Acute-phase proteins in patients with head and neck cancer treated with interleukin 2/interferon alfa

G L Clayman1, F J Liu, H E Savage

  • 1Department of Head and Neck Surgery, University of Texas M.D. Anderson Cancer Center, Houston.

Insights

Elevated C-reactive protein and low C3 complement levels correlate with toxic effects during interleukin-2/interferon-alfa immunotherapy for head and neck cancer. Acute-phase proteins did not impact immune cell function in this study.

Area of Science:

  • Immunology
  • Oncology
  • Biochemistry

Background:

  • Biologic response modifiers, such as interleukin-2/interferon-alfa, can cause adverse reactions.
  • Acute-phase proteins (APPs) are potential mediators of these toxicities.
  • Patients with unresectable head and neck squamous cell carcinoma often receive immunotherapy.

Purpose of the Study:

  • To investigate the relationship between circulating acute-phase proteins and clinical toxic effects during interleukin-2/interferon-alfa immunotherapy.
  • To assess the impact of serum APPs on the in vitro immunomodulatory capacity of lymphokine-activated killer (LAK) cells.

Main Methods:

  • Prospective study of nine patients with head and neck squamous cell carcinoma receiving interleukin-2/interferon-alfa.
  • Measurement of seven acute-phase proteins and C3 complement levels.
  • Assessment of autologous serum's effect on LAK cell induction using chromium release assays.

Main Results:

  • Haptoglobin and C-reactive protein (CRP) levels were elevated pretreatment.
  • Toxic events correlated significantly with elevated CRP and decreased C3 complement levels.
  • No correlation was found between serum APP levels and inhibition of LAK cell cytotoxicity.

Conclusions:

  • Elevated CRP and reduced C3 complement are associated with interleukin-2/interferon-alfa toxicity in head and neck cancer patients.
  • Acute-phase proteins do not appear to inhibit LAK cell induction in this context.
  • Further research is needed to elucidate the role of CRP and complement in immunotherapy-related toxicity.

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