"Understanding cancer processes is a key toward effective targeted therapy. My laboratory explores unconventional roles for chromatin modifiers – the factors the most altered in cancers. These proteins are easily targetable by drugs and the plasticity of epigenetic events makes them a powerful target for reversion of disease phenotype. The Distinguished Scientist Award allows us to decipher the mechanisms of tumorigenesis of DIPG in order to identify new therapies based on patients’ genotypes. It is an honor to be recognized by the Sontag Foundation to tackle the deadliest childhood cancer."

- Dr. Capucine Van Rechem

Dr. Van Rechem's Biosketch

Academic Appointments

  • Assistant Professor, Pathology, Stanford University School of Medicine, 2018-present

 

About DSA-Funded Research

Pediatric brain tumors are the primary cause of cancer death in children. The deadliest childhood cancers are Diffuse Intrinsic Pontine Gliomas (DIPG), accounting for 10% of pediatric brain cancers. Under 1% of patients survive 5 years after diagnosis. Genetically, 80% of DIPG patients have a mutation, K27M, in the histone H3. Histones are proteins that pack our genome and can be modified by chemical groups, allowing our genome to be read like a book. Histones and their chemical groups alter how our genome is read; they lead to consequences such as cell death. The K27M mutation prevents the chemical groups’ protective activity, altering the story and keeping DIPG cells alive. In DIPG, the K27M mutation is found in histones H3.3 and H3.1. These two patient subgroups differ in prognoses and response to standard therapy. Therefore, DIPGs may include multiple diseases with distinct specificities. Understanding the differences at the molecular level is necessary for defining specific therapies and curing patients. The fundamental difference between H3.3 and H3.1 is their expression across a cell’s life cycle, or when the words are present in the story. We hypothesize that DIPG subgroups have distinct mechanisms that lead to tumorigenesis. The mechanisms will be uncovered by studying the diseases in a cell cycle specific manner. I developed a novel approach to address this pioneering hypothesis. Ultimately, we will not only greatly improve our understanding of DIPGs, but also unravel new strategies for targeted therapies and potentially more effective treatments for this incurable childhood disease.

 

Accolades

“Dr. Van Rechem shows great promise of becoming a leader in her field. During her postdoctoral training at MGH/Harvard, Capucine studied epigenetic factors through two unusual perspectives which not only demonstrate her distinguished achievement of extraordinary promise in epigenetics and diseases research but also that she can do highly creative research. Her innovative studies will significantly advance our basic knowledge and will also have great potential for translating novel discovery to the development of new targeted therapies.”

Dr. Thomas J. Montine
Stanford University

"Capucine is fearless and willing to ask unconventional questions at a basic science level that will have profound therapeutic implications. I can speak first hand to this fact as Capucine changed our view of how chromatin factors impact cytoplasmic events such as translation (two back-to-back Van Rechem et al. 2015 Cancer Discovery papers), while developing strategies for epigenomics that allowed us to uncover new principals related to the direct role chromatin has on cell cycle phases."

Johnathan Whetstine, PhD
Professor, Jack Schultz Basic Science Endowed Chair, Program Leader Cancer Epigenetics
Fox Chase Cancer Center 

 

 

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