I am currently a Posdoctoral Fellow in the laboratory of Dr. Irving Weissman, a world-renowned researcher at the Stanford University School of Medicine’s Institute for Stem Cell Biology and Regenerative Medicine. Building upon my previous experience in genetics, cancer biology, and small RNA signaling, during my appointment in Dr. Weissman’s lab I am applying the principles of forward genetics to identify and study genes involved in immune evasion by tumors. This work has the potential to open major avenues of research in basic biology, and to identify novel mechanisms and agents for anti-cancer immunotherapy.

Honors & Awards

  • CRI Irvington Postdoctoral Fellowship, Cancer Research Institute (06/14-Present)
  • Richard C. Parker Memorial Award for Outstanding and Innovative Doctoral Research, Columbia University, Department of Microbiology and Immunology (March 2013)

Professional Education

  • Bachelor of Arts, University of California Berkeley (2006)
  • Master of Arts, Columbia University (2007)
  • Master of Philosophy, Columbia University (2009)
  • Doctor of Philosophy, Columbia University (2013)

Stanford Advisors

Research & Scholarship

Current Research and Scholarly Interests

My research applies the principles of forward genetics to screen for important regulators of the immune system, particularly in the context of anti-cancer immune surveillance. By investigating and untangling the regulatory networks that control immune activation or repression in response to cancer, we can design novel drugs to manipulate these pathways to therapeutic benefit in patients.

Lab Affiliations


All Publications

  • tRNA-derived microRNA modulates proliferation and the DNA damage response and is down-regulated in B cell lymphoma PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Maute, R. L., Schneider, C., Sumazin, P., Holmes, A., Califano, A., Basso, K., Dalla-Favera, R. 2013; 110 (4): 1404-1409


    Sequencing studies from several model systems have suggested that diverse and abundant small RNAs may be derived from tRNA, but the function of these molecules remains undefined. Here, we demonstrate that one such tRNA-derived fragment, cloned from human mature B cells and designated CU1276, in fact possesses the functional characteristics of a microRNA, including a DICER1-dependent biogenesis, physical association with Argonaute proteins, and the ability to repress mRNA transcripts in a sequence-specific manner. Expression of CU1276 is abundant in normal germinal center B cells but absent in germinal center-derived lymphomas, suggesting a role in the pathogenesis of this disease. Furthermore, CU1276 represses endogenous RPA1, an essential gene involved in many aspects of DNA dynamics, and consequently, expression of this tRNA-derived microRNA in a lymphoma cell line suppresses proliferation and modulates the molecular response to DNA damage. These results establish that functionally active microRNAs can be derived from tRNA, thus defining a class of genetic entities with potentially important biological roles.

    View details for DOI 10.1073/pnas.1206761110

    View details for Web of Science ID 000314453900056

    View details for PubMedID 23297232

  • A Mutation in Mouse Pak1ip1 Causes Orofacial Clefting while Human PAK1IP1 Maps to 6p24 Translocation Breaking Points Associated with Orofacial Clefting. PloS one Ross, A. P., Mansilla, M. A., Choe, Y., Helminski, S., Sturm, R., Maute, R. L., May, S. R., Hozyasz, K. K., Wójcicki, P., Mostowska, A., Davidson, B., Adamopoulos, I. E., Pleasure, S. J., Murray, J. C., Zarbalis, K. S. 2013; 8 (7)


    Orofacial clefts are among the most common birth defects and result in an improper formation of the mouth or the roof of the mouth. Monosomy of the distal aspect of human chromosome 6p has been recognized as causative in congenital malformations affecting the brain and cranial skeleton including orofacial clefts. Among the genes located in this region is PAK1IP1, which encodes a nucleolar factor involved in ribosomal stress response. Here, we report the identification of a novel mouse line that carries a point mutation in the Pak1ip1 gene. Homozygous mutants show severe developmental defects of the brain and craniofacial skeleton, including a median orofacial cleft. We recovered this line of mice in a forward genetic screen and named the allele manta-ray (mray). Our findings prompted us to examine human cases of orofacial clefting for mutations in the PAK1IP1 gene or association with the locus. No deleterious variants in the PAK1IP1 gene coding region were recognized, however, we identified a borderline association effect for SNP rs494723 suggesting a possible role for the PAK1IP1 gene in human orofacial clefting.

    View details for DOI 10.1371/journal.pone.0069333

    View details for PubMedID 23935987

  • Identification of the Human Mature B Cell miRNome IMMUNITY Basso, K., Sumazin, P., Morozov, P., Schneider, C., Maute, R. L., Kitagawa, Y., Mandelbaum, J., Haddad, J., Chen, C., Califano, A., Dalla-Favera, R. 2009; 30 (5): 744-752


    The full set of microRNAs (miRNAs) in the human genome is not known. Because presently known miRNAs have been identified by virtue of their abundant expression in a few cell types, many tissue-specific miRNAs remain unrevealed. To understand the role of miRNAs in B cell function and lymphomagenesis, we generated short-RNA libraries from normal human B cells at different stages of development (naive, germinal center, memory) and from a Burkitt lymphoma cell line. A combination of cloning and computational analysis identified 178 miRNAs (miRNome) expressed in normal and/or transformed B cell libraries. Most notably, the B cell miRNome included 75 miRNAs which to our knowledge have not been previously reported and of which 66 have been validated by RNA blot and/or RT-PCR analyses. Numerous miRNAs were expressed in a stage- or transformation-specific fashion in B cells, suggesting specific functional or pathologic roles. These results provide a resource for studying the role of miRNAs in B cell development, immune function, and lymphomagenesis.

    View details for DOI 10.1016/j.immuni.2009.03.017

    View details for Web of Science ID 000266356900016

    View details for PubMedID 19446474

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