N. P., Doan, A., Colace, S. I., Guinipero, T., Otterson, D., Kaplan, J. A., Hinson, A., Pommert, L., Wayne, A. S., Bhojwani, D., Burke, M. J. 2022; 69 (10)

    View details for DOI 10.1002/pbc.29812

    View details for Web of Science ID 000813817300001

    View details for PubMedID 35726868

  • Outcomes of Hispanic and non-Hispanic white pediatric and young adult patients with B-cell acute lymphoblastic leukemia after commercial tisagenlecleucel. Vandris, P., Chao, K., Baggott, C., Phillips, C. L., Qayed, M., Rossoff, J., Lim, S., Winestone, L. E., Stefanski, H. E., Talano, J. M., Margossian, S., Verneris, M. R., Myers, G., Karras, N. A., Brown, P. A., Satwani, P., Mackall, C., Curran, K. J., Laetsch, T., Schultz, L. M. LIPPINCOTT WILLIAMS & WILKINS. 2022

    View details for Web of Science ID 000863680300019

https://orcid.org/0000-0003-4163-3165