Anti-tumor immunoglobulin M increases lung metastasis in an experimental model of malignant melanoma

Nu Man Tsai, Bing Mae Chen, Shao Lun Wei, Cheng-Wen Wu Lee, Steve R. Roffler*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

3 Scopus citations


Cancer metastasis involves distinct steps that depend on complicated tumor-host interactions. The hematogenous dissemination of tumor cells may be facilitated by factors that promote the arrest and adherence of cancer cells in capillaries. We examined whether anti-tumor monoclonal immunoglobulin M (IgM) antibodies promoted the hematogenous dissemination of B 16 melanoma cells in syngeneic mice. IgM monoclonal antibodies were generated that selectively bind to B 16 melanoma cells as compared to syngeneic fibroblasts, lymphocytes or Lewis lung carcinoma cells. Incubation of B16-BL6 or B 16-F0 melanoma cells with these IgM anti-tumor antibodies significantly increased the number of lung colonies as compared with control antibodies. Moreover, intraperitoneal injection of specific antibody also significantly increased lung colonization. All anti-tumor antibodies promoted the aggregation of B 16 melanoma cells. A chemically generated immunoglobulin G (IgG)-like fragment of an anti-tumor IgM antibody displayed greatly reduced tumor aggregation and, in contrast to intact IgM, did not significantly increase lung colonization of B16 melanoma cells. Neither intact IgM nor the IgG-like fragment enhanced the in vitro invasiveness of B 16 melanoma cells across Matrigel-coated membranes. Our results, therefore, suggest that besides their beneficial anti-tumor effects, anti-tumor IgM antibodies may also promote the hematogenous dissemination of cancer cells.

Original languageEnglish
Pages (from-to)103-109
Number of pages7
JournalClinical and Experimental Metastasis
Issue number2
StatePublished - 14 Apr 2003


  • Aggregation
  • IgM
  • Melanoma
  • Metastasis
  • Monoclonal antibodies
  • Tumor antigens

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