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Janus Kinase Signaling: Oncogenic Criminal of Lymphoid Cancers

Boheng Li1, Qin Wan1, Zhubo Li1

  • 1College of Pharmaceutical Sciences, Southwest University, Chongqing 400715, China.

Cancers
|October 23, 2021
PubMed

Insights

Janus kinase (JAK) abnormalities drive lymphoid cancers by over-activating the JAK/STAT pathway. This review covers JAK mutations, signaling, and therapeutic inhibition strategies for treating these malignancies.

Area of Science:

  • Molecular Biology
  • Oncology
  • Immunology

Background:

  • Janus kinase (JAK) proteins mediate cytokine signaling by activating signal transducers and activators of transcription (STAT).
  • Aberrant JAK/STAT pathway activation is implicated in various cancers, particularly lymphoid malignancies.
  • Emerging evidence suggests non-canonical and nuclear functions for JAK tyrosine kinases.

Purpose of the Study:

  • To review the role of JAK deregulation in lymphoid malignancies.
  • To discuss the upstream regulation of JAK expression.
  • To summarize current and emerging therapeutic strategies targeting the JAK pathway in lymphoid cancers.

Main Methods:

  • Literature review of studies on JAK signaling, mutations, and therapeutic interventions.
  • Analysis of the JAK/STAT pathway's role in lymphoid cancers.
  • Discussion of noncanonical JAK functions.

Main Results:

  • Mutations and fusions lead to JAK deregulation, driving lymphoid malignancies.
  • Upstream signaling nodes significantly influence JAK expression.
  • The JAK/STAT pathway is dysregulated in lymphoid cancers, with JAKs potentially playing nuclear roles.
  • JAK inhibitors show efficacy, especially in combination therapies.

Conclusions:

  • JAK deregulation is a key driver of lymphoid malignancies.
  • Targeting the JAK pathway, including its noncanonical roles, offers promising therapeutic strategies.
  • Combination therapies involving JAK inhibitors may enhance treatment outcomes for lymphoid cancers.
Keywords:
JAK/STATinhibitorlymphomamyeloma

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