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Ribosomopathies and the paradox of cellular hypo- to hyperproliferation. | LitMetric

Ribosomopathies and the paradox of cellular hypo- to hyperproliferation.

Blood

Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, MD.

Published: February 2015

AI Article Synopsis

  • - Ribosomopathies are congenital disorders caused by defects in ribosomal proteins or biogenesis factors, leading to issues like bone marrow failure and increased cancer risks as individuals age.
  • - The phenomenon where these conditions shift from low to high cell proliferation is known as "Dameshek's riddle," which poses a challenge in understanding the hematology behind these diseases.
  • - Recent cancer studies have identified mutations in ribosomal proteins linked to various cancers, prompting a deeper exploration into the connections between ribosomal dysfunctions and cancer development.

Article Abstract

Ribosomopathies are largely congenital diseases linked to defects in ribosomal proteins or biogenesis factors. Some of these disorders are characterized by hypoproliferative phenotypes such as bone marrow failure and anemia early in life, followed by elevated cancer risks later in life. This transition from hypo- to hyperproliferation presents an intriguing paradox in the field of hematology known as "Dameshek's riddle." Recent cancer sequencing studies also revealed somatically acquired mutations and deletions in ribosomal proteins in T-cell acute lymphoblastic leukemia and solid tumors, further extending the list of ribosomopathies and strengthening the association between ribosomal defects and oncogenesis. In this perspective, we summarize and comment on recent findings in the field of ribosomopathies. We explain how ribosomopathies may provide clues to help explain Dameshek's paradox and highlight some of the open questions and challenges in the field.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4342353PMC
http://dx.doi.org/10.1182/blood-2014-10-569616DOI Listing

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