BFAM Member Spotlights

Meet the members of the Stanford Medicine Black Faculty Affinity Meetings (BFAM), a network created through OFDD's Community Support Initiative. BFAM is intended to provide networking and social engagement opportunities for Stanford Medicine faculty across all clinical lines and departments.

Allyson Spence, MD, PhD

Department of Medicine/Oncology

VA Palo Alto Oncologist

Something you wouldn’t know just by looking at me.
I enjoy playing the piano

What are some of your favorite social activities?
Musical events

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Clinical Assistant Professor, Medicine - Oncology

acampb1@stanford.edu

Bio

Allyson Spence MD, PhD is a Clinical Assistant Professor of Medicine in the Stanford University School of Medicine. She received her MD, PhD in the MSTP program at Vanderbilt University School of Medicine, studying basic mechanisms of transcription using Saccharomyces cerevisiae as a model system in the laboratory of Dr. Tony Weil. She went on to an internship and residency at the University of Pennsylvania before returning to Stanford to complete her Oncology fellowship training. She did a postdoctoral fellowship at Stanford in the department of Molecular Biology under the auspices of Dr. Margaret Fuller, where she was the recipient of a career award. She has transitioned from basic science research to clinical medicine where she sees patients diagnosed with breast cancer. Additionally, she has an appointment at the Palo Alto VA as a staff oncologist where she focuses on women's cancers and women at high risk of developing breast and gynecologic cancers. She is involved in several translational research projects at the VA, as well as being involved in clinical trials.

Publications

DREF Genetically Counteracts Mi-2 and Caf1 to Regulate Adult Stem Cell Maintenance. PLoS genetics Angulo, B., Srinivasan, S., Bolival, B. J., Olivares, G. H., Spence, A. C., Fuller, M. T. 2019; 15 (6): e1008187 More

Abstract

Active adult stem cells maintain a bipotential state with progeny able to either self-renew or initiate differentiation depending on extrinsic signals from the surrounding microenvironment. However, the intrinsic gene regulatory networks and chromatin states that allow adult stem cells to make these cell fate choices are not entirely understood. Here we show that the transcription factor DNA Replication-related Element Factor (DREF) regulates adult stem cell maintenance in the Drosophila male germline. A temperature-sensitive allele of DREF described in this study genetically separated a role for DREF in germline stem cell self-renewal from the general roles of DREF in cell proliferation. The DREF temperature-sensitive allele caused defects in germline stem cell self-renewal but allowed viability and division of germline stem cells as well as cell viability, growth and division of somatic cyst stem cells in the testes and cells in the Drosophila eye. Germline stem cells mutant for the temperature sensitive DREF allele exhibited lower activation of a TGF-beta reporter, and their progeny turned on expression of the differentiation factor Bam prematurely. Results of genetic interaction analyses revealed that Mi-2 and Caf1/p55, components of the Nucleosome Remodeling and Deacetylase (NuRD) complex, genetically antagonize the role of DREF in germline stem cell maintenance. Taken together, these data suggest that DREF contributes to intrinsic components of the germline stem cell regulatory network that maintains competence to self-renew.

View details for DOI 10.1371/journal.pgen.1008187

View details for PubMedID 31226128
The actin-binding protein profilin is required for germline stem cell maintenance and germ cell enclosure by somatic cyst cells DEVELOPMENT Shields, A. R., Spence, A. C., Yamashita, Y. M., Davies, E. L., Fuller, M. T. 2014; 141 (1): 73-82 More

Abstract

Specialized microenvironments, or niches, provide signaling cues that regulate stem cell behavior. In the Drosophila testis, the JAK-STAT signaling pathway regulates germline stem cell (GSC) attachment to the apical hub and somatic cyst stem cell (CySC) identity. Here, we demonstrate that chickadee, the Drosophila gene that encodes profilin, is required cell autonomously to maintain GSCs, possibly facilitating localization or maintenance of E-cadherin to the GSC-hub cell interface. Germline specific overexpression of Adenomatous Polyposis Coli 2 (APC2) rescued GSC loss in chic hypomorphs, suggesting an additive role of APC2 and F-actin in maintaining the adherens junctions that anchor GSCs to the niche. In addition, loss of chic function in the soma resulted in failure of somatic cyst cells to maintain germ cell enclosure and overproliferation of transit-amplifying spermatogonia.

View details for DOI 10.1242/dev.101931

View details for PubMedID 24346697

View details for PubMedCentralID PMC3865751

see all 2 publications

BFAM Member Spotlights

Allyson Spence, MD, PhD

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