Bio


Amy Fan is an Immunology PhD candidate in Dr. Ravi Majeti's lab, with research interests in immunology, stem cell biology, and cancer. Her thesis work investigates the mechanism of blood cancer progression in patients with inherited mutations in the RUNX1 gene. Prior to joining Stanford in 2016, she earned her B.S. in Biology from MIT and worked for two years at the Broad Institute of MIT & Harvard. Outside of lab, she devotes time to teaching, mentoring, and diversity advocacy, and she likes to relax by dancing, hiking, and painting.

Honors & Awards


  • Amgen Scholar, Amgen Foundation (Jun - Aug 2014)
  • Gene Brown Prize for Teaching, MIT Department of Biology (June 2015)
  • Stanford Graduate Fellowship, Stanford University (September 2016)
  • NSF Graduate Research Fellowship, National Science Foundation (March 2017)
  • Stanford Biosciences Travel Grant, Stanford Biosciences (Aug 2018)
  • Excellence in Advocacy, Stanford Diversity & Advocacy Committee (May 2019)
  • Community Impact Award, Stanford Alumni Association (May 2019)
  • Excellence in Service to Grad Students, Stanford Biosciences (June 2019)
  • Best Graduate Student Talk, Stanford Immunology (November 2020)
  • ASH Abstract Achievement Award, American Society of Hematology (November 2020)
  • Gerald J. Lieberman Fellowship, Stanford University (May 2021)
  • James W. Lyons Award, Stanford University (May 2021)
  • Experimental Hematology Travel Grant, ISEH (August 2021)

Professional Affiliations and Activities


  • Member, International Society of Experimental Hematology (2018 - Present)

Education & Certifications


  • BS, Massachusetts Institute of Technology, Biology (2015)

Current Research and Scholarly Interests


Germline mutations in RUNX1 cause an autosomal dominant disorder characterized by lifelong thrombocytopenia and increased risk of progression to acute myeloid leukemia (AML). Indeed, unlike sporadic AML, which commonly presents in the elderly, the average age of onset for RUNX1 familial AML cases is 35, with over one-third of patients developing leukemia as a child. While megakaryocyte defects have been shown to be a cell-autonomous effect of RUNX1 mutations in hematopoietic stem and progenitor cells (HSPCs), the mechanisms by which germline RUNX1 mutations progress to leukemia remains unclear. Interestingly, RUNX1 is also expressed in bone marrow mesenchymal stromal cells (BM-MSCs), which have been shown to contribute to the pathogenesis of some hematopoietic malignancies. The goal of my thesis research is to determine how RUNX1 mutations may be contributing to leukemogenesis through both cell autonomous and non-autonomous mechanisms.

Lab Affiliations


Work Experience


  • Academic Research Technician, Broad Institute of MIT & Harvard (January 2015 - May 2016)

    Investigate how heterogeneous regulation of LPS modifications by PhoPQ and PmrAB in S. Typhimurium modulate Type I IFN response in mouse macrophages. Developed single-cell RNA-Seq method to simultaneously probe host and pathogen transcriptomes.

    Location

    Cambridge, MA

All Publications


  • Black In Immuno: harnessing social media and digital platforms to connect the dots. Nature reviews. Immunology Babdor, J., Fan, A. C., Wane, M., Mbiribindi, B., Mobley, A. S., Noel, J. C., Kouame, E. 2021

    View details for DOI 10.1038/s41577-021-00645-5

    View details for PubMedID 34744170

  • Black in Immuno Week: Who We Are, What We Did, and Why It Matters. Journal of immunology (Baltimore, Md. : 1950) Kouame, E., Noel, J. C., Wane, M., Babdor, J., Caslin, H. L., Fan, A., Mbiribindi, B., Sattler, S., Mobley, A. S. 2021; 207 (8): 1941-1947

    Abstract

    Our organization, Black in Immuno (@BlackInImmuno), was formed in September 2020 to celebrate, support, and amplify Black voices in immunology when social media campaigns like #BlackInTheIvory illuminated the shared overt and covert issues of systemic racism faced by Black researchers in all facets of science, technology, engineering, art, and mathematics. Black in Immuno was cofounded by a group of Black immunology trainees working at multiple institutions globally: Joel Babdor, E. Evonne Jean, Elaine Kouame, Alexis S. Mobley, Justine C. Noel, and Madina Wane. We devised Black in Immuno Week, held November 22-28, 2020, as a global celebration of Black immunologists. The week was designed to advocate for increased diversity and accessibility in immunology, amplify Black excellence in immunology, and create a community of Black immunologists who can support each other to flourish despite barriers in academia and other job sectors. The week contained live panels and scientific talks, a casual networking mixer, online advocacy and amplification sessions, and a series of wellness events. Our live-streamed programs reached over 300 individuals, and thousands of people kept the conversations going globally using #BlackInImmuno and #BlackInImmunoWeek on social media from five continents. Below, we highlight the events and significant takeaways of the week.

    View details for DOI 10.4049/jimmunol.2100667

    View details for PubMedID 34607907

  • Niche-directed therapy in acute myeloid leukemia: optimization of stem cell competition for niche occupancy. Leukemia & lymphoma Patel, S. A., Dalela, D., Fan, A. C., Lloyd, M. R., Zhang, T. Y. 2021: 1-9

    Abstract

    Acute myeloid leukemia (AML) is an aggressive malignancy of stem cell origin that contributes to significant morbidity and mortality. The long-term prognosis remains dismal given the high likelihood for primary refractory or relapsed disease. An essential component of relapse is resurgence from the bone marrow. To date, the murine hematopoietic stem cell (HSC) niche has been clearly defined, but the human HSC niche is less well understood. The design of niche-based targeted therapies for AML must account for which cellular subsets compete for stem cell occupancy within respective bone marrow microenvironments. In this review, we highlight the principles of stem cell niche biology and discuss translational insights into the AML microenvironment as of 2021. Optimization of competition for niche occupancy is important for the elimination of measurable residual disease (MRD). Some of these novel therapeutics are in the pharmacologic pipeline for AML and may be especially useful in the setting of MRD.

    View details for DOI 10.1080/10428194.2021.1966779

    View details for PubMedID 34407733

  • Reprogramming cancer into antigen presenting cells as a novel immunotherapy. Linde, M. H., Gurev, S. F., Phan, P., Zhao, F., Gars, E. J., Stafford, M., Kohnke, T., Marshall, P. L., Fan, A. C., Dove, C. G., Linde, I. L., Miller, L. P., Majzner, R. G., Zhang, T., Majeti, R. AMER ASSOC CANCER RESEARCH. 2021
  • NOT-Gated CD93 CAR T Cells Effectively Target AML with Minimized Endothelial Cross-Reactivity. Blood cancer discovery Richards, R. M., Zhao, F., Freitas, K. A., Parker, K. R., Xu, P., Fan, A., Sotillo, E., Daugaard, M., Oo, H. Z., Liu, J., Hong, W. J., Sorensen, P. H., Chang, H. Y., Satpathy, A. T., Majzner, R. G., Majeti, R., Mackall, C. L. 2021; 2 (6): 648-665

    Abstract

    Chimeric antigen receptor (CAR) T cells hold promise for the treatment of acute myeloid leukemia (AML), but optimal targets remain to be defined. We demonstrate that CD93 CAR T cells engineered from a novel humanized CD93-specific binder potently kill AML in vitro and in vivo but spare hematopoietic stem and progenitor cells (HSPC). No toxicity is seen in murine models, but CD93 is expressed on human endothelial cells, and CD93 CAR T cells recognize and kill endothelial cell lines. We identify other AML CAR T-cell targets with overlapping expression on endothelial cells, especially in the context of proinflammatory cytokines. To address the challenge of endothelial-specific cross-reactivity, we provide proof of concept for NOT-gated CD93 CAR T cells that circumvent endothelial cell toxicity in a relevant model system. We also identify candidates for combinatorial targeting by profiling the transcriptome of AML and endothelial cells at baseline and after exposure to proinflammatory cytokines.CD93 CAR T cells eliminate AML and spare HSPCs but exert on-target, off-tumor toxicity to endothelial cells. We show coexpression of other AML targets on endothelial cells, introduce a novel NOT-gated strategy to mitigate endothelial toxicity, and demonstrate use of high-dimensional transcriptomic profiling for rational design of combinatorial immunotherapies.See related commentary by Velasquez and Gottschalk, p. 559. This article is highlighted in the In This Issue feature, p. 549.

    View details for DOI 10.1158/2643-3230.BCD-20-0208

    View details for PubMedID 34778803

    View details for PubMedCentralID PMC8580619

  • IL-3 RESCUES PROLIFERATIVE DEFECTS IN INFLAMMATION-SENSITIVE RUNX1 DEFICIENT HUMAN HEMATOPOIETIC STEM AND PROGENITOR CELLS Fan, A., Azizi, A., Dutta, R., Nakauchi, Y., Nuno, K., Zhao, F., Reinisch, A., Majeti, R. ELSEVIER SCIENCE INC. 2020: S59
  • Azacitidine and Ascorbate Inhibit the Competitive Outgrowth of Human TET2 Mutant HSPCs in a Xenograft Model of Pre-Leukemia Nakauchi, Y., Thomas, D., Sharma, R., Corces, M., Reinisch, A., Cruz, D., Koehnke, T., Karigane, D., Fan, A., Majeti, R. AMER SOC HEMATOLOGY. 2018
  • scDual-Seq: mapping the gene regulatory program of Salmonella infection by host and pathogen single-cell RNA-sequencing GENOME BIOLOGY Avital, G., Avraham, R., Fan, A., Hashimshony, T., Hung, D. T., Yanai, I. 2017; 18: 200

    Abstract

    The interaction between a pathogen and a host is a highly dynamic process in which both agents activate complex programs. Here, we introduce a single-cell RNA-sequencing method, scDual-Seq, that simultaneously captures both host and pathogen transcriptomes. We use it to study the process of infection of individual mouse macrophages with the intracellular pathogen Salmonella typhimurium. Among the infected macrophages, we find three subpopulations and we show evidence for a linear progression through these subpopulations, supporting a model in which these three states correspond to consecutive stages of infection.

    View details for DOI 10.1186/s13059-017-1340-x

    View details for Web of Science ID 000413769600001

    View details for PubMedID 29073931

    View details for PubMedCentralID PMC5658913

  • A highly multiplexed and sensitive RNA-seq protocol for simultaneous analysis of host and pathogen transcriptomes. Nature protocols Avraham, R., Haseley, N., Fan, A., Bloom-Ackermann, Z., Livny, J., Hung, D. T. 2016; 11 (8): 1477-1491

    Abstract

    The ability to simultaneously characterize the bacterial and host expression programs during infection would facilitate a comprehensive understanding of pathogen-host interactions. Although RNA sequencing (RNA-seq) has greatly advanced our ability to study the transcriptomes of prokaryotes and eukaryotes separately, limitations in existing protocols for the generation and analysis of RNA-seq data have hindered simultaneous profiling of host and bacterial pathogen transcripts from the same sample. Here we provide a detailed protocol for simultaneous analysis of host and bacterial transcripts by RNA-seq. Importantly, this protocol details the steps required for efficient host and bacteria lysis, barcoding of samples, technical advances in sample preparation for low-yield sample inputs and a computational pipeline for analysis of both mammalian and microbial reads from mixed host-pathogen RNA-seq data. Sample preparation takes 3 d from cultured cells to pooled libraries. Data analysis takes an additional day. Compared with previous methods, the protocol detailed here provides a sensitive, facile and generalizable approach that is suitable for large-scale studies and will enable the field to obtain in-depth analysis of host-pathogen interactions in infection models.

    View details for DOI 10.1038/nprot.2016.090

    View details for PubMedID 27442864