More research

A few other interesting cancer-related research reports in the news lately:

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Researchers at the Institute for Myeloma and Bone Cancer Research in Los Angeles have found out how tumors create their own blood supply. They looked at tumor cells from Multiple Myeloma (a bone marrow cancer). The tumor cells release a protein called pleiotrophin (PTN), which affects white blood cells, changing them into cells that form the lining of blood vessels. These new blood vessel linings become incorporated into the blood vessels within the tumors, connecting the tumor to the body's main blood supply. It's kind of sci-fi, almost: alien invader mutates itself and finds a way to live if its host.

But it's potentially big news, and not just for myeloma patients, but for all cancer patients. There are a bunch of different approaches to cancer research, theories about how to cure it, and one approach works on the premise that if you can somehow cut off a tumor's blood supply, you can starve the tumor. This myeloma research sounds like it could be a significant piece to that puzzle.

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Another study, more directly linked to my present condition, comes from the Centre for Medical Oncology Laboratory in London. (I can't get the link to work, unfortunately.)

These researchers have been focusing on how and why the slow-growing Follicular NHL cellss transform into a more agressive form of NHL. It's a tough article to read, very technical, and (as some of us discussed in the support group) a little controversial, in that it leaves some questions unanswered. Basically, the authors of the study say that fNHL and t-fNHL (fNHL that has transformed into a more aggressive form) come from the same mutated cell. One cell mutates from a normal lymphocite (a kind of white blood cell). Then it sometimes reproduces as fNHL, and sometimes as t-fNHL.

Knowing how the tranforming begins is important for future research -- it has a lot to do with that "personalization" trend, because the research involves looking at antigens that are specific to each patient's tumors. But it also may say something more general: if the defective "parent" lymphocite cells can be identified, it might be easier to find a way to wipe them out. Doctors could harvest normal "parent" lymphocite cells, kill off everything with heavy chemo, and reintroduce the harvested normal cells through an auto stem cell transplant.


Controversial, as I said, but potentially exciting. There are some NHL researchers who are looking at the results of auto SCTs and the long-term survival rates that come from them, and saying this is our best chance at a cure. This research, if it all holds up under scrutiny, may give them some strong evidence.

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Finally, I've seen an abstract for this articel, but it hasn't officially been published yet. It's the most recent data from the National LymphoCare Study. The study was begun because there was so little data on fNHL patients outside of clinical trials. A trial might look at a few hundred people and determine that a treatment is effective, but then no one knows how effective it really is. The LymphoCare Study is descriptive -- they aren't giving anyone any treatments, they've following patients to find out how they're bing treated, for how long, etc. The hope is that they can find some pattern in helping decide which treatments, and in what order, work best.

Between 2004 and 2007, they followed 2,728 fNHL patients. They looked at the initial treatment. Watch and wait was used for 17.7% of patients. Rituxin on its own was used for 13.9%. About 6% went into a clinical trial. Radiation therapy, 5.6%; chemotherapy only, 3.2%. Chemotherapy plus rituxin was the biggest group at 51.9%.

Of the chemotherapy plus rituxingroup, R-CHOP was used in 55.0%; R-CVP in 23.1%; rituxin plus fludarabine, 15.5%. Others were the remaining 6.4%.

They conclude that there is a wide variety of treatment approaches (no kidding), and that having some consistency in initial treatment might also help in determining the best course of treatment after relapse. It's a good thing -- we need to know what's going on.

There's more out there. I'll try to update with more soon.