In case you've forgotten, there is a new type of anti-cancer treatment available called targeted therapy, which attacks specific molecular targets on the outside or within the malignant cell. Such agents differ from standard chemotherapy, which disables or destroys cells that happen to be rapidly dividing, whether they are malignant or benign. On the contrary, targeted therapy medications attach themselves to one or more specific receptors that have control over discrete cellular functions vital to the growth, survival, invasion and immortality of the cancer cell. Everyone understand? No? Perhaps it will help if I let an expert explain it. Here's how Dr. George Sledge from Indiana University describes targeted therapy:
A targeted therapy should attack a biologically important process (usually, though not necessarily, a single molecule), preferably one central to a hallmark of cancer. The target should be measurable in the clinic, and measurement of the target (in either quantitative or qualitative terms) should correlate with clinical outcome when the targeted therapy is administered.
Seems simple enough, doesn't it? If you think it is easy to learn the biology of the cancer cell, its many targets and the mechanism of action of targeted agents, try explaining all this to patients. I personally would have better luck translating Sanskrit than explaining malignant cell biology. For example, if I want to explain how the new pill sorafenib works I have to open my little précis with something like this:
The vascular endothelial growth factor (VEGF) family of angiogenic growth factors includes six secreted glycoproteins referred to as VEGF-A, VEGF-B, VEGF-C, VEGF-D, VEGF-E, placenta growth factor (PlGF)-1, and PlGF-2. These receptors consist of an extracellular domain that binds specific VEGF ligands, a transmembrane domain, and an intracellular region that contains a tyrosine kinase domain. Ligand-receptor interaction induces the activation of the tyrosine kinase domain of the VEGFRs, which finally leads to the activation of intracellular signaling transduction pathways that are involved in regulating cellular proliferation and survival, such as the Raf/mitogen-activated protein kinase-extracellular signal-regulated kinase (MEK)/extracellular signal-regulated kinase (ERK) and the phosphatidylinositol 3' kinase (PI3K)/protein kinase B (Akt) pathways.
The first time I tried to explain this to a patient he put a wastebasket over his head and began to bark like a dog. I therefore decided to use a visual aid to get my message of hope across. After calming him down I showed him this cartoon:
He gave me a look like a vacationer reading an Uzbekistani menu. Undaunted, I racked my brain to come up with a better way to describe how this treatment stops the engine of the cancer cell from receiving the message to start up. I came up with this idea and tried to spit it out to my patient, who was now trying to sneak out the door:
"Think of cancer cell receptors as champion runners ready to sprint across the countryside in a relay race. Each runner passes a deadly baton to the next, containing the secrets of the cell's ability to wreak havoc. When the final runner reaches the gates of the nucleus he gives the baton to the keepers within, who use it to awaken a murdering army of invaders.
"The runners, however, cannot start until they hear the starter's pistol go off. That is their weak spot, and our side knows it. Targeted agents are trained to snatch the starter before he can pull the trigger and tie him up, leaving rows upon rows of runners crouched and ready, waiting for a signal we hope they will never hear."
I've never been confused by targeted thearpy. To me it was putting flags on evil cells so that they can easily be destroyed.
I'm just concerned that it doesn't flag some good cells as well as the evil ones.
Okay, I probably need to re-read this article a few more times before I understand it, but I just wanted to say that is an excellent line drawing of the Flying Spaghetti Monster you have there ...
I concur with Llewelly. The colors are pretty.
I am laughing out loud in cubeland. This cracks me up and you are trying too hard. Why not just tell your patient that "This treatment works by stopping the engine of the cancer cell from receiving the message to start up." Actually you are making me feel smart because I figured out on my own that Herceptin works by binding to the Her2/neu receptors on the outside of cells and disallowing them to overexpress.