Sumana Shashidhar, MS, MA, has extensive experience as a research scientist in industry and academia. Her career at Stanford has spanned over 19 years, beginning in the Department of Blood and Marrow Transplantation (BMT), and currently at the Stanford Center for Clinical Research (SCCR). The focus of her applied science research was on the development of hematopoietic progenitor cell based therapies to prevent opportunistic infections in the setting of stem cell transplant. Her clinical research experience includes investigator-initiated and industry-sponsored drug/device trials in cancer and non-cancer settings.

In her current role as the Associate Director for Clinical Research Operations at SCCR, Sumana helps support and promote impactful clinical research conducted by faculty within the Department of Medicine (DoM), and across Stanford University. She serves as a liaison across cross-functional areas and schools, as well as external organizations and agencies. She is passionate about the participant experience and in bringing clinical trials to under-served and under-represented populations.

Current Role at Stanford

Associate Director - Clinical Research Operations
Stanford Center for Clinical Research

Education & Certifications

  • MA, San Jose State University, CA, Molecular and Microbiology (2001)
  • MS, University of Mysore, India, Biotechnology (1997)
  • BS, University of Mysore, India, Biochemistry, Botany, and Microbiology (1995)

All Publications

  • Why digital health trials can fail: Lessons learned from a randomized trial of health coaching and virtual cardiac rehabilitation. Cardiovascular digital health journal Olivier, C. B., Middleton, S. K., Purington, N., Shashidhar, S., Hereford, J., Mahaffey, K. W., Turakhia, M. P. 2021; 2 (2): 101-108


    We performed a trial to evaluate the efficacy of a blended intervention with personalized health coaching and virtual cardiac rehabilitation to improve medication adherence and risk factors. The trial was terminated early. Here, we describe findings from a root cause analysis and lessons learned.SmartGUIDE was an open-label, single-center trial that randomized participants with coronary artery disease who were prescribed a statin and/or P2Y12 inhibitor 1:1 to either usual care or the added use of a mobile app with components of cardiac rehabilitation paired with personal virtual coaching. The primary outcome was medication adherence: proportion of days covered (PDC). The planned sample size was 132. We performed a root cause analysis to evaluate processes from study development to closure.During trial conduct, the technology start-up withdrew the intervention. The study was terminated early with 63 participants randomized and data from 26 available for analysis. The median PDC was high in both groups (intervention group 94%, interquartile range [IQR] 88%-96%; control group: 99%, IQR 95%-100%). Root cause analysis identified factors for not achieving trial objectives: key factors that limited enrollment (inclusion criteria, low penetration of compatible smartphones), participant retention or engagement (poor app product, insufficient technology support), and suboptimal choice of a technology partner (technology start-up's inexperience in health care, poor product design, inadequate fundraising).We identified important and preventable factors leading to trial failure. These factors may be common across digital health trials and may explain prior observations that many such trials are never completed. Careful vetting of technology partners and more pragmatic study designs may prevent these missteps.

    View details for DOI 10.1016/j.cvdhj.2021.01.003

    View details for PubMedID 35265897

    View details for PubMedCentralID PMC8890340

  • A double-blind, randomized, placebo-controlled pilot trial to evaluate safety and efficacy of vorapaxar on arteriovenous fistula maturation. The journal of vascular access Olivier, C. B., Sundaram, V., Chertow, G. M., Shashidhar, S., McDonnell, L. K., Ding, V. Y., Desai, M., Mahaffey, K. W., Mell, M. 2019: 1129729819887269


    BACKGROUND: Protease-activated receptor-1 antagonism by vorapaxar could facilitate arteriovenous fistula maturation but may increase bleeding risk.OBJECTIVE: The primary objective of the Vorapaxar Study for Maturation of arteriovenous fistula for Hemodialysis Access (VorapAccess) was to determine if vorapaxar improves arteriovenous fistula functional maturation in patients with end-stage renal disease.METHODS: VorapAccess was a randomized, placebo-controlled, double-blind pilot trial comparing 2.5mg vorapaxar per day with placebo for twelve weeks starting on day two after arteriovenous fistula creation. The primary outcome was time to functional maturation defined as successful cannulation for six hemodialysis sessions within three weeks. The planned sample size was 50 participants. The study was terminated early after withdrawal of planned financial support. Given the small number of randomized patients, we performed descriptive analyses without inference testing.RESULTS: A total of 13 participants were randomly allocated study drug (six vorapaxar and seven placebo). The median age was 56years and seven participants (54%) were female. The median (minimum-maximum) days to functional maturation were 169 (77-287)days in the vorapaxar group and 145 (48-198)days in the placebo group. Six of the 13 (46%) participants had arteriovenous fistula functional maturation within 180days; two of six (33%) in the vorapaxar group and four of seven (57%) in the placebo group. There was one bleeding event in the placebo group.CONCLUSION: Fewer than half of participants had functional maturation within 180days after surgery, suggesting a major need for agents or strategies that enhance arteriovenous fistula maturation.

    View details for DOI 10.1177/1129729819887269

    View details for PubMedID 31774037

  • Co-transplantation of pure blood stem cells with antigen-specific but not bulk T cells augments functional immunity PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Mueller, A. M., Shashidhar, S., Kuepper, N. J., Kohrt, H. E., Florek, M., Negrin, R. S., Brown, J. M., Shizuru, J. A. 2012; 109 (15): 5820-5825


    Impaired immunity is a fundamental obstacle to successful allogeneic hematopoietic cell transplantation. Mature graft T cells are thought to provide protection from infections early after transplantation, but can cause life-threatening graft-vs.-host disease. Human CMV is a major pathogen after transplantation. We studied reactivity against the mouse homologue, murine CMV (MCMV), in lethally irradiated mice given allogeneic purified hematopoietic stem cells (HSCs) or HSCs supplemented with T cells or T-cell subsets. Unexpectedly, recipients of purified HSCs mounted superior antiviral responses compared with recipients of HSC plus unselected bulk T cells. Furthermore, supplementation of purified HSC grafts with CD8(+) memory or MCMV-specific T cells resulted in enhanced antiviral reactivity. Posttransplantation lymphopenia promoted massive expansion of MCMV-specific T cells when no competing donor T cells were present. In recipients of pure HSCs, naive and memory T cells and innate lymphoid cell populations developed. In contrast, the lymphoid pool in recipients of bulk T cells was dominated by effector memory cells. These studies show that pure HSC transplantations allow superior protective immunity against a viral pathogen compared with unselected mature T cells. This reductionist transplant model reveals the impact of graft composition on regeneration of host, newly generated, and mature transferred T cells, and underscores the deleterious effects of bulk donor T cells. Our findings lead us to conclude that grafts composed of purified HSCs provide an optimal platform for in vivo expansion of selected antigen-specific cells while allowing the reconstitution of a naive T-cell pool.

    View details for DOI 10.1073/pnas.1120237109

    View details for PubMedID 22440752

  • Early CMV Viremia Is Associated with Impaired Viral Control following Nonmyeloablative Hematopoietic Cell Transplantation with a Total Lymphoid Irradiation and Antithymocyte Globulin Preparative Regimen BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION Schaenman, J. M., Shashidhar, S., Rhee, C., Wong, J., Navato, S., Wong, R. M., Ho, D. Y., Arai, S., Johnston, L., Brown, J. M. 2011; 17 (5): 693-702


    The reconstitution of immune function after hematopoietic cell transplant (HCT) plays an important role in the control of viral infections. Both donor and recipient cytomegalovirus (CMV) serostatus has been shown to contribute to effective immune function; however, the influence of a nonmyeloablative preparative (NMA) regimen using total lymphoid irradiation (TLI) and antithymocyte globulin (ATG) on antiviral immune reconstitution has not yet been described. In 117 recipients of NMA HCT patients following ATG and TLI, not unexpectedly, CMV viremia was seen in approximately 60% of the seropositive patients regardless of donor serostatus, and recipient seropositivity significantly increased the odds of CMV viremia after transplant in a multivariate analysis. The administration of ATG and TLI resulted in a strikingly earlier viremia in the posttransplant period when compared to the previously reported timing of viremia following myeloablative preparative regimens, especially for transplant recipients who were seropositive for CMV with seronegative donors. Furthermore, early viremia in the setting of a CMV naïve donor was associated with a delay in functional antiviral control. These observations demonstrate the dynamic nature of immunity in relation to CMV antigen exposure in the complex environment resulting from NMA conditions where both donor and residual recipient immune response affect viral control.

    View details for DOI 10.1016/j.bbmt.2010.08.010

    View details for Web of Science ID 000290061500012

    View details for PubMedID 20736077

  • Combined Effects of Interleukin-7 and Stem Cell Factor Administration on Lymphopoiesis after Murine Bone Marrow Transplantation BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION Chung, B., Min, D., Joo, L. W., Krampf, M. R., Huang, J., Yang, Y., Shashidhar, S., Brown, J., Dudl, E. P., Weinberg, K. I. 2011; 17 (1): 48-60


    The decreased ability of the thymus to generate T cells after bone marrow transplantation (BMT) is a clinically significant problem. Interleukin (IL)-7 and stem cell factor (SCF) induce proliferation, differentiation, and survival of thymocytes. Although previous studies have shown that administration of recombinant human IL-7 (rhIL-7) after murine and human BMT improves thymopoiesis and immune function, whether administration of SCF exerts similar effects is unclear. To evaluate independent or combinatorial effects of IL-7 and SCF in post-BMT thymopoiesis, bone marrow (BM)-derived mesenchymal stem cells transduced ex vivo with the rhIL-7 or murine SCF (mSCF) genes were cotransplanted with T cell-depleted BM cells into lethally irradiated mice. Although rhIL-7 and mSCF each improved immune reconstitution, the combination treatment had a significantly greater effect than either cytokine alone. Moreover, the combination treatment significantly increased donor-derived common lymphoid progenitors (CLPs) in BM, suggesting that transplanted CLPs expand more rapidly in response to IL-7 and SCF and may promote immune reconstitution. Our findings demonstrate that IL-7 and SCF might be therapeutically useful for enhancing de novo T cell development. Furthermore, combination therapy may allow the administration of lower doses of IL-7, thereby decreasing the likelihood of IL-7-mediated expansion of mature T cells.

    View details for DOI 10.1016/j.bbmt.2010.07.027

    View details for Web of Science ID 000286173400003

    View details for PubMedID 20713165

  • The impact of regulatory T cells on T-cell immunity following hematopoietic cell transplantation BLOOD Nguyen, V. H., Shashidhar, S., Chang, D. S., Ho, L., Kambham, N., Bachmann, M., Brown, J. M., Negrin, R. S. 2008; 111 (2): 945-953


    Regulatory T cells (Tregs) prevent graft-versus-host disease (GvHD) by inhibiting the proliferation and function of conventional T cells (Tcons). However, the impact of Tregs on T-cell development and immunity following hematopoietic cell transplantation (HCT) is unknown. Using a murine GvHD model induced by Tcons, we demonstrate that adoptive transfer of Tregs leads to (1) abrogration of GvHD, (2) preservation of thymic and peripheral lymph node architecture, and (3) an accelerated donor lymphoid reconstitution of a diverse TCR-Vbeta repertoire. The resultant enhanced lymphoid reconstitution in Treg recipients protects them from lethal cytomegalovirus (MCMV) infection. By contrast, mice that receive Tcons alone have disrupted lymphoid organs from GvHD and remain lymphopenic with a restricted TCR-Vbeta repertoire and rapid death on MCMV challenge. Lymphocytes from previously infected Treg recipients generate secondary response specific to MCMV, indicating long-term protective immunity with transferred Tregs. Thymectomy significantly reduces survival after MCMV challenge in Treg recipients compared with euthymic controls. Our results indicate that Tregs enhance immune reconstitution by preventing GvHD-induced damage of the thymic and secondary lymphoid microenvironment. These findings provide new insights into the role of Tregs in affording protection to lymphoid stromal elements important for T-cell immunity.

    View details for DOI 10.1182/blood-2007-07-103895

    View details for PubMedID 17916743

  • Protection against lethal Aspergillus fumigatus infection in mice by allogeneic myeloid progenitors is not major histocompatibility complex restricted 45th Annual Meeting and Exhibition of the American-Society-of-Hematology Arber, C., Bitmansour, A., Shashidhar, S., Wang, S., Tseng, B., Brown, J. M. UNIV CHICAGO PRESS. 2005: 1666–71


    Invasive fungal infections are a leading cause of morbidity and mortality after myelotoxic chemotherapy or radiation exposure. The resulting depletion of myeloid precursors under these conditions appears to be the factor that limits approaches to accelerate immune reconstitution. In a murine model of myeloablation after radiation exposure, we demonstrated that highly purified common myeloid and granulocyte-monocyte progenitors (CMPs/GMPs) accelerated myeloid recovery and, thus, enhanced innate immunity as measured by survival after a lethal challenge with Aspergillus fumigatus. Of greatest significance was the demonstration that the protection afforded by CMPs/GMPs was not major histocompatibility complex restricted. Furthermore, the effect of CMP/GMP cellular therapy was additive with that of liposomal amphotericin B treatment. These observations greatly expand the potential donor pool and, thus, the clinical utility of CMP/GMP cellular therapy in patients with myeloid depletion.

    View details for Web of Science ID 000232333000022

    View details for PubMedID 16206084

  • Single infusion of myeloid progenitors reduces death from Aspergillus fumigatus following chemotherapy-induced neutropenia BLOOD Bitmansour, A., Cao, T. M., Chao, S., Shashidhar, S., Brown, J. M. 2005; 105 (9): 3535-3537


    Hematopoietic progenitors committed to the myeloid lineage, the common myeloid and granulocyte-monocyte progenitors (CMP/GMP), have been shown to protect against opportunistic pathogens following myeloablative radiation; however, the efficacy of this approach has not been studied in the setting of chemotherapy-induced neutropenia. In this mouse model, the infusion of CMP/GMP on the day after 5-fluorouracil (5-FU) administration (D+1) resulted in a significant increase in the number of splenic neutrophils by D+8 when compared with 5-FU-only controls (P = .02), the majority of which were CMP/GMP-derived (54%). Moreover, 19% and 28% of neutrophils in the blood and bone marrow, respectively, were CMP/GMP-derived. Survival following intranasal challenge with the fungus Aspergillus fumigatus was significantly higher in CMP/GMP-infused mice than the controls (56% and 33% respectively; P = .019). Thus, a single infusion of CMP/GMP enhances tissue neutrophil content and increases survival against a lethal challenge with A fumigatus in the setting of chemotherapy-induced neutropenia.

    View details for DOI 10.1182/blood-2004-2004-07-2676

    View details for Web of Science ID 000228797400029

    View details for PubMedID 15576478

    View details for PubMedCentralID PMC1895020

  • GPR56 is a GPCR that is overexpressed in gliomas and functions in tumor cell adhesion ONCOGENE Shashidhar, S., Lorente, G., Nagavarapu, U., Nelson, A., Kuo, J., Cummins, J., Nikolich, K., Urfer, R., Foehr, E. D. 2005; 24 (10): 1673-1682


    GPR56 (also known as TM7XN1) is a newly discovered orphan G-protein-coupled receptor (GPCR) of the secretin family that has a role in the development of neural progenitor cells and has been linked to developmental malformations of the human brain. GPR56 diverges from other secretin-like family members in that it has an extremely large N-terminal extracellular region (381 amino acids) and contains a novel feature among this new subclass, consisting of four cysteine residues that define a GPCR proteolytic site (GPS motif) located just before the first transmembrane spanning domain. The rest of the amino-terminal domain contains a large number of possible N- and O-linked glycosylation sites similar to mucin-like proteins. These features suggest a role in cell-cell, or cell-matrix interactions. Here, we demonstrate upregulation of GPR56 in glioblastoma multiforme tumors using functional genomics. Immunohistochemistry studies confirmed the expression of GPR56 protein in a majority of glioblastoma/astrocytoma tumor samples with undetectable levels of expression in normal adult brain tissue. Immunofluorescence analysis of human glioma cells using anti-GPR56 antibodies demonstrate that GPR56 is expressed on the leading edge of membrane filopodia and colocalizes with alpha-actinin. Purified recombinant GPR56 extracellular domain protein inhibits glioma cell adhesion and causes abnormal cytoskeletal morphology and cell rounding. These results indicate that the extracellular domain may compete for unidentified ligand(s), and block the normal function of GPR56 in cell attachment. In reporter assays, overexpression of GPR56 activates the NF-kappaB, PAI-1 and TCF transcriptional response elements. These pathways have been implicated in cytoskeletal signaling, adhesion and tumor biology. The above results indicate that GPR56 serves as an adhesion GPCR and is involved in adhesion signaling.

    View details for DOI 10.1038/sj.onc.1208395

    View details for Web of Science ID 000227345100003

    View details for PubMedID 15674329