Ragini Adams, MD is a Clinical Assistant Professor in the Division of Pediatric Hematology, Oncology, Stem Cell Transplant and Regenerative Medicine at the Lucile Packard Children's Hospital, Stanford University School of Medicine. Dr. Adams obtained her BS in Biology at the Massachusetts Institute of Technology where she also completed her thesis in the field of Medical Anthropology. She then joined the Stanford University Cancer Center where she managed clinical trials related to the the study of biomarkers in Diffuse Large B Cell Lymphoma. She then earned her MD from the East Tennessee State University Quillen College of Medicine. Dr. Adams completed a residency in Pediatrics at Georgetown University where her research focused on multidisciplinary therapies for retinoblastoma and hepatoblastoma. Currently, Dr. Adams is dedicated to the personal and comprehensive care of her pediatric hematology and oncology patients extending across of a variety of diseases. Dr. Adams's present research in the Alizadeh Lab is focused on using circulating tumor DNA to genetically profile and monitor pediatric patients diagnosed with Hodgkin Lymphoma. In 2021, Dr. Adams completed her fellowship in Pediatric Hematology and Oncology at Stanford University. Dr. Adams is a board certified pediatrician and is also practicing in Pediatric Urgent Care.
- Pediatric Hodgkin Lymphoma
- Circulating Tumor DNA
- Pediatric Hematology-Oncology
Clinical Assistant Professor, Pediatrics - Hematology & Oncology
Honors & Awards
Tashia and John Morgridge Endowed Postdoctoral Fellow, Stanford Maternal and Child Health Research Institute (MCHRI) (2019 - 2021)
Fellowship: Stanford University Pediatric Hematology Oncology Fellowship (2021) CA
Board Certification: American Board of Pediatrics, Pediatrics (2018)
Residency: MedStar Georgetown University Pediatrics Program (2018) DC
Medical Education: East Tennessee State University Medicine (2015) TN
Board Certification, American Board of Pediatrics, General Pediatrics (2018)
Residency, Georgetown University, Pediatrics (2018)
MD, East Tennessee State University Quillen College of Medicine (2015)
BS, Massachusetts Institute of Technology, Biology, Anthropology (2008)
Current Research and Scholarly Interests
Circulating tumor DNA (ctDNA) is DNA that is released by tumor cells into the blood of the host; it is a fraction of all the cell free DNA (cfDNA) that is present. Because ctDNA contains the mutations of the original tumor, it is detectable using next generation sequencing and is an accurate surrogate measure of tumor burden. Therefore, ctDNA is an emerging biomarker in Hodgkin Lymphoma (HL) that is specific, quantifiable, and can be measured by noninvasive means. Using ctDNA to explore the genetic landscape of pediatric HL and monitor the response of these patients to therapy has never been done before and is my current focus of study.
- Evans Syndrome Medscape. 2020
Pathophysiological significance and therapeutic targeting of germinal center kinase in diffuse large B-cell lymphoma.
2016; 128 (2): 239-248
Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of non-Hodgkin lymphoma (NHL), yet 40-50% of patients will eventually succumb to their disease demonstrating a pressing need for novel therapeutic options. Gene expression profiling has identified messenger RNA's that lead to transformation, but critical events transforming cells are normally executed by kinases. Therefore, we hypothesized that previously unrecognized kinases may contribute to DLBCL pathogenesis. We performed the first comprehensive analysis of global kinase activity in DLBCL, to identify novel therapeutic targets, and discovered that Germinal Center Kinase (GCK) was extensively activated. GCK RNA interference and small molecule inhibition induced cell cycle arrest and apoptosis in DLBCL cell lines and primary tumors in vitro and decreased the tumor growth rate in vivo, resulting in a significantly extended lifespan of mice bearing DLBCL xenografts. GCK expression was also linked to adverse clinical outcome in a cohort of 151 primary DLBCL patients. These studies demonstrate, for the first time, that GCK is a molecular therapeutic target in DLBCL tumors and that inhibiting GCK may significantly extend DLBCL patient survival. Since the majority of DLBCL tumors (~80%) exhibit activation of GCK, this therapy may be applicable to most patients.
View details for DOI 10.1182/blood-2016-02-696856
View details for PubMedID 27151888
The effect of iron- and light-limitation on phytoplankton communities of deep chlorophyll maxima of the western Pacific Ocean
JOURNAL OF MARINE RESEARCH
2010; 68 (2): 283–308
View details for DOI 10.1357/002224010793721433
View details for Web of Science ID 000285702200005
Lymphoma cell VEGFR2 expression detected by immunohistochemistry predicts poor overall survival in diffuse large B cell lymphoma treated with immunochemotherapy (R-CHOP)
BRITISH JOURNAL OF HAEMATOLOGY
2010; 148 (2): 235-244
Diffuse large B cell lymphoma (DLBCL) is clinically and biologically heterogeneous. In most cases of DLBCL, lymphoma cells co-express vascular endothelial growth factor (VEGF) and its receptors VEGFR1 and VEGFR2, suggesting autocrine in addition to angiogenic effects. We enumerated microvessel density and scored lymphoma cell expression of VEGF, VEGFR1, VEGFR2 and phosphorylated VEGFR2 in 162 de novo DLBCL patients treated with R-CHOP (rituximab, cyclophosphamide, vincristine, doxorubicin and prednisone)-like regimens. VEGFR2 expression correlated with shorter overall survival (OS) independent of International Prognostic Index (IPI) (P = 0.0028). Phosphorylated VEGFR2 (detected in 13% of cases) correlated with shorter progression-free survival (PFS, P = 0.044) and trended toward shorter OS on univariate analysis. VEGFR1 was not predictive of survival on univariate analysis, but it did correlate with better OS on multivariate analysis with VEGF, VEGFR2 and IPI (P = 0.036); in patients with weak VEGFR2, lack of VEGFR1 coexpression was significantly correlated with poor OS independent of IPI (P = 0.01). These results are concordant with our prior finding of an association of VEGFR1 with longer OS in DLBCL treated with chemotherapy alone. We postulate that VEGFR1 may oppose autocrine VEGFR2 signalling in DLBCL by competing for VEGF binding. In contrast to our prior results with chemotherapy alone, microvessel density was not prognostic of PFS or OS with R-CHOP-like therapy.
View details for DOI 10.1111/j.1365-2141.2009.07942.x
View details for PubMedID 19821819