Mechanisms of paraneoplastic syndromes of colon-26: involvement of interleukin 6 in hypercalcemia

Cytokine. 1993 Sep;5(5):463-8. doi: 10.1016/1043-4666(93)90037-6.


The precise mechanisms responsible for increased calcium levels in patients with cancer are not fully understood. In a recent study, the participation of interleukin (IL)-6 as an important mediator of key parameters of cancer cachexia in the colon-26 adenocarcinoma was reported. Here, we show that in addition to cachexia, C-26 tumour bearing mice also develop hypercalcemia. Treatment of these mice with 5' deoxyfluorouridine significantly reduces tumour size and inhibits both hypercalcemia, cachexia, and elevated serum IL-6. Moreover, monoclonal antibody to mouse IL-6 prevents both the cachexia and the hypercalcemia and reduces serum IL-6 levels in C-26 tumour bearing hosts. The administration of a bisphosphonate compound (Clodronate) reverses the hypercalcemia but has no effect on tumour burden, serum IL-6 levels, or wasting. We conclude that tumour-derived IL-6 plays a role in the pathogenesis of the C-26 associated hypercalcemia, and that the increase of serum calcium does not by itself mediate cachexia.

MeSH terms

  • Adenocarcinoma / blood*
  • Adenocarcinoma / complications
  • Animals
  • Colonic Neoplasms / blood*
  • Colonic Neoplasms / complications
  • Hypercalcemia / etiology*
  • Interleukin-6 / physiology*
  • Mice
  • Mice, Inbred Strains
  • Paraneoplastic Syndromes / blood*
  • Random Allocation


  • Interleukin-6