Bio

Clinical Focus


  • Pediatric Hematology
  • Pediatric Oncology
  • Pediatric Stem Cell Transplantation
  • Pediatrics

Academic Appointments


Honors & Awards


  • Member, Stanford Society of Physician Scholare (2010 -present)
  • Paul and Yuanbi Fellow of Pediatrics, Department of Pediatrics (10/01/2009-9/30/2010)
  • MD Scholar, California Institute of Regenerative Medicine (10/01/2010-present)

Boards, Advisory Committees, Professional Organizations


  • Reviewer, Pediatrics On Call (2013 - Present)

Professional Education


  • Board Certification: Pediatric Hematology-Oncology, American Board of Pediatrics (2013)
  • Fellowship:Stanford University School of Medicine (2012) CA
  • Board Certification: Pediatrics, American Board of Pediatrics (2010)
  • Residency:Univ of Chicago - Pritzker School of Medicine (2009) IL
  • Medical Education:Univ of Chicago - Pritzker School of Medicine (2006) IL
  • Doctor of Philosophy, University of Chicago, Genetics, Cell Biology (2004)
  • Doctor of Medicine, University of Chicago (2006)

Stanford Advisors


Research & Scholarship

Current Research and Scholarly Interests


Currently, I am involved research in a number of fields:

BASIC:
1) the role of the retinoblastoma family of tumor suppressor proteins in the regulation of thymic cellularity and its downstream effect on the immune system
2) immune reconstitution following therapy
3) enhancing immune response to cancer antigens

TRANSLATIONAL:
1) Development of primary retinoblastoma samples as a model system for the study of pediatric cancers and of cell (pluri)potency and differentiation status

CLINICAL (all at various stages of progress):
1) Transplantation for Hodkgin Disease
2) Late effects of transplantation

Clinical Trials


  • Cancer Biology of Retinoblastoma Recruiting

    Many children with the childhood cancer, Retinoblastoma, have surgery to remove the tumor and sometimes the entire eye. The purpose of this study is to collect the extra tissue from patients who undergo tumor removal for laboratory experiments that will help us understand not only what occurs in retinoblastoma cells but also how cells normally function. Some of these studies will include an evaluation of how cells control the way that genes are expressed, how cells "know" to become retinal cells, how cells remain retinal cells, how cells lose their identity as retinal cells, what changes make retinoblastoma cells different from normal retinal cells, and what changes make some retinoblastomas worse than others.

    View full details

Lab Affiliations


Publications

Journal Articles


  • Inactivation of the RB family prevents thymus involution and promotes thymic function by direct control of Foxn1 expression. journal of experimental medicine Garfin, P. M., Min, D., Bryson, J. L., Serwold, T., Edris, B., Blackburn, C. C., Richie, E. R., Weinberg, K. I., Manley, N. R., Sage, J., Viatour, P. 2013; 210 (6): 1087-1097

    Abstract

    Thymic involution during aging is a major cause of decreased production of T cells and reduced immunity. Here we show that inactivation of Rb family genes in young mice prevents thymic involution and results in an enlarged thymus competent for increased production of naive T cells. This phenotype originates from the expansion of functional thymic epithelial cells (TECs). In RB family mutant TECs, increased activity of E2F transcription factors drives increased expression of Foxn1, a central regulator of the thymic epithelium. Increased Foxn1 expression is required for the thymic expansion observed in Rb family mutant mice. Thus, the RB family promotes thymic involution and controls T cell production via a bone marrow-independent mechanism, identifying a novel pathway to target to increase thymic function in patients.

    View details for DOI 10.1084/jem.20121716

    View details for PubMedID 23669396

  • Expression of the Arf tumor suppressor gene is controlled by Tgf beta 2 during development DEVELOPMENT Freeman-Anderson, N. E., Zheng, Y., McCalla-Martin, A. C., Treanor, L. M., Zhao, Y. D., Garfin, P. M., He, T., Mary, M. N., Thornton, J. D., Anderson, C., Gibbons, M., Saab, R., Baumer, S. H., Cunningham, J. M., Skapek, S. X. 2009; 136 (12): 2081-2089

    Abstract

    The Arf tumor suppressor (also known as Cdkn2a) acts as an oncogene sensor induced by ;abnormal' mitogenic signals in incipient cancer cells. It also plays a crucial role in embryonic development: newborn mice lacking Arf are blind due to a pathological process resembling severe persistent hyperplastic primary vitreous (PHPV), a human eye disease. The cell-intrinsic mechanism implied in the oncogene sensor model seems unlikely to explain Arf regulation during embryo development. Instead, transforming growth factor beta2 (Tgfbeta2) might control Arf expression, as we show that mice lacking Tgfbeta2 have primary vitreous hyperplasia similar to Arf(-/-) mice. Consistent with a potential linear pathway, Tgfbeta2 induces Arf transcription and p19(Arf) expression in cultured mouse embryo fibroblasts (MEFs); and Tgfbeta2-dependent cell cycle arrest in MEFs is maintained in an Arf-dependent manner. Using a new model in which Arf expression can be tracked by beta-galactosidase activity in Arf(lacZ/+) mice, we show that Tgfbeta2 is required for Arf transcription in the developing vitreous as well as in the cornea and the umbilical arteries, two previously unrecognized sites of Arf expression. Chemical and genetic strategies show that Arf promoter induction depends on Tgfbeta receptor activation of Smad proteins; the induction correlates with Smad2 phosphorylation in MEFs and Arf-expressing cells in vivo. Chromatin immunoprecipitation shows that Smads bind to genomic DNA proximal to Arf exon 1beta. In summary, Tgfbeta2 and p19(Arf) act in a linear pathway during embryonic development. We present the first evidence that p19(Arf) expression can be coupled to extracellular cues in normal cells and suggest a new mechanism for Arf control in tumor cells.

    View details for DOI 10.1242/dev.033548

    View details for Web of Science ID 000266296400012

    View details for PubMedID 19465598

  • Prostacyclin release by rat cardiac fibroblasts - Inhibition of collagen expression HYPERTENSION Yu, H., Gallagher, A. M., Garfin, P. M., Printz, M. P. 1997; 30 (5): 1047-1053

    Abstract

    Cardiac fibroblasts, as the source of extracellular matrix for the left ventricle, subserve important functions to cardiac remodeling and fibrotic development following myocardial infarction or with pressure-overload cardiac hypertrophy. The fibroblast may be the target cell for angiotensin-converting enzyme inhibitors (ACEI) that are cardioprotective and reverse collagen deposition and remodeling but whose mechanisms of action remain controversial. Because we previously documented phenotypic differences between cardiac fibroblasts from the spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) left ventricle, the present study evaluated whether phenotypic differences also exist in the release of endogenous arachidonic acid metabolites or in the activation of phospholipase D, and the importance of observed differences to the formation of collagen and the mechanism of action of ACEI. The experimental design compared endogenous sources of arachidonic acid with exogenous prelabeling of cells. Angiotensin II stimulated greater arachidonic acid release than bradykinin, and WKY cells were more responsive than SHR. The major prostanoid formed by cardiac fibroblasts was prostaglandin I2 (PGI2), with more prostacyclin production by WKY cells than SHR cells both under nonstimulated conditions and in response to angiotensin II or bradykinin. Beraprost, a PGI2 analogue, was shown to decrease growth rate and DNA synthesis of fibroblasts and to inhibit mRNA expression for collagen types I and III, with SHR cells being less responsive to beraprost than WKY cells. These results potentially implicate eicosanoid metabolism, particularly PGI2, in collagen formation, fibrotic development, and cardiac remodeling, and they imply that the SHR genetic hypertension model may be predisposed to excess cardiac fibrosis.

    View details for Web of Science ID A1997YE99000008

    View details for PubMedID 9369254

Conference Proceedings


  • Autologous Transplantation for Hodgkin disease: A Tale of Two Eras Garfin, P. M., Luna-Fineman, S., Amylon, M., Kharbanda, S., Weinberg, K. I., Willert, J. R., Porteus, M., Link, M., Agarwal, R. ELSEVIER SCIENCE INC. 2013: S247-S247
  • RB Controls Size, Cellularity, and T Cell Output of the Mouse Thymus Garfin, P. M., Viatour, P., Min, D., Bryson, J., Weinberg, K. I., Manley, N. R., Sage, J. AMER SOC HEMATOLOGY. 2012

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