The Instutute of Physics released news last week about what they call a "breakthrough in radiotherapy." Traditional radiation is pretty good at focusing on tumors, but some healthy tissue does get destroyed in the process, causing some nasty side effects. The "breakthrough" involves combining radiation therapy with an MRI. The MRI allows more focused aiming of the radiation, but it also provides the radiation oncologist with a "real time" view of the tumor, so the beam can be adjusted in response to the tumor shrinking or moving. Radiation isn't necessarily used in later stage follicular NHL like mine, but it sometimes is used on a stubborn node that won't respond to chemo when the rest of them have, so this could be personally useful. Plus, it's just good news for cancer patients in general.
Another general cancer research report with implications for lymphoma: Researchers think they have uncovered a communication pathway that allows the immune system to coordinate and fight off cancer. They speculate that when that sytem breaks down, cancers are allowed to grow. It's a theory I've read about before: the body is constantly developing mutated cells, and constatntly fighting them off, and when they can't fight them, they turn into cancer. (It's a theory that's hard to prove, because we only see the failures of the system.) According to these researchers, that failure of the system comes from a breakdown in the interferon pathway -- that communication system in the immune system. Once that pathway breaks down, the system can't fight off developing cancer cells on its own. This is important for lymphoma research because it might explain why lymphoma vaccines, which seem so darn promising, haven't had the expected results. Maybe accounting for the interferon pathway problem will result in a more effective vaccine. I know the lymphoma specialist, Dr C, that I saw when I was first diagnosed, was very excited about the vaccine approach. So maybe in a few years we'll see it work.
This next one is more directly lymphoma-related. It's from a press release describing a Journal of Clinical Oncology article on early clinical trials of Veltuzamab, a monoclonal antibody that could be an alternative to Rituxin. Like Rituxin, it targets CD20 proteins on lymphocytes. But here's the key difference: Rituxin is made from both human and mouse proteins, while Veltuzamab is made from only human proteins. As a result, it's likely to create fewer rejection problems than Rituxin. Rituxin is usually given very slowly, often over a period of up to 8 hours, and with Benedril, so any adverse reactions can be taken care of immediately. Veltuzamab seems to cause fewer of these allergic reactions, and so can be given much more quickly. The responses to it are otherwise similar to Rituxin. The same company is also running trials for another antibody, Epratuzumab, that targets CD22 proteins, and has been used effectively in a recent trial. My guess is this company will soon start to combine Epratuzumab and Veltuzamab and see how that works as eithera first-line therapy or as a Rituxin substitute for standard chemo regimens. But that's just a guess....
Veltuzamab isn't the only humanized monoclonal antibody out there in trials. Another company recently started clinical trials for its humanized monoclonal antibody, known as R7159. (You can tell it's still in trials because the marketing department hasn't given it a cool name with an X or a Z in it yet.) This one is similar to that other one with a Z in the name -- derived from human proteins, so there's less chance of rejection or allergic reaction. Initial trials for R7159 look very good -- at least comparable to Rituxin, maybe even a little more effective. I'm not privy to the science behind all of these antibodies, but it seems like they all have slightly different, and they claim slightly better mechanisms for identifying and attaching to CD20 (or other) proteins on lymphocytes.