The findings have boosted the investigation of targeted therapies to disable this molecular 'bodyguard' and increase a patient's ability to fight the blood cancer.
The study was conducted by a team of researchers led by Margaret Shipp at Dana-Farber Cancer Institute.
The biological trademark of Hodgkin lymphoma is a type of giant, mutant white blood cell called the Reed-Sternberg cell that is found in the lymph node tumors, which can reach the size of a basketball.
The blood cell contain only about 5 percent cancerous Reed-Sternberg cells while the rest are different types of immune cells recruited to fight the tumor, but they are ineffective.
The immune army includes different types of T cells, such as T helper 1 (Th1) cells designed to recognize and kill foreign infectious agents and sometimes tumors, T helper 2 (Th2) cells, which normally control allergic responses, and T regulatory (Treg) cells that suppress other T-cell types and shut down an immune response when the job is done.
The Hodgkin tumors are overloaded with Th2 and Treg cells that act as bodyguards for the cancer by weakening the Th1 immune response against it.
As part of the study researchers hunted the source of the cancer cells' protection using gene microarray chips, and looked for genes that were active in Reed-Sternberg cells but not in cells of another non-Hodgkin B-cell lymphoma.
It was found that a gene called Gal1 was up to 30 times more active in the Reed-Sternberg cells, causing them to secrete large quantities of a protein -- Gal1 or Galectin 1 -- that turned down the Th1 immune response.
"These observations provide an important explanation for why you have this ineffective immune response in Hodgkin lymphoma," Shipp said.
The findings of the study were published in the Proceedings of the National Academy of Sciences.