Genistein induces G2 arrest in malignant B cells by decreasing IL-10 secretion

Amal Mansour, Brian McCarthy, Stephan K. Schwander, Victor Chang, Sergei Kolenko, Sreekrishna Donepudi, Janet Lee, Elizabeth Raveche

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


Chronic B cell malignancies are often chemoresistant and the development of new therapeutic modalities is a high priority. Many B cell malignancies have autocrine production of IL-10, which regulates B cell growth and differentiation. Here we demonstrate that the soy isoflavone genistein, a tyrosine kinase inhibitor, rapidly decreased IL-10 secretion followed by upregulation of IFNγ and inhibition of cell proliferation with predominantly G2 arrest. The antiproliferative effects of genistein were reversed by the addition of exogenous IL-10. Genistein downregulated cdc25C and cdk1 as well as anti-apoptotic proteins survivin and Ian-5. After genistein withdrawal, the G2M arrested cells reentered the cell cycle and underwent apoptosis, which was significantly augmented by fludarabine. We conclude that genistein can sensitize malignant B cells to the action of other chemotherapeutic agents by modulating the cytokine profile and controlling cell cycle progression.

Original languageEnglish (US)
Pages (from-to)1597-1605
Number of pages9
JournalCell Cycle
Issue number12
StatePublished - Dec 2004

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Developmental Biology
  • Cell Biology


  • B cell malignancy
  • Fludarabine
  • Genistein
  • IL-10
  • Ian5
  • Survivin


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