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Tanja Gruber, MD

  • Tanja Andrea Gruber
  • “Information is power. When families understand what you're doing and why, that helps us work together.”

It's important to me that patients have state-of-the-art care and a team that really cares about them. Its emotionally very difficult to have cancer or have a child with cancer, and we work hard to support patients and their families throughout the journey. It's very much a family affair.

Making sure the family and patient are informed is paramount, and I spend a lot of time explaining the treatment in detail. Information is power, and when families understand what you're doing and why, that helps us work together on decision-making. By the end of treatment, families often say to me, “I know so much, I could be a doctor.”

I want patients to look forward to coming to the clinic as much as I look forward to seeing them. It's a long journey, and I'm honored to be a part of their lives, standing beside them in the fight to beat cancer. Helping patients feel better and providing them with the best treatment available are my top priorities.

Trabajo y educación

Educación

University of Southern California, Los Angeles, CA, 05/16/2003

Últimos años de residencia

Children's Hospital Los Angeles Pediatric Residency, Los Angeles, CA, 06/30/2006

Subespecialidad

Childrens Hospital Los Angeles Hematology Oncology Fellowship, Los Angeles, CA, 07/31/2009

Certificado(s) de especialidad

Pediatric Hematology-Oncology, American Board of Pediatrics

Experiencia

Acute Myelogenous Leukemia

High-Risk Leukemia

Todo Publicaciones

DNA Methylation Clusters and Their Relation to Cytogenetic Features in Pediatric AML. Cancers Lamba, J. K., Cao, X., Raimondi, S., Downing, J., Ribeiro, R., Gruber, T. A., Rubnitz, J., Pounds, S. 2020; 12 (10)

Abstract

Acute Myeloid Leukemia (AML) is characterized by recurrent genetic and cytogenetic lesions that are utilized for risk stratification and for making treatment decisions. In recent years, methylation dysregulation has been extensively studied and associated with risk groups and prognosis in adult AML, however, such studies in pediatric AML are limited. Moreover, the mutations in epigenetic genes such as DNMT3A, IDH1 or IDH2 are almost absent or rare in pediatric patients as compared to their abundance in adult AML. In the current study, we evaluated methylation patterns that occur with or independent of the well-defined cytogenetic features in pediatric AML patients enrolled on multi-site AML02 clinical trial (NCT00136084). Our results demonstrate that unlike adult AML, cytosine DNA methylation does not result in significant unique clusters in pediatric AML, however, DNA methylation signatures correlated significantly with the most common and recurrent cytogenetic features. Paired evaluation of DNA methylation and expression identified genes and pathways of biological relevance that hold promise for novel therapeutic strategies. Our results further demonstrate that epigenetic signatures occur complimentary to the well-established chromosomal/mutational landscape, implying that dysregulation of oncogenes or tumor suppressors might be leveraging both genetic and epigenetic mechanisms to impact biological pathways critical for leukemogenesis.

View details for DOI 10.3390/cancers12103024

View details for PubMedID 33080932

The genomic landscape of juvenile myelomonocytic leukemia NATURE GENETICS Stieglitz, E., Taylor-Weiner, A. N., Chang, T. Y., Gelston, L. C., Wang, Y., Mazor, T., Esquivel, E., Yu, A., Seepo, S., Olsen, S. R., Rosenberg, M., Archambeault, S. L., Abusin, G., Beckman, K., Brown, P. A., Briones, M., Carcamo, B., Cooper, T., Dahl, G. V., Emanuel, P. D., Fluchel, M. N., Goyal, R. K., Hayashi, R. J., Hitzler, J., Hugge, C., Liu, Y. L., Messinger, Y. H., Mahoney, D. H., Monteleone, P., Nemecek, E. R., Roehrs, P. A., Schore, R. J., Stine, K. C., Takemoto, C. M., Toretsky, J. A., Costello, J. F., Olshen, A. B., Stewart, C., Li, Y., Ma, J., Gerbing, R. B., Alonzo, T. A., Getz, G., Gruber, T. A., Golub, T. R., Stegmaier, K., Loh, M. L. 2015; 47 (11): 1326-?

Abstract

Juvenile myelomonocytic leukemia (JMML) is a myeloproliferative neoplasm (MPN) of childhood with a poor prognosis. Mutations in NF1, NRAS, KRAS, PTPN11 or CBL occur in 85% of patients, yet there are currently no risk stratification algorithms capable of predicting which patients will be refractory to conventional treatment and could therefore be candidates for experimental therapies. In addition, few molecular pathways aside from the RAS-MAPK pathway have been identified that could serve as the basis for such novel therapeutic strategies. We therefore sought to genomically characterize serial samples from patients at diagnosis through relapse and transformation to acute myeloid leukemia to expand knowledge of the mutational spectrum in JMML. We identified recurrent mutations in genes involved in signal transduction, splicing, Polycomb repressive complex 2 (PRC2) and transcription. Notably, the number of somatic alterations present at diagnosis appears to be the major determinant of outcome.

View details for DOI 10.1038/ng.3400

View details for PubMedID 26457647