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

  • Medical Oncology

Academic Appointments

Professional Education

  • Board Certification: American Board of Internal Medicine, Medical Oncology (2021)
  • Board Certification: American Board of Internal Medicine, Hematology (2021)
  • 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

  • Emerging strategies: PARP inhibitors in combination with immune checkpoint blockade in BRCA1 and BRCA2 mutation-associated and triple-negative breast cancer. Breast cancer research and treatment Gupta, T., Vinayak, S., Telli, M. 2022


    Poly (adenosine diphosphate-ribose) polymerase (PARP) inhibitor monotherapy in germline BRCA1 and BRCA2 mutation-associated metastatic breast cancer is a well-tolerated and an effective therapeutic strategy, however, the durability of response can be limited. Checkpoint inhibitors targeting the PD-1/PD-L1 axis as monotherapy in metastatic triple-negative breast cancer (mTNBC) have a limited role due to low response rates, but are capable of long, durable responses. Combination PARP inhibition with checkpoint blockade is an emerging area of investigation with potential synergy to produce robust responses with durability. Mechanistically, PARP inhibition activates the stimulator of interferon gene (STING) pathway to promote dendritic cell and T lymphocyte recruitment, increases tumor neoantigens, and upregulates PD-L1 expression to increase the immunogenicity of the tumor and thereby potentially enhance responses to immunotherapy. Several clinical trials have reported early results on PARP inhibitor and PD-1/PD-L1 checkpoint inhibitor combinations. All studies have shown safety and tolerability of this combination regimen. In advanced breast cancer associated with a germline BRCA1 or BRCA2 mutation, response rates have been high and similar to what is observed with PARP inhibitor monotherapy. Additional follow-up is needed to see if combination with a checkpoint inhibitor can lead to a clinically meaningful extension of durability of response in patients with germline mutations in BRCA1 and BRCA2. In unselected mTNBC in the 1st-3rd line setting, response rates of combined PARP inhibitor and PD-1/PD-L1 inhibitors have ranged from 18-21%, with higher rates of response among those with alterations in homologous recombination DNA repair pathway genes. Multiple ongoing studies will report additional data on combinations of PARP inhibitors and checkpoint blockade in the future and this combination strategy remains an active area of investigation.

    View details for DOI 10.1007/s10549-022-06780-4

    View details for PubMedID 36318381

  • Incident comorbidities after tamoxifen or aromatase inhibitor therapy in a racially and ethnically diverse cohort of women with breast cancer. Breast cancer research and treatment Gupta, T., Purington, N., Liu, M., Han, S., Sledge, G., Schapira, L., Kurian, A. W. 2022


    As survival with early-stage, hormone receptor (HR)-positive breast has improved, it is essential to understand the long-term risks of incident comorbidities with different adjuvant endocrine therapy (ET) options.Women treated with tamoxifen and/or an aromatase inhibitor (AI) for stages 1-3, HR-positive/HER2-negative breast cancer from 2000 to 2016 in either of two healthcare systems in the San Francisco Bay Area were included. We considered the following comorbidities: cerebrovascular accidents, congestive heart failure, dementia, depression/anxiety, diabetes mellitus, hyperlipidemia, myocardial infarction, non-alcoholic steatohepatitis, osteoporosis/fracture, peripheral vascular disease, and venous thromboembolism. Cause-specific Cox proportional hazards models were fit to time-to-new-diagnosis for each comorbidity, accounting for death as a competing risk. Hazard ratios (HR) and 95% confidence intervals (CI) for tamoxifen versus AI were reported.Among 2,902 analyzed patients, the median age at diagnosis was 58.3 years; 67.6% were non-Hispanic white, 22.3% Asian, 7.5% Hispanic, and 1.7% non-Hispanic Black. Half (54.7%) used AIs only, 27.6% used tamoxifen only and 17.7% used both tamoxifen and AIs sequentially. Tamoxifen was associated with a lower risk of osteoporosis than AI (multivariable HR 0.45, 95% CI 0.32-0.62). No other incident comorbidity risk varied between users of tamoxifen versus AIs.In a diverse, multi-institutional, contemporary breast cancer cohort, the only incident comorbidity that differed between ET options was osteoporosis, a known side effect of AIs. These results may inform clinical decision-making about ET, and reassure patients who have bothersome symptoms on AIs that they are unlikely to develop worse comorbidities if they switch to tamoxifen.

    View details for DOI 10.1007/s10549-022-06716-y

    View details for PubMedID 36030472

  • Neoadjuvant Therapy in Breast Cancer: Histologic Changes and Clinical Implications. Surgical pathology clinics Troxell, M. L., Gupta, T. 2022; 15 (1): 57-75


    Cytotoxic or endocrine therapy before surgery (neoadjuvant) for breast cancer has become standard of care, affording the opportunity to assess and quantify response in the subsequent resection specimen. Correlation with radiology, cassette mapping, and histologic review with a semi-quantitative reporting system such as residual cancer burden (RCB) provides important prognostic data that may guide further therapy. The tumor bed should be identified histologically, often as a collagenized zone devoid of normal breast epithelium, with increased vasculature. Identification of residual treated carcinoma may require careful high power examination, as residual tumor cells may be small and dyscohesive; features are widely variable and include hyperchromatic small, large, or multiple nuclei with clear, foamy, or eosinophilic cytoplasm. Calculation of RCB requires residual carcinoma span in 2 dimensions, estimated carcinoma cellularity (% area), number of involved lymph nodes, and span of largest nodal carcinoma. These RCB parameters may differ from AJCC staging measurements, which depend on only contiguous carcinoma in breast and lymph nodes.

    View details for DOI 10.1016/j.path.2021.11.004

    View details for PubMedID 35236634

  • 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; 2: 1-10


    As genetic testing expands, patients are increasingly found to carry pathogenic variants in cancer susceptibility genes that are less familiar to most clinicians, specifically genes other than those causing hereditary breast ovarian cancer syndrome (BRCA1 and BRCA2) and Lynch syndrome. Little is known about the subsequent behaviors of such patients in terms of managing cancer risks and informing relatives.All adult patients who were counseled and tested at the Stanford Cancer Genetics Clinic from January 2013 to July 2015 and had a pathogenic variant in a non-BRCA1/2, non-Lynch syndrome gene were invited to participate in a telephone interview about adherence to risk-reducing recommendations, genetic testing by relatives, and new cancer incidence.Fifty-seven (40%) of 142 eligible patients were successfully contacted, and all 57 patients participated; median follow-up was 677 days (range, 247 to 1,401 days). Most patients (82%; 95% CI, 70% to 90%) recalled that a risk-reducing intervention (screening, medication, or surgery) was recommended, and most patients (85%; 95% CI, 72% to 93%) adhered to the recommendation. Nearly all patients (91%; 95% CI, 81% to 97%) shared results with relatives, and most patients (78%; 95% CI, 64% to 88%) reported that a relative was subsequently tested. During the follow-up period, 9% of patients (95% CI, 3% to 19%) developed second cancers, and in 14% of patients (95% CI, 7% to 26%), a first-degree relative developed cancer, some of which were detected by recommended screening.Patients with a pathogenic variant in a less familiar cancer susceptibility gene report high adherence to risk-reducing interventions. Furthermore, in the 57 carriers and subsequently tested relatives with two years of follow-up, a total of three cancers (one in a proband and two in relatives) were detected through interventions recommended on the basis of the pathogenic variant. These results suggest a potential benefit of genetic counseling and testing for pathogenic variants in less familiar genes.

    View details for DOI 10.1200/PO.18.00167

    View details for PubMedID 35135157

  • 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