A drug used for renal cell cancer turns out to block the multiple receptor tyrosine kinases prevalent in many cancer cells.
Kinases empower proteins and peptides to act by attaching high energy phosphate bonds to supply energy in the form of electrons. Pain neurons have their own tyrosine kinases, ie kinases which act on pain proteins where an attachment at the amino acid tyrosine is important.
You will recall from multiple articles at this site that tyrosine kinase B (Trk B) is a marker that any given sensory neuron is a PAIN neuron. Cancer cells routinely set up their own tyrosine kinases to affect growth of new blood vessels and other growth matters on which cancer depends. These multiple receptor tyrosine kinases are as the name implies capable of activating many tyrosine kinase receptors.
It turns out that sunitinib might just be able to block the tyrosine kinase active in pain neurons. A Dr. Di Lorenzo is just now publishing in the J Clin Oncology (2007) 25: 2858-9 an article suggesting that sunitinib might well be able to block neuropathic pain by interfering with Tyrosine Kinase B.
Here is another new potential avenue for help from a drug which already exists. How we wish the NIDCR/NIH had the money to jump on these thinss. We are not waiting patiently to be free of the burning pain. Write to your congressmen asking for funding at NIH for BASIC pain research.