Dr. Gupta is a medical oncologist in the Stanford University Department of Medicine, Division of Medical Oncology. In her clinical practice and research, she is dedicated to advancing the understanding and management of breast cancer.

She is a recent recipient of the American Society of Clinical Oncology (ASCO)/Conquer Cancer 2020 Bonadonna Breast Cancer Research Grant. This grant supports her work as the co-investigator of a clinical trial evaluating the ctDNA status changes during adjuvant treatment of patients with early-stage triple-negative breast cancer who do not respond completely to neoadjuvant chemotherapy.

Dr. Gupta was a member of the combined bachelors/MD program at the University of California – San Diego. She graduated summa cum laude and was inducted into the Gold Humanism in Medicine Honor Society. She completed internship and residency in Internal Medicine at Stanford, during which time she was a recipient of the Julian Wolfsohn Award for clinical achievements in Internal Medicine and was inducted into the Alpha Omega Alpha Honor Medical Society. She then served as a Chief Resident and Clinical Instructor in Internal Medicine. Subsequently, she stayed on at Stanford for fellowship training in Hematology and Medical Oncology.

Clinical Focus

  • Oncology

Academic Appointments

Professional Education

  • Fellowship: Stanford University Division of Oncology (2021) CA
  • Medical Education: University of California San Diego School of Medicine (2014) CA
  • Residency: Stanford University Internal Medicine Residency (2018) CA
  • Board Certification: American Board of Internal Medicine, Internal Medicine (2017)

All Publications

  • Incident comorbidities in a diverse cohort of women treated for early-stage, hormone receptor-positive breast cancer Gupta, T., Purington, N., Liu, M., Han, S., Sledge, G., Schapira, L., Kurian, A. AMER ASSOC CANCER RESEARCH. 2021
  • Online Communities as Sources of Peer Support for People Living With Cancer: A Commentary JOURNAL OF ONCOLOGY PRACTICE Gupta, T., Schapira, L. 2018; 14 (12): 725-+
  • Pathogenic variants in less familiar cancer susceptibility genes: what happens after genetic testing? JCO Precision Oncology Hall, E. T., Parikh, D., Caswell-Jin, J. L., Gupta, T., Mills, M. A., Kingham, K. E., Koff, R., Ford, J. M., Kurian, A. W. 2018

    View details for DOI 10.1200/PO.18.00167

  • Pathogenic germline mutations in emerging cancer genes: What happens after panel testing? Hall, E., Parikh, D., Gupta, T., Caswell, J., Mills, M., Kingham, K., Koff, R., Ford, J. M., Kurian, A. W. AMER SOC CLINICAL ONCOLOGY. 2017
  • Racial/ethnic differences in multiple-gene sequencing results for hereditary cancer risk. Genetics in medicine : official journal of the American College of Medical Genetics Caswell-Jin, J. L., Gupta, T. n., Hall, E. n., Petrovchich, I. M., Mills, M. A., Kingham, K. E., Koff, R. n., Chun, N. M., Levonian, P. n., Lebensohn, A. P., Ford, J. M., Kurian, A. W. 2017


    PurposeWe examined racial/ethnic differences in the usage and results of germ-line multiple-gene sequencing (MGS) panels to evaluate hereditary cancer risk.MethodsWe collected genetic testing results and clinical information from 1,483 patients who underwent MGS at Stanford University between 1 January 2013 and 31 December 2015.ResultsAsians and Hispanics presented for MGS at younger ages than whites (48 and 47 vs. 55; P = 5E-16 and 5E-14). Across all panels, the rate of pathogenic variants (15%) did not differ significantly between racial groups. Rates by gene did differ: in particular, a higher percentage of whites than nonwhites carried pathogenic CHEK2 variants (3.8% vs. 1.0%; P = 0.002). The rate of a variant of uncertain significance (VUS) result was higher in nonwhites than whites (36% vs. 27%; P = 2E-4). The probability of a VUS increased with increasing number of genes tested; this effect was more pronounced for nonwhites than for whites (1.1% absolute difference in VUS rates testing BRCA1/2 vs. 8% testing 13 genes vs. 14% testing 28 genes), worsening the disparity.ConclusionIn this diverse cohort undergoing MGS testing, pathogenic variant rates were similar between racial/ethnic groups. By contrast, VUS results were more frequent among nonwhites, with potential significance for the impact of MGS testing by race/ethnicity.GENETICS in MEDICINE advance online publication, 27 July 2017; doi:10.1038/gim.2017.96.

    View details for PubMedID 28749474

  • Considering the vascular hypothesis for the pathogenesis of small intestinal atresia: A case control study of genetic factors AMERICAN JOURNAL OF MEDICAL GENETICS PART A Gupta, T., Yang, W., Iovannisci, D. M., Carmichael, S. L., Stevenson, D. K., Shaw, G. M., Lammer, E. J. 2013; 161A (4): 702-710


    Small intestinal atresia (SIA) is a rare congenital occlusion of the small intestine. SIA development, particularly in the jejunum and ileum, has been associated with in utero disruption of vascular supply. However, the number of studies of the vascular hypothesis is limited. This study considers the vascular hypothesis by exploring risks associated with 32 SNPs of genes involved in vascular processes of homocysteine metabolism, coagulation, cell-cell interactions, inflammatory response, and blood pressure regulation. A total of 206 SIA cases were ascertained by the California Birth Defects Monitoring Program, and 573 infants with no major congenital anomalies by their first birthday were selected as controls. Genomic DNA was genotyped for 32 SNPs involving the following genes: MTHFR, F2, F5, F7, SERPINE1, FGB, ITGA2, ITGB3, SELE, ICAM1, MMP3, TNF, LTA, NOS3, AGTR1, AGT, NPPA, ADD1, SCNN1A, GNB3, and ADRB2. Risks were estimated as odds ratios, adjusted for maternal age and race, with 95% confidence intervals. Cases were considered collectively and by subgroups based on atresia location (duodenal/jejunum/ileum). Three SNPs had reduced risk: SERPINE1 11053 T/G, MMP3 (-1171) A6/A5, and ADRB2 gln27glu. Two had increased risk: ITGA2 873 G/A and NPPA 2238 T/C. No intestinal subphenotypes showed a unique pattern of SNP associations. The association of two SNPs with increased risk lends some, albeit limited, support to vascular impairment as a possible mechanism leading to SIA. These results also identify genes meriting further exploration in SIA studies. Hence, this study makes an important contribution by exploring the long-held but not well-investigated vascular hypothesis.

    View details for DOI 10.1002/ajmg.a.35775

    View details for Web of Science ID 000316631300012