Rituxan, part 2

More on Rituxan. Even though I;ve written about it a couple of dozen times in the last two years, it's worth giving everyone the full tutorial from the beginning:


The way Rituxan works is really fascinating. Like a natural antibody, it recognizes the invader that is was programmed to find. In this case, it looks for something called CD-20, a protein on the surface of the follicular lymphoma cell. (It's on lots of non-lymphoma cells, too, so Rituxin wipes out some healthy cells along the way.)


Once it finds the CD-20 protein on a cell, the Rituxan...well, it sorta...um.....


Actually, researchers have no idea why it works to kill off the lymphoma cells. That, to me, is what's so fascinating.


That's not totally true, that they have no idea -- it's just kind of funny to say. They have some idea. Researchers think that Rituxan works in several ways (but they're not really completely sure).


The first way is by Apoptosis, or natural cell death. Every cell in the body is programmed to die at some point; when a cell's "suicide switch" is turned off, you end up with cancer -- runaway cells that won't die. Rituxin may cause apoptosis by turning that suicide switch back on.


Another possibility is called Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC). For this one, the antibody joining to the cell somehow triggers an immune response, so the antibody hold onto the cancer cell on one end, and then attaches to another immune cell with the other end, and that wipes out the cancer cell.


Still another possibility is called Complement-Dependent Cytotoxicity (CDC), where the antibody somehow damages the surface of the cancer cell, and the contents leak out, which results in its being killed off.


Rituxan might also work by making it hard for cancer cells to divide, or by signalling to the immune system in some other way that the cancer cell is indeed an invader, and should be eliminated.


Genentech, which manufactures Rituxan, has a very cool video showing how these processes work. Talk about Star Wars-type stuff -- you can almost see Luke Skywalker flying past the cancer cells in his X-wing.

So researchers have some idea that these three processes kill off the cells, but they don't know if they all work at the same time, or one works at a time, or if they influence each other somehow. My guess is that as we learn more about the genetic makeup of the cells, we'll have some clue. I'm guessing there will be differentiations between types of fNHL, and Rituxan will work differently depending on the type. But that's just a guess.

Rituxan does OK by itself, but its real miracle work happens when it is combined with other treatments, especially chemotherapy (which is why I'd be taking R-CVP, not just CVP). Since Rituxan has been added to chemotherapy, the Overall Survival rate for Follicular NHL has nearly doubled. (Or so it is speculated; not enough people have died to say for sure.)

So, Rituxan is a very good thing. Like I said -- my new Best Friend.