Could this spell aloha to melanoma?

A vaccine that produces a delayed-type hypersensitivity immune response shows promise

By Samuel Munson

The blas� approach to soaking up the rays during the 70s and 80s made melanoma the fastest growing cancer among American men. Slathering on UV sunscreen has curbed melanoma somewhat but it still counts for about 48,000 cases annually in the US and 3,500 here in Canada. Each year in the US and Canada over 7,000 and 700 people die respectively.

Vaccines for cancers have been in development for decades. Now a melanoma vaccine is making waves in the fight against skin cancer. In the February 1 issue of the Journal of Clinical Oncology, Dr David Berd of the Thomas Jefferson University in Philadelphia reported on a five-year follow-up of 214 patients who received a trial melanoma vaccine.

The patients selected had cancer that had spread from the skin to the lymph nodes, prompting removal of the nodes as a means of obstructing the cancer's march.

The guts of the vaccine were the cancer cells themselves. In one batch, these autologous cells were chemically tagged with dinitrophenyl � a compound that would stimulate the immune system. Other cells were left untagged. Both cell types were injected into the patient after being mixed with bacille Calmette-Guerin (an 'industry standard' way of revving up the immune system).

The immune response to autologous cells doesn't involve antibody production. Rather, T-cells and macrophages slowly gear up, migrate to the site of the action, and physically attack the tumour cells. This "delayed-type hypersensitivity" can be a good thing in battling cancer.

The five-year overall survival rate of the 214 patients was 44%, much higher than the typical rate of 20-25%. Further, those patients whose immune system kicked into gear slowly had double the overall survival rate (almost 60%) when compared to those without this immune response (29%).

Surprisingly, this beneficial immune response appeared to pack an extra punch if the tumour cells weren't tagged. In patients who relapsed, the overall survival rate in those having an immune response to unmodified cells was 25%, compared to only 12% in those who had an immune response to tagged cells.

Critics point out that in clinical applications, it may be difficult to differentiate whether an immune response is due to a chemical tag on the tumour cells, and not to a component of the tumour cells themselves. As well, those who did better may have been healthier to begin with, particularly in terms of their immune system, than those who didn't fair as well.

Dr Berd hopes that a large-scale clinical trial by the company that owns the vaccine can help iron out such issues. For the time being, this provocative data serves as a reminder of the complexity of the antitumour immune system and should not be discounted.