Bio

Dr. Caely Yanikoglu is a Clinical Assistant Professor of Dermatology at Stanford. Dr. Yanikoglu received her Bachelor of Science degree with distinction from the University of Michigan. She received her medical degree from Columbia University in New York, where she was inducted into the Alpha Omega Alpha honor society. She completed her residency in dermatology at Stanford University Medical Center and served as chief resident in her final year. Dr. Yanikoglu’s clinical interest is general medical dermatology, including skin cancer, acne, psoriasis, atopic dermatitis, and dermatologic surgery.

Clinical Focus

  • Dermatology

Academic Appointments

Professional Education

  • Board Certification: American Board of Dermatology, Dermatology (2021)
  • Residency, Stanford University Department of Dermatology
  • Medical School, Columbia University Vagelos College of Physicians and Surgeons
  • Undergraduate, University of Michigan

Contact

  • Academic
    caelyah@stanford.edu
    University - Staff Department: Dermatology Position: Clinical Assistant Professor
    • 5800 HOLLIS ST
    • Bldg. 1, 4th floor - POD 5
    • MC7841
    • EMERYVILLE,  California  94608 
  • Clinical (Primary)  Stanford Dermatology 450 Broadway St Pavilion B 4th Fl MC 5338 Redwood City, CA 94063 (650) 721-3476 (fax)

Additional Clinical Info

All Publications

  • Disseminated non-Langerhans cell histiocytosis with an IRF2BP2-NTRK1 gene fusion identified by next-generation sequencing. JAAD case reports Chan, W. H., Shah, A., Bae, G., Hambro, C., Martin, B. A., Brown, R., Novoa, R., Kwong, B. Y. 2020; 6 (11): 1156–58

    View details for DOI 10.1016/j.jdcr.2020.05.032

    View details for PubMedID 33134460

  • Neutrophil Extracellular Traps Induce Human Th17 Cells: Effect of Psoriasis-Associated TRAF3IP2 Genotype. The Journal of investigative dermatology Lambert, S., Hambro, C. A., Johnston, A., Stuart, P. E., Tsoi, L. C., Nair, R. P., Elder, J. T. 2019; 139 (6): 1245-1253

    Abstract

    Psoriasis lesions are rich in IL-17-producing T cells as well as neutrophils, which release webs of DNA-protein complexes known as neutrophil extracellular traps (NETs). Because we and others have observed increased NETosis in psoriatic lesions, we hypothesized that NETs contribute to increased T helper type 17 (Th17) cells in psoriasis. After stimulating peripheral blood mononuclear cells with anti-CD3/CD28 beads for 7 days, we found significantly higher percentages of CD3+CD4+IL-17+ (Th17) cells in the presence versus absence of NETs, as assessed by flow cytometry, IL-17 ELISA, and IL17A/F and RORC mRNAs. Memory, but not naïve, T cells were competent and monocytes were required for CD3/CD28-mediated Th17 induction, with or without NETs. Th17 induction was enhanced by the T allele of rs33980500 (T/C), a psoriasis risk-associated variant in the TRAF3IP2 gene encoding the D10N variant of Act1, a key mediator of IL-17 signal transduction. Global transcriptome analysis of CD3/CD28-stimulated peripheral blood mononuclear cells by RNA sequencing confirmed the stimulatory effects of NETs, demonstrated NET-induced enhancement of cytokine gene expression, and verified that the effect of Act1 D10N was greater in the presence of NETs. Collectively, these results implicate NETs and the Act1 D10N variant in human Th17 induction from peripheral blood mononuclear cells, with ramifications for immunogenetic studies of psoriasis and other autoimmune diseases.

    View details for DOI 10.1016/j.jid.2018.11.021

    View details for PubMedID 30528823

    View details for PubMedCentralID PMC7092801

  • Trichophyton rubrum tinea capitis in an HIV-positive patient with generalized dermatophytosis. JAAD case reports Hambro, C. A., Yin, N. C., Yang, C., Husain, S., Silvers, D. N., Grossman, M. E. 2017; 3 (1): 19-21

    View details for DOI 10.1016/j.jdcr.2016.10.011

    View details for PubMedID 28050591

    View details for PubMedCentralID PMC5192346

  • Dopamine and opioid systems interact within the nucleus accumbens to maintain monogamous pair bonds. eLife Resendez, S. L., Keyes, P. C., Day, J. J., Hambro, C., Austin, C. J., Maina, F. K., Eidson, L. N., Porter-Stransky, K. A., Nevárez, N., McLean, J. W., Kuhnmuench, M. A., Murphy, A. Z., Mathews, T. A., Aragona, B. J. 2016; 5

    Abstract

    Prairie vole breeder pairs form monogamous pair bonds, which are maintained through the expression of selective aggression toward novel conspecifics. Here, we utilize behavioral and anatomical techniques to extend the current understanding of neural mechanisms that mediate pair bond maintenance. For both sexes, we show that pair bonding up-regulates mRNA expression for genes encoding D1-like dopamine (DA) receptors and dynorphin as well as enhances stimulated DA release within the nucleus accumbens (NAc). We next show that D1-like receptor regulation of selective aggression is mediated through downstream activation of kappa-opioid receptors (KORs) and that activation of these receptors mediates social avoidance. Finally, we also identified sex-specific alterations in KOR binding density within the NAc shell of paired males and demonstrate that this alteration contributes to the neuroprotective effect of pair bonding against drug reward. Together, these findings suggest motivational and valence processing systems interact to mediate the maintenance of social bonds.

    View details for DOI 10.7554/eLife.15325

    View details for PubMedID 27371827

    View details for PubMedCentralID PMC4972541