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TOX expression and role in CTCL.

L Y McGirt1,2, C A Degesys3, V E Johnson2

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|June 28, 2016
PubMed
Summary
This summary is machine-generated.

Thymocyte selection-associated HMG box protein (TOX) shows diagnostic utility in mycosis fungoides (MF) and early-stage cutaneous T-cell lymphomas (CTCL). GATA3 regulates TOX, offering insights into MF development and potential therapeutic targets.

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Area of Science:

  • Oncology
  • Dermatology
  • Molecular Biology

Background:

  • Cutaneous T-cell lymphomas (CTCL), including mycosis fungoides (MF), are challenging to diagnose early due to a lack of reliable markers.
  • Increased expression of thymocyte selection-associated HMG box protein (TOX) is observed in MF/CTCL, prompting investigation into its diagnostic and functional roles.

Purpose of the Study:

  • To evaluate TOX expression across the spectrum of CTCL, including MF precursors like large plaque parapsoriasis (LPP).
  • To elucidate the implications of altered TOX expression in CTCL pathogenesis and identify its regulatory mechanisms.

Main Methods:

  • TOX protein expression was assessed via staining in MF, CD30(+) lymphoproliferative disorders (LPD), LPP, benign inflammatory dermatoses (BID), and normal skin (NS).
  • CTCL cell lines were used to investigate the regulation of TOX expression, including the role of GATA3 and therapeutic agents.

Main Results:

  • TOX was positive in 73.6% of MF cases, with a positive predictive value of 86.7% for MF diagnosis.
  • TOX expression was also observed in 70.0% of LPP cases and was more common in Black patients with MF.
  • GATA3 knockdown reduced TOX mRNA and protein levels in CTCL cells, and TOX expression decreased with CTCL therapeutics.

Conclusions:

  • TOX serves as a valuable diagnostic marker for MF and is also present in LPP, suggesting a role in MF development.
  • GATA3 is identified as a regulator of TOX, providing new insights into the molecular mechanisms underlying CTCL.
  • These findings highlight TOX's diagnostic utility and potential involvement in MF pathogenesis, with implications for understanding CTCL biology.