Study of Rpl22 in MDS and AML

Abstract

Increasing evidence from our lab and others supports that ribosomal proteins play a critical role in development(1) and diseases including bone marrow disease (2) in addition to its essential role in protein synthesis. We found Rpl22 is dispensable for protein biosynthesis but regulates transformation and hematopoiesis (1, 3). Previously I have determined that Rpl22 functions as a haploinsufficient tumor suppressor in a mouse T-cell lymphoma model by activating NFB and its target Lin28B (3). Recently we also found that Rpl22 knockout mice exhibit an MDS-like phenotype associated with anemia and abnormal bone marrow (BM) hematopoiesis. Consistent with what we observed in our mouse model, our collaborator found that Rpl22 was mutated or deleted in some MDS and AML patients.

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Document Details

Document Type
Technical Report
Publication Date
Oct 01, 2015
Accession Number
AD1003214

Entities

People

  • Shuyun Rao

Organizations

  • Fox Chase Cancer Center

Tags

DTIC Thesaurus Topics

  • Abstracts
  • Biomedical Research
  • Blood
  • Bone Marrow
  • Bone Marrow Cells
  • Bones
  • Cancer
  • Cells
  • Diseases And Disorders
  • Gene Expression
  • Hematologic Diseases
  • Hematopoiesis
  • Lymphocytes
  • Neoplasms
  • Phenotypes
  • Proteins
  • Stem Cells

Fields of Study

  • Biology

Readers

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  • Immunology and Pathology
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