Dr. Sun is a chief fellow and third-year fellow in Hematology & Oncology 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.

In residency and fellowship at Stanford, he led clinical research to help advance the treatment of aggressive lung cancers including small-cell lung cancer and other high grade neuroendocrine tumors. He has published in The New England Journal of Medicine, Nature, Science and The Journal of Thoracic Oncology, among others. He is currently a co-investigator in an investigator-initiated phase 1 trial in small cell lung cancer.

He will be joining the Pleasanton hematology/oncology practice of Stanford Medicine Partners in Aug 2023. He is fluent in Cantonese and Mandarin.

Google scholar profile:

Honors & Awards

  • Best Research, Stanford Internal Medicine Residency Research Symposium (2020)
  • Poster Walk Presenter Travel Award, The European Neuroendocrine Tumor Society (2020)
  • 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 (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

  • Chief Fellow, Stanford University School of Medicine, Hematology/Oncology (2023)
  • Fellowship, Stanford University School of Medicine, Hematology/Oncology (2023)
  • Residency, Stanford University School of Medicine, Internal Medicine (2020)
  • Masters, Yale University School of Medicine, MHS (2017)
  • Medical School, Yale University School of Medicine, MD (2017)
  • Undergraduate, Columbia College, Columbia University, BA (2011)

All Publications

  • Exploratory genomic analysis of high grade neuroendocrine neoplasms across diverse primary sites. Endocrine-related cancer Sun, T. Y., Zhao, L., Van Hummelen, P., Martin, B., Hornbacker, K., Lee, H., Xia, L. C., Padda, S. K., Ji, H. P., Kunz, P. 2022


    High grade (grade 3) neuroendocrine neoplasms (G3 NENs) have poor survival outcomes. From a clinical standpoint, G3 NENs are usually grouped regardless of primary site and treated similarly. Little is known regarding the underlying genomics of these rare tumors, especially when compared across different primary sites. We performed whole transcriptome (n = 46), whole exome (n = 40) and gene copy number (n = 43) sequencing on G3 NEN FFPE samples from diverse organs (in total 17 were lung, 16 were gastroenteropancreatic, 13 other). G3 NENs despite arising from diverse primary sites did not have gene expression profiles that were easily segregated by organ of origin. Across all G3 NENs, TP53, APC, RB1 and CDKN2A were significantly mutated. The CDK4/6 cell cycling pathway was mutated in 95% of cases, with upregulation of oncogenes within this pathway. G3 NENs had high tumor mutation burden (mean 7.09 mutations/MB), with 20% having >10 mutations/MB. Two somatic copy number alterations were significantly associated with worse prognosis across tissue types: focal deletion 22q13.31 (HR, 7.82; p = 0.034) and arm amplification 19q (HR, 4.82; p = 0.032). This study is among the most diverse genomic study of high-grade neuroendocrine neoplasms. We uncovered genomic features previously unrecognized for this rapidly fatal and rare cancer type that could have potential prognostic and therapeutic implications.

    View details for DOI 10.1530/ERC-22-0015

    View details for PubMedID 36165930

  • Lung Neuroendocrine Tumors: How Does Molecular Profiling Help? Current oncology reports Sun, T. Y., Hendifar, A., Padda, S. K. 2022


    Lung neuroendocrine tumors (NETs)-typical carcinoids and atypical carcinoids-have unique molecular alterations that are distinct from neuroendocrine carcinomas of the lung and non-small cell lung cancers. Here, we review the role of molecular profiling in the prognosis and treatment of lung NETs.There have been no recently identified molecular prognostic factors for lung NETs and none that have been routinely used to guide management of patients with lung NETs. Previous findings suggest that patients with loss of chromosome 11q may have a worse prognosis along with upregulation of anti-apoptotic pathways (e.g., loss of CD44 and OTP protein expression). Lung NETs rarely harbor driver mutations commonly found in non-small cell lung cancer (NSCLC) or TP53/RB1 mutations found universally in small cell lung cancer. Lung NETs also have low tumor mutation burden and low PD-L1 expression. Everolimus, an mTOR inhibitor and the only FDA approved therapy for unresectable lung NETs, is an effective treatment but the presence of a molecular alteration in the PI3K/AKT/mTOR pathway is not known to predict treatment response. The predominant mutations in lung NETs occur in genes regulating chromatin remodeling and histone modification, with potential targeted therapies emerging in clinical trials. Lung NETs have recurring alterations in genes that regulate the epigenome. Future targeted therapy interfering with epigenetic pathways may hold promise.

    View details for DOI 10.1007/s11912-022-01253-9

    View details for PubMedID 35305210

  • Diffuse Idiopathic Pulmonary Neuroendocrine Cell Hyperplasia (DIPNECH): Clinical Characteristics and Progression to Carcinoid Tumor European Respiratory Journal Sun, T. 2021
  • US phase 1 first-in-human study of taletrectinib (DS-6051b/AB-106), a ROS1/TRK inhibitor, in patients with advanced solid tumors. Clinical cancer research : an official journal of the American Association for Cancer Research Papadopoulos, K. P., Borazanci, E. n., Shaw, A. T., Katayama, R. n., Shimizu, Y. n., Zhu, V. W., Sun, T. Y., Wakelee, H. A., Madison, R. n., Schrock, A. B., Senaldi, G. n., Nakao, N. n., Hanzawa, H. n., Masaya, T. n., Isoyama, T. n., Nakamaru, K. n., Deng, C. n., Li, M. n., Fran, F. n., Zhao, Q. n., Gao, Y. n., Seto, T. n., Janne, P. A., Ou, S. I. 2020


    Taletrectinib (DS-6051b/AB-106) is an oral, tyrosine kinase inhibitor of ROS1 and NTRK with potent pre-clinical activity against ROS1 G2032R solvent-front mutation among others. We report the first-in-human US-phase 1 results of taletrectinib.Patients ≥18 years old with neuroendocrine tumors, with tumor-induced pain, or tumors harboring ROS1/NTRK rearrangements were eligible. Accelerated titration followed by modified continuous reassessment method and escalation with overdose control was used (50-1200 mg once daily [QD] or 400 mg twice daily). Primary objectives were safety/tolerability, and maximum tolerated dose (MTD) determination. Secondary objectives were food-effect pharmacokinetics and antitumor activity.A total of 46 patients were enrolled. Steady-state peak concentration (Cmax) and exposure (AUC0-8) increased dose dependently from 50 mg to 800 mg QD doses. The ratio of the geometric mean of AUC0-24 between low-fat-diet-fed/fasted state was 123% (90% confidence interval: 104% - 149%). Dose-limiting toxicities (grade 3 transaminases increase) occurred in 2 patients (1200 mg QD dose). MTD was 800 mg QD. Most common treatment-related adverse events (TRAEs) were nausea (47.8%), diarrhea (43.5%), and vomiting (32.6%). Pain score reductions were observed in the 800 mg QD-dose cohort. Confirmed ORR was 33.3% among the 6 RECIST-evaluable crizotinib-refractory ROS1+ NSCLC patients. One TPM3-NTRK1 differentiated thyroid cancer patient achieving a confirmed partial response (PR) of 27 months at data cutoff. We identified a cabozantinib-sensitive ROS1 L2086F as an acquired taletrectinib-resistance mutation.Taletrectinib has manageable toxicities at the MTD of 800 mg daily. Preliminary efficacy was observed in crizotinib-refractory ROS1+ NSCLC patients.

    View details for DOI 10.1158/1078-0432.CCR-20-1630

    View details for PubMedID 32591465

  • Steroid-Sparing Therapy for Tyrosine Kinase Inhibitor-Induced Pneumonitis. Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer Sun, T. Y., Sung, A. W., Neal, J. W. 2019; 14 (4): e75-e77

    View details for DOI 10.1016/j.jtho.2018.11.030

    View details for PubMedID 30922583

  • Tumor heterogeneity and testing discrepancy confound ROS1 detection in NSCLC. Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer Sun, T. Y., Stehr, H., Suarez, C. J., Wakelee, H. A. 2019

    View details for DOI 10.1016/j.jtho.2019.03.011

    View details for PubMedID 30914313

  • Single-Cell Analysis Reveals a Hair Follicle Dermal Niche Molecular Differentiation Trajectory that Begins Prior to Morphogenesis DEVELOPMENTAL CELL Gupta, K., Levinsohn, J., Linderman, G., Chen, D., Sun, T., Dong, D., Taketo, M., Bosenberg, M., Kluger, Y., Choate, K., Myung, P. 2019; 48 (1): 17-+


    Delineating molecular and cellular events that precede appendage morphogenesis has been challenging due to the inability to distinguish quantitative molecular differences between cells that lack histological distinction. The hair follicle (HF) dermal condensate (DC) is a cluster of cells critical for HF development and regeneration. Events that presage emergence of this distinctive population are poorly understood. Using unbiased single-cell RNA sequencing and in vivo methods, we infer a sequence of transcriptional states through which DC cells pass that begins prior to HF morphogenesis. Our data indicate that Wnt/β-catenin signaling is required to progress into an intermediate stage that precedes quiescence and differentiation. Further, we provide evidence that quiescent DC cells are recent progeny of selectively proliferating cells present prior to morphogenesis and that are later identified in the peri-DC zone during DC expansion. Together, these findings provide an inferred path of molecular states that lead to DC cell differentiation.

    View details for DOI 10.1016/j.devcel.2018.11.032

    View details for Web of Science ID 000455007100009

    View details for PubMedID 30595533

    View details for PubMedCentralID PMC6361530

  • 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 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


    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
  • Stromal re-organization in hair follicle development and cancer suppression Sun, T., Greco, V., Myung, P. ELSEVIER SCIENCE INC. 2016: S16
  • 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


    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


    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


    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


    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