Crystal Botham, Ph.D. is Director of the Office of Pediatric Research Development in the Department of Pediatrics at Stanford University ( Dr. Botham provides strategic advice to faculty and others to enable competitive funding applications and productive research programs.

Dr. Botham is also the Director & Founder of the Biosciences Grant Writing Academy ( The Grant Writing Academy supports graduate and postdoctoral trainees in developing and articulating research strategies to tackle important scientific questions.

Current Role at Stanford

• Providing individualized grantsmanship assistance to postdoctoral fellows and faculty
• Editing and critically evaluating grant applications to improve funding potential
• Interpreting sponsor requirements and providing strategic advice
• Identifying a diverse portfolio of funding opportunities
• Designing and facilitating courses to enable postdoctoral fellows to develop competitive Career Development applications
• Developing and presenting at workshops on grant writing and proposal submission
• Coordinating completion of subcontracts and large collaborative projects

Institute Affiliations

Honors & Awards

  • Collaboration Award, Department of Pediatrics, Stanford University (2021)
  • Trainee Abstract Award, American Association of Immunologists (2011)
  • Tashia and John Morgridge Endowed Postdoctoral Fellow, Child Health Research Institute (CHRI) at Stanford University (2009-2011)
  • Ruth L. Kirschstein National Research Service Award (F32AI082936), NIH, NIAID (2009-2010)
  • Winning image for Journal cover, May issue of PLoS Pathogen (2008)
  • Predoctoral Fellowship Award, American Heart Association- Pacific Mountain (2005-2006)
  • Summer Research Award, Department of Biology, University of the Pacific (2002)
  • Award for Summer Research, Max and Victoria Dreyfus Foundation at the University of the Pacific (2001)
  • Participant, Colgate University's Study Group at NIH (2001)
  • Outstanding recognition for poster presentation, Pacific Undergraduate Research Conference (2000)
  • Outstanding recognition for speech presentation, West Coast Biological Sciences Undergraduate Research Conference (2000)

Education & Certifications

  • Certification, Stanford University, Strategic Decision and Risk Management (2016)
  • Certification, Stanford University, Stanford Advanced Project Management (2014)
  • Postdoctoral Fellow, Stanford University, Immunology (2011)
  • Ph.D., University of Oregon, Biology (2007)
  • B.S., University of the Pacific, Biology (2001)

All Publications

  • Ten simple rules for writing compelling recommendation letters. PLoS computational biology Kong, J. H., Steele, L. J., Botham, C. M. 2021; 17 (2): e1008656

    View details for DOI 10.1371/journal.pcbi.1008656

    View details for PubMedID 33630854

  • Biosciences Proposal Bootcamp: Structured peer and faculty feedback improves trainees' proposals and grantsmanship self-efficacy. PloS one Botham, C. M., Brawn, S. n., Steele, L. n., Barrón, C. B., Kleppner, S. R., Herschlag, D. n. 2020; 15 (12): e0243973


    Grant writing is an essential skill to develop for academic and other career success but providing individual feedback to large numbers of trainees is challenging. In 2014, we launched the Stanford Biosciences Grant Writing Academy to support graduate students and postdocs in writing research proposals. Its core program is a multi-week Proposal Bootcamp designed to increase the feedback writers receive as they develop and refine their proposals. The Proposal Bootcamp consisted of two-hour weekly meetings that included mini lectures and peer review. Bootcamp participants also attended faculty review workshops to obtain faculty feedback. Postdoctoral trainees were trained and hired as course teaching assistants and facilitated weekly meetings and review workshops. Over the last six years, the annual Bootcamp has provided 525 doctoral students and postdocs with multi-level feedback (peer and faculty). Proposals from Bootcamp participants were almost twice as likely to be funded than proposals from non-Bootcamp trainees. Overall, this structured program provided opportunities for feedback from multiple peer and faculty reviewers, increased the participants' confidence in developing and submitting research proposals, while accommodating a large number of participants.

    View details for DOI 10.1371/journal.pone.0243973

    View details for PubMedID 33370337

  • How to design a winning fellowship proposal. Nature Botham, C. M., Evans, T. M. 2018; 563 (7730): 283

    View details for DOI 10.1038/d41586-018-07297-x

    View details for PubMedID 30401856

  • Ten simple rules for scientists: Improving your writing productivity. PLoS computational biology Peterson, T. C., Kleppner, S. R., Botham, C. M. 2018; 14 (10): e1006379

    View details for PubMedID 30286072

  • Ten simple rules for writing a career development award proposal PLOS COMPUTATIONAL BIOLOGY Botham, C. M., Arribere, J. A., Brubaker, S. W., Beier, K. T. 2017; 13 (12): e1005863

    View details for PubMedID 29240828

    View details for PubMedCentralID PMC5730102

  • Ten Simple Rules for Writing a Postdoctoral Fellowship PLOS COMPUTATIONAL BIOLOGY Yuan, K., Cai, L., Ngok, S., Ma, L., Botham, C. M. 2016; 12 (7): e1004934

    View details for PubMedID 27415752

    View details for PubMedCentralID PMC4945040

  • Clinical trials of adult stem cell therapy for peripheral artery disease. Methodist DeBakey cardiovascular journal Botham, C. M., Bennett, W. L., Cooke, J. P. 2013; 9 (4): 201-205


    Peripheral artery disease (PAD) refers to noncoronary vascular disease affecting the peripheral arteries. Most commonly the term is applied to occlusive arterial disease affecting the limb arteries, typically due to atherosclerosis. Preclinical studies indicate that a variety of stem cell therapies provide growth factors and cytokines for therapeutic angiogenesis. Small clinical trials with bone marrow mononuclear cells, as well as other cell types, have shown promise. However, mechanisms of therapeutic effect, if any, are not understood. Definitive clinical trials are needed to determine if there are any beneficial effects on functional capacity or morbidity.

    View details for PubMedID 24298310

  • Endothelial Cells Derived From Nuclear Reprogramming CIRCULATION RESEARCH Wong, W. T., Huang, N. F., Botham, C. M., Sayed, N., Cooke, J. P. 2012; 111 (10): 1363-1375


    The endothelium plays a pivotal role in vascular homeostasis, regulating the tone of the vascular wall, and its interaction with circulating blood elements. Alterations in endothelial functions facilitate the infiltration of inflammatory cells and permit vascular smooth muscle proliferation and platelet aggregation. Therefore, endothelial dysfunction is an early event in disease processes including atherosclerosis, and because of its critical role in vascular health, the endothelium is worthy of the intense focus it has received. However, there are limitations to studying human endothelial function in vivo, or human vascular segments ex vivo. Thus, methods for endothelial cell (EC) culture have been developed and refined. Recently, methods to derive ECs from pluripotent cells have extended the scientific range of human EC studies. Pluripotent stem cells may be generated, expanded, and then differentiated into ECs for in vitro studies. Constructs for molecular imaging can also be employed to facilitate tracking these cells in vivo. Furthermore, one can generate patient-specific ECs to study the effects of genetic or epigenetic alterations on endothelial behavior. Finally, there is the opportunity to apply these cells for vascular therapy. This review focuses on the generation of ECs from stem cells; their characterization by genetic, histological, and functional studies; and their translational applications.

    View details for DOI 10.1161/CIRCRESAHA.111.247213

    View details for Web of Science ID 000310501300017

    View details for PubMedID 23104878

    View details for PubMedCentralID PMC3526979

  • Identification of genetic modifiers of CagA-induced epithelial disruption in Drosophila. Frontiers in cellular and infection microbiology Reid, D. W., Muyskens, J. B., Neal, J. T., Gaddini, G. W., Cho, L. Y., Wandler, A. M., Botham, C. M., Guillemin, K. 2012; 2: 24-?


    Helicobacter pylori strains containing the CagA protein are associated with high risk of gastric diseases including atrophic gastritis, peptic ulcers, and gastric cancer. CagA is injected into host cells via a Type IV secretion system where it activates growth factor-like signaling, disrupts cell-cell junctions, and perturbs host cell polarity. Using a transgenic Drosophila model, we have shown that CagA expression disrupts the morphogenesis of epithelial tissues such as the adult eye. Here we describe a genetic screen to identify modifiers of CagA-induced eye defects. We determined that reducing the copy number of genes encoding components of signaling pathways known to be targeted by CagA, such as the epidermal growth factor receptor (EGFR), modified the CagA-induced eye phenotypes. In our screen of just over half the Drosophila genome, we discovered 12 genes that either suppressed or enhanced CagA's disruption of the eye epithelium. Included in this list are genes involved in epithelial integrity, intracellular trafficking, and signal transduction. We investigated the mechanism of one suppressor, encoding the epithelial polarity determinant and junction protein Coracle, which is homologous to the mammalian Protein 4.1. We found that loss of a single copy of coracle improved the organization and integrity of larval retinal epithelia expressing CagA, but did not alter CagA's localization to cell junctions. Loss of a single copy of the coracle antagonist crumbs enhanced CagA-associated disruption of the larval retinal epithelium, whereas overexpression of crumbs suppressed this phenotype. Collectively, these results point to new cellular pathways whose disruption by CagA are likely to contribute to H. pylori-associated disease pathology.

    View details for DOI 10.3389/fcimb.2012.00024

    View details for PubMedID 22919616

  • Cationic Lipid/DNA Complex-Adjuvanted Influenza A Virus Vaccination Induces Robust Cross-Protective Immunity JOURNAL OF VIROLOGY Hong, D. K., Chang, S., Botham, C. M., Giffon, T. D., Fairman, J., Lewis, D. B. 2010; 84 (24): 12691-12702


    Influenza A virus is a negative-strand segmented RNA virus in which antigenically distinct viral subtypes are defined by the hemagglutinin (HA) and neuraminidase (NA) major viral surface proteins. An ideal inactivated vaccine for influenza A virus would induce not only highly robust strain-specific humoral and T-cell immune responses but also cross-protective immunity in which an immune response to antigens from a particular viral subtype (e.g., H3N2) would protect against other viral subtypes (e.g., H1N1). Cross-protective immunity would help limit outbreaks from newly emerging antigenically novel strains. Here, we show in mice that the addition of cationic lipid/noncoding DNA complexes (CLDC) as adjuvant to whole inactivated influenza A virus vaccine induces significantly more robust adaptive immune responses both in quantity and quality than aluminum hydroxide (alum), which is currently the most widely used adjuvant in clinical human vaccination. CLDC-adjuvanted vaccine induced higher total influenza virus-specific IgG, particularly for the IgG2a/c subclass. Higher levels of multicytokine-producing influenza virus-specific CD4 and CD8 T cells were induced by CLDC-adjuvanted vaccine than with alum-adjuvanted vaccine. Importantly, CLDC-adjuvanted vaccine provided significant cross-protection from either a sublethal or lethal influenza A viral challenge with a different subtype than that used for vaccination. This superior cross-protection afforded by the CLDC adjuvant required CD8 T-cell recognition of viral peptides presented by classical major histocompatibility complex class I proteins. Together, these results suggest that CLDC has particular promise for vaccine strategies in which T cells play an important role and may offer new opportunities for more effective control of human influenza epidemics and pandemics by inactivated influenza virus vaccine.

    View details for DOI 10.1128/JVI.00769-10

    View details for PubMedID 20943978

  • A transgenic Drosophila model demonstrates that the Helicobacter pylori CagA protein functions as a eukaryotic Gab adaptor PLOS PATHOGENS Botham, C. M., Wandler, A. M., Guillemin, K. 2008; 4 (5)


    Infection with the human gastric pathogen Helicobacter pylori is associated with a spectrum of diseases including gastritis, peptic ulcers, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue lymphoma. The cytotoxin-associated gene A (CagA) protein of H. pylori, which is translocated into host cells via a type IV secretion system, is a major risk factor for disease development. Experiments in gastric tissue culture cells have shown that once translocated, CagA activates the phosphatase SHP-2, which is a component of receptor tyrosine kinase (RTK) pathways whose over-activation is associated with cancer formation. Based on CagA's ability to activate SHP-2, it has been proposed that CagA functions as a prokaryotic mimic of the eukaryotic Grb2-associated binder (Gab) adaptor protein, which normally activates SHP-2. We have developed a transgenic Drosophila model to test this hypothesis by investigating whether CagA can function in a well-characterized Gab-dependent process: the specification of photoreceptors cells in the Drosophila eye. We demonstrate that CagA expression is sufficient to rescue photoreceptor development in the absence of the Drosophila Gab homologue, Daughter of Sevenless (DOS). Furthermore, CagA's ability to promote photoreceptor development requires the SHP-2 phosphatase Corkscrew (CSW). These results provide the first demonstration that CagA functions as a Gab protein within the tissue of an organism and provide insight into CagA's oncogenic potential. Since many translocated bacterial proteins target highly conserved eukaryotic cellular processes, such as the RTK signaling pathway, the transgenic Drosophila model should be of general use for testing the in vivo function of bacterial effector proteins and for identifying the host genes through which they function.

    View details for DOI 10.1371/journal.ppat.1000064

    View details for Web of Science ID 000256668900012

    View details for PubMedID 18483552

  • Helicobacter pylori CagA induces AGS cell elongation through a cell retraction defect that is independent of Cdc42, Rac1, and Arp2/3 INFECTION AND IMMUNITY Bourzac, K. M., Botham, C. M., Guillemin, K. 2007; 75 (3): 1203-1213


    Helicobacter pylori, which infects over one-half the world's population, is a significant risk factor in a spectrum of gastric diseases, including peptic ulcers and gastric cancer. Strains of H. pylori that deliver the effector molecule CagA into host cells via a type IV secretion system are associated with more severe disease outcomes. In a tissue culture model of infection, CagA delivery results in a dramatic cellular elongation referred to as the "hummingbird" phenotype, which is characterized by long, thin cellular extensions. These actin-based cytoskeletal rearrangements are reminiscent of structures that are regulated by Rho GTPases and the Arp2/3 complex. We tested whether these signaling pathways were important in the H. pylori-induced cell elongation phenotype. Contrary to our expectations, we found that these molecules are dispensable for cell elongation. Instead, time-lapse video microscopy revealed that cells infected by cagA(+) H. pylori become elongated because they fail to release their back ends during cell locomotion. Consistent with a model in which CagA causes cell elongation by inhibiting the disassembly of adhesive cell contacts at migrating cells' lagging ends, immunohistochemical analysis revealed that focal adhesion complexes persist at the distal tips of elongated cell projections. Thus, our data implicate a set of signaling molecules in the hummingbird phenotype that are different than the molecules previously suspected.

    View details for DOI 10.1128/IAI.01702-06

    View details for Web of Science ID 000244733900014

    View details for PubMedID 17194805