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Cancer Vaccines: A Two-pronged Attack?

Date:
January 27, 2005
Source:
Ludwig Institute For Cancer Research
Summary:
The latest findings in cancer vaccine development suggest that cancer vaccines may have two modes of action; specific immunization and non-specific activation of immune cells paralyzed by the tumor.

Brussels (January 17, 2005) -- The latest findings in cancer vaccine development suggest that cancer vaccines may have two modes of action; specific immunization and non-specific activation of immune cells paralyzed by the tumor.

The human immune system fights cancer partly through the production of many populations of specialized immune cells called cytolytic T cells (CTL). Each CTL population recognizes a different, specific marker, an 'antigen', on the cancer cell surface. Cancer vaccines are designed to tip the balance in favor of the immune system by stimulating the production of CTLs against the particular antigen in the vaccine. However, in back-to-back articles published today in the Journal of Experimental Medicine, investigators at the Brussels Branch of the Ludwig Institute for Cancer Research (LICR) and Brussel's Louvain University have shown that a cancer vaccine not only specifically stimulates the production of CTLs against the vaccine antigen, it also non-specifically activates spontaneously produced CTL populations against multiple cancer antigens.

According to Dr. Thierry Boon, the Director of the LICR Brussels Branch, this observation opens a new way of thinking about how cancer vaccines might work. "We have always thought that cancer vaccines could only be effective if massive numbers of vaccine-specific CTLs were produced. But it seems that, in about 10% of patients with metastatic melanoma, the vaccine might actually be reawakening different CTL populations that have been effectively deactivated by the tumor."

The research team also found that metastases were enriched with inactive CTLs, and they are now assessing exactly how vaccination can 'spark' the reactivation of CTLs. "We believe that these CTLs in the metastatic lesions could potentially eliminate the bulk of the tumor," says Dr. Boon. "Now we have to elucidate why this non-specific process works in some patients and not in others, and then to learn how to harness this effect to help even more people with cancer."

###

This study was published by a team comprised of researchers from the Brussels Branch of the Ludwig Institute for Cancer Research at Louvain University, Belgium, and the Laboratory of Experimental Surgery, Liege University, Liege, Belgium.

The Ludwig Institute for Cancer Research (LICR) is the largest international academic institute dedicated to understanding and controlling cancer. With ten Branches in seven countries, and numerous Affiliates and Clinical Trial Centers in many others, the scientific network that is LICR quite literally covers the globe. The uniqueness of LICR lies not only in its size and scale, but also in its philosophy and ability to drive its results from the laboratory into the clinic. LICR has developed an impressive portfolio of reagents, knowledge, expertise, and intellectual property, and has also assembled the personnel, facilities, and practices necessary to patent, clinically evaluate, license, and thus translate, the most promising aspects of its own laboratory research into cancer therapies.


Story Source:

The above story is based on materials provided by Ludwig Institute For Cancer Research. Note: Materials may be edited for content and length.


Cite This Page:

Ludwig Institute For Cancer Research. "Cancer Vaccines: A Two-pronged Attack?." ScienceDaily. ScienceDaily, 27 January 2005. <www.sciencedaily.com/releases/2005/01/050126112737.htm>.
Ludwig Institute For Cancer Research. (2005, January 27). Cancer Vaccines: A Two-pronged Attack?. ScienceDaily. Retrieved April 20, 2014 from www.sciencedaily.com/releases/2005/01/050126112737.htm
Ludwig Institute For Cancer Research. "Cancer Vaccines: A Two-pronged Attack?." ScienceDaily. www.sciencedaily.com/releases/2005/01/050126112737.htm (accessed April 20, 2014).

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