Transglutaminase 2 expression in acute myeloid leukemia: Association with adhesion molecule expression and leukemic blast motility

Andrew Pierce, Anthony D. Whetton, Stefan Meyer, Farhad Ravandi-Kashani, Gautam Borthakur, Kevin R. Coombes, Nianxiang Zhang, Steven Kornblau

Research output: Contribution to journalArticlepeer-review

17 Scopus citations


Acute myeloid leukemia (AML) is a heterogenous disease with differential oncogene association, outcome and treatment regimens. Treatment strategies for AML have improved outcome but despite increased molecular biological information AML is still associated with poor prognosis. Proteomic analysis on the effects of a range of leukemogenic oncogenes showed that the protein transglutaminase 2 (TG2) is expressed at greater levels as a consequence of oncogenic transformation. Further analysis of this observation was performed with 511 AML samples using reverse phase proteomic arrays, demonstrating that TG2 expression was higher at relapse than diagnosis in many cases. In addition elevated TG2 expression correlated with increased expression of numerous adhesion proteins and many apoptosis regulating proteins, two processes related to leukemogenesis. TG2 has previously been linked to drug resistance in cancer and given the negative correlation between TG2 levels and peripheral blasts observed increased TG2 levels may lead to the protection of the leukemic stem cell due to increased adhesion/reduced motility. TG2 may therefore form part of a network of proteins that define poor outcome in AML patients and potentially offer a target to sensitize AML stem cells to drug treatment.

Original languageEnglish (US)
Pages (from-to)2216-2224
Number of pages9
Issue number14
StatePublished - Jul 2013
Externally publishedYes


  • Acute myeloid leukemia
  • Biomedicine
  • Reverse phase protein array
  • Transglutaminase2

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology


Dive into the research topics of 'Transglutaminase 2 expression in acute myeloid leukemia: Association with adhesion molecule expression and leukemic blast motility'. Together they form a unique fingerprint.

Cite this