Dr. Baker is a Clinical Assistant Professor in the Division of Immunology and Rheumatology at Stanford University with a focus on patient care, bench research, and clinical trials. He studied at Harvard Medical School and trained in Internal Medicine at the Massachusetts General Hospital. He subsequently came to Stanford for his fellowship in Rheumatology, and spent several years in the laboratory of Dr. William Robinson conducting basic research related to characterizing novel autoantibodies in ANCA-vasculitis and investigating the immune profile of patients with IgG4-related disease. Under the mentorship of Dr. Mark Genovese, he has authored several investigator-initiated clinical trials with a focus on sarcoidosis, Sjogren's syndrome, and IgG4-related disease. He serves as one of the founders and Co-Directors of the Stanford Multidisciplinary Sarcoidosis Program.
- IgG4-related disease
- Sjogren's syndrome
- Cardiac sarcoidosis
- Systemic lupus erythematosus
- Rheumatoid Arthritis
Clinical Assistant Professor, Medicine - Immunology & Rheumatology
Honors & Awards
Translational Research and Applied Medicine Award, Stanford University (9/1/18 - 9/1/19)
Scientist Development Award, Rheumatology Research Foundation (2/1/17 - 1/31/18)
KL2 Stanford Spectrum Mentored Career Development Award, National Institutes of Health (7/1/17 - 6/30/19)
Distinguished Fellow Award, American College of Rheumatology (11/28/16)
Bevra Hahn Distinguished Fellow Scholarship, California Rheumatology Alliance (5/24/16)
Ruth L. Kirschstein National Research Service Award, National Institutes of Health (7/1/16 - 1/31/17)
ACR/EULAR Exchange Program Award, American College of Rheumatology (6/12/17)
Master of Science, Stanford University, EPIDM-MS (2019)
Board Certification: Internal Medicine, American Board of Internal Medicine (2014)
Fellowship:Stanford University Rheumatology Fellowship (2016) CA
Board Certification: Rheumatology, American Board of Internal Medicine (2016)
Residency:Massachusetts General Hospital Internal Medicine Residency (2014) MA
Medical Education:Harvard Medical School (2011) MA
Bachelor of Arts, Pomona College (2004)
Sarilumab in Patients With Glucocorticoid-Dependent Sarcoidosis
The purpose of this study is to compare the effectiveness and the safety of sarilumab in patients with glucocorticoid-dependent sarcoidosis.
A Crossover Study to Compare RAYOS to IR Prednisone to Improve Fatigue and Morning Symptoms for SLE
To compare the effect of RAYOS® versus immediate-release (IR) prednisone on fatigue as measured by Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-F).
Stanford is currently not accepting patients for this trial. For more information, please contact Mark Genovese, 650-498-5630.
Safety and Efficacy of Filgotinib and Lanraplenib in Adults With Lupus Membranous Nephropathy (LMN)
The primary objective of this study is to evaluate the efficacy of filgotinib and lanreplenib (previously GS-9876) in adults with Lupus Membranous Nephropathy (LMN).
Stanford is currently not accepting patients for this trial.
- Dermatomyositis Associated With a Skull Base Chondrosarcoma JCR-JOURNAL OF CLINICAL RHEUMATOLOGY 2019; 25 (4): E50–E53
TNF-alpha inhibition for the treatment of cardiac sarcoidosis.
Seminars in arthritis and rheumatism
Tumor necrosis factor alpha (TNF-α) inhibitors are increasingly being used for treating refractory cardiac sarcoidosis. There is a theoretical risk, however, that these therapies can worsen heart failure, and reports on efficacy and safety are lacking.We conducted a retrospective review of all cardiac sarcoidosis patients seen at Stanford University from 2009 to 2018. Data were collected on patient demographics, diagnostic testing, and treatment outcomes.We identified 77 cardiac sarcoidosis patients, of which 20 (26%) received TNF-α inhibitor treatment. The majority were treated for progressive heart failure or tachyarrhythmia, along with worsening imaging findings. All TNF-α inhibitor treated patients demonstrated meaningful benefit, as assessed by changes in advanced imaging, echocardiographic measures of cardiac function, and prednisone use.A large cohort (n = 77) of cardiac sarcoidosis patients has been treated at Stanford University. Roughly one-fourth of these patients (n = 20) received TNF-α inhibitors. Of these patients, none had worsening heart failure and all saw clinical benefit. These results help support the use of TNF-α inhibitors for the treatment of cardiac sarcoidosis based on real-world evidence and highlight the need for future prospective studies.
View details for DOI 10.1016/j.semarthrit.2019.11.004
View details for PubMedID 31806154
Security and Privacy Qualities of Medical Devices: An Analysis of FDA Postmarket Surveillance
2012; 7 (7)
Medical devices increasingly depend on computing functions such as wireless communication and Internet connectivity for software-based control of therapies and network-based transmission of patients' stored medical information. These computing capabilities introduce security and privacy risks, yet little is known about the prevalence of such risks within the clinical setting.We used three comprehensive, publicly available databases maintained by the Food and Drug Administration (FDA) to evaluate recalls and adverse events related to security and privacy risks of medical devices.Review of weekly enforcement reports identified 1,845 recalls; 605 (32.8%) of these included computers, 35 (1.9%) stored patient data, and 31 (1.7%) were capable of wireless communication. Searches of databases specific to recalls and adverse events identified only one event with a specific connection to security or privacy. Software-related recalls were relatively common, and most (81.8%) mentioned the possibility of upgrades, though only half of these provided specific instructions for the update mechanism.Our review of recalls and adverse events from federal government databases reveals sharp inconsistencies with databases at individual providers with respect to security and privacy risks. Recalls related to software may increase security risks because of unprotected update and correction mechanisms. To detect signals of security and privacy problems that adversely affect public health, federal postmarket surveillance strategies should rethink how to effectively and efficiently collect data on security and privacy problems in devices that increasingly depend on computing systems susceptible to malware.
View details for DOI 10.1371/journal.pone.0040200
View details for Web of Science ID 000306956300012
View details for PubMedID 22829874
View details for PubMedCentralID PMC3400651
Enhancement of DNA tumor vaccine efficacy by gene gun-mediated codelivery of threshold amounts of plasmid-encoded helper antigen
2009; 113 (1): 37-45
Nucleic acid-based vaccines are effective in infectious disease models but have yielded disappointing results in tumor models when tumor-associated self-antigens are used. Incorporation of helper epitopes from foreign antigens into tumor vaccines might enhance the immunogenicity of DNA vaccines without increasing toxicity. However, generation of fusion constructs encoding both tumor and helper antigens may be difficult, and resulting proteins have unpredictable physical and immunologic properties. Furthermore, simultaneous production of equal amounts of highly immunogenic helper and weakly immunogenic tumor antigens in situ could favor development of responses against the helper antigen rather than the antigen of interest. We assessed the ability of 2 helper antigens (beta-galactosidase or fragment C of tetanus toxin) encoded by one plasmid to augment responses to a self-antigen (lymphoma-associated T-cell receptor) encoded by a separate plasmid after codelivery into skin by gene gun. This approach allowed adjustment of the relative ratios of helper and tumor antigen plasmids to optimize helper effects. Incorporation of threshold (minimally immunogenic) amounts of helper antigen plasmid into a DNA vaccine regimen dramatically increased T cell-dependent protective immunity initiated by plasmid-encoded tumor-associated T-cell receptor antigen. This simple strategy can easily be incorporated into future vaccine trials in experimental animals and possibly in humans.
View details for DOI 10.1182/blood-2008-01-136267
View details for Web of Science ID 000262162800010
View details for PubMedID 18832136
View details for PubMedCentralID PMC2614641