Bio

Bio


Thomas Sun is a resident physician in Internal Medicine at Stanford. He graduated summa cum laude with honors in philosophy from Columbia University, and received his medical degree from Yale University. He spent an additional year while in medical school in the basic science laboratory of Dr. Valentina Greco investigating the tumor microenvironment as a potential target for antitumor therapy. His career goal is to pursue a hem/onc fellowship with a focus on clinical research.

Honors & Awards


  • First Place, Society of Hospital Medicine Essay Competition (2018)
  • Finalist, Best Clinical Vignette, American College of Physicians Northern California Competition (2017)
  • Paul R. Bergstresser Travel Award, Society for Investigative Dermatology (2016)
  • Farr Scholarship, Yale University School of Medicine (2015)
  • Howard I. Jacoby Presidential Scholarship, Columbia University (2008-2011)
  • Adam Leroy Jones Prize, Columbia University, best essay in philosophy of science or foundation of logic (2011)
  • Finalist, Davis Peace Prize (2011)
  • Goldman Sachs Global Leader, Goldman Sachs, Institute of International Education (2009)
  • USAID Global Health Fellowship, United States Agency for International Development (2009)

Professional Education


  • Internal Medicine Residency, Stanford University School of Medicine (2020)
  • MHS, Yale University School of Medicine, Master of Health Science (2017)
  • MD, Yale University School of Medicine (2017)
  • BA, Columbia College, Columbia University, Philosophy (2011)

Publications

All Publications


  • Lengthy progression-free survival and intracranial activity of cabozantinib in patients with crizotinib and ceritinib-resistant ROS1-positive non-small-cell lung cancer. Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer Sun, T. Y., Niu, X., Chakraborty, A., Neal, J. W., Wakelee, H. A. 2018

    View details for DOI 10.1016/j.jtho.2018.08.2030

    View details for PubMedID 30217491

  • To be guided by instinct New England Journal of Medicine Sun, T. 2018: 1004-1005

    View details for DOI 10.1056/NEJMp1805651

  • Preclinical Advances with Multiphoton Microscopy in Live Imaging of Skin Cancers JOURNAL OF INVESTIGATIVE DERMATOLOGY Sun, T., Haberman, A. M., Greco, V. 2017; 137 (2): 282–87

    Abstract

    Conventional, static analyses have historically been the bedrock and tool of choice for the study of skin cancers. Over the past several years, in vivo imaging of tumors using multiphoton microscopy has emerged as a powerful preclinical tool for revealing detailed cellular behaviors from the earliest moments of tumor development to the final steps of metastasis. Multiphoton microscopy allows for deep tissue penetration with relatively minor phototoxicity, rendering it an effective tool for the long-term observation of tumor evolution. This review highlights some of the recent preclinical insights gained using multiphoton microscopy and suggests future advances that could enhance its power in revealing the mysteries of skin tumor biology.

    View details for DOI 10.1016/j.jid.2016.08.033

    View details for Web of Science ID 000392469700007

    View details for PubMedID 27847119

    View details for PubMedCentralID PMC5258832

  • Transformation from md to MD Sun, T. in-Training. 2017
  • Niche-induced cell death and epithelial phagocytosis regulate hair follicle stem cell pool NATURE Mesa, K. R., Rompolas, P., Zito, G., Myung, P., Sun, T. Y., Brown, S., Gonzalez, D. G., Blagoev, K. B., Haberman, A. M., Greco, V. 2015; 522 (7554): 94–U236

    Abstract

    Tissue homeostasis is achieved through a balance of cell production (growth) and elimination (regression). In contrast to tissue growth, the cells and molecular signals required for tissue regression remain unknown. To investigate physiological tissue regression, we use the mouse hair follicle, which cycles stereotypically between phases of growth and regression while maintaining a pool of stem cells to perpetuate tissue regeneration. Here we show by intravital microscopy in live mice that the regression phase eliminates the majority of the epithelial cells by two distinct mechanisms: terminal differentiation of suprabasal cells and a spatial gradient of apoptosis of basal cells. Furthermore, we demonstrate that basal epithelial cells collectively act as phagocytes to clear dying epithelial neighbours. Through cellular and genetic ablation we show that epithelial cell death is extrinsically induced through transforming growth factor (TGF)-β activation and mesenchymal crosstalk. Strikingly, our data show that regression acts to reduce the stem cell pool, as inhibition of regression results in excess basal epithelial cells with regenerative abilities. This study identifies the cellular behaviours and molecular mechanisms of regression that counterbalance growth to maintain tissue homeostasis.

    View details for DOI 10.1038/nature14306

    View details for Web of Science ID 000355543400036

    View details for PubMedID 25849774

    View details for PubMedCentralID PMC4457634

  • beta-Catenin Activation Regulates Tissue Growth Non-Cell Autonomously in the Hair Stem Cell Niche SCIENCE Deschene, E. R., Myung, P., Rompolas, P., Zito, G., Sun, T., Taketo, M. M., Saotome, I., Greco, V. 2014; 343 (6177): 1353–56

    Abstract

    Wnt/β-catenin signaling is critical for tissue regeneration. However, it is unclear how β-catenin controls stem cell behaviors to coordinate organized growth. Using live imaging, we show that activation of β-catenin specifically within mouse hair follicle stem cells generates new hair growth through oriented cell divisions and cellular displacement. β-Catenin activation is sufficient to induce hair growth independently of mesenchymal dermal papilla niche signals normally required for hair regeneration. Wild-type cells are co-opted into new hair growths by β-catenin mutant cells, which non-cell autonomously activate Wnt signaling within the neighboring wild-type cells via Wnt ligands. This study demonstrates a mechanism by which Wnt/β-catenin signaling controls stem cell-dependent tissue growth non-cell autonomously and advances our understanding of the mechanisms that drive coordinated regeneration.

    View details for DOI 10.1126/science.1248373

    View details for Web of Science ID 000333108500037

    View details for PubMedID 24653033

    View details for PubMedCentralID PMC4096864

  • Spontaneous tumour regression in keratoacanthomas is driven by Wnt/retinoic acid signalling cross-talk NATURE COMMUNICATIONS Zito, G., Saotome, I., Liu, Z., Ferro, E. G., Sun, T. Y., Nguyen, D. X., Bilguvar, K., Ko, C. J., Greco, V. 2014; 5: 3543

    Abstract

    A fundamental goal in cancer biology is to identify the cells and signalling pathways that are keys to induce tumour regression. Here we use a spontaneously self-regressing tumour, cutaneous keratoacanthoma (KAs), to identify physiological mechanisms that drive tumour regression. By using a mouse model system that recapitulates the behaviour of human KAs, we show that self-regressing tumours shift their balance to a differentiation programme during regression. Furthermore, we demonstrate that developmental programs utilized for skin hair follicle regeneration, such as Wnt, are hijacked to sustain tumour growth and that the retinoic acid (RA) signalling pathway promotes tumour regression by inhibiting Wnt signalling. Finally, we find that RA signalling can induce regression of malignant tumours that do not normally spontaneously regress, such as squamous cell carcinomas. These findings provide new insights into the physiological mechanisms of tumour regression and suggest therapeutic strategies to induce tumour regression.

    View details for DOI 10.1038/ncomms4543

    View details for Web of Science ID 000334303700003

    View details for PubMedID 24667544

    View details for PubMedCentralID PMC3974217

  • DNase Inhibits Gardnerella vaginalis Biofilms In Vitro and In Vivo JOURNAL OF INFECTIOUS DISEASES Hymes, S. R., Randis, T. M., Sun, T., Ratner, A. J. 2013; 207 (10): 1491–97

    Abstract

    Bacterial vaginosis is a highly prevalent and poorly understood polymicrobial disorder of the vaginal microbiota, with significant adverse sequelae. Gardnerella vaginalis predominates in bacterial vaginosis. Biofilms of G. vaginalis are present in human infections and are implicated in persistent disease, treatment failure, and transmission. Here we demonstrate that G. vaginalis biofilms contain extracellular DNA, which is essential to their structural integrity. Enzymatic disruption of this DNA specifically inhibits biofilms, acting on both newly forming and established biofilms. DNase liberates bacteria from the biofilm to supernatant fractions and potentiates the activity of metronidazole, an antimicrobial agent used in the treatment of bacterial vaginosis. Using a new murine vaginal colonization model for G. vaginalis, we demonstrate >10-fold inhibition of G. vaginalis colonization by DNase. We conclude that DNase merits investigation as a potential nonantibiotic adjunct to existing bacterial vaginosis therapies in order to decrease the risk of chronic infection, recurrence, and associated morbidities.

    View details for DOI 10.1093/infdis/jit047

    View details for Web of Science ID 000318106600004

    View details for PubMedID 23431033

    View details for PubMedCentralID PMC3627197

  • The Effect of Epoxidized Safflower Oil on the Properties of Polyvinyl Chloride Films JOURNAL OF ELASTOMERS AND PLASTICS Sun, T., Thom, R. 2010; 42 (2): 129–37