So, you say that there is a magic bullet! A drug that will cure all types of cancer! Come on, lets get real, NO, it is not true, At Least Not Yet.
I don’t usually comment on early stage (animal model) research because we simply are not rats, zebra fish, dogs or monkeys. This, I am sure about. I have been receiving some rather over the top questions about the recent discovery of the magic bullet, the cure to all cancers.
Let me share what I believe is the confusion.
A recent on-line article in “Science Now”, titled One Drug to Shrink All Tumors said that a single drug can shrink or cure human breast, ovary, colon, bladder, brain, liver, and prostate tumors that have been transplanted into mice. The treatment, an antibody that blocks a “do not eat” signal normally displayed on tumor cells, coaxes the immune system to destroy the cancer cells, or to eat the tumor cell.
A decade ago, biologist Irving Weissman of the Stanford University School of Medicine in Palo Alto, California, discovered that leukemia cells produce higher levels of a protein called CD47 than do healthy cells. They found that this protein, CD47serves as a marker for the immune system that blocks the immune system from destroying the tumor cel, or as they coined the phrase, a sign that says do not eat me. They theorized that cancers take advantage of this marker to trick the immune system into ignoring them, allowing them to continue to grow and spread.
Dr. Weissman’s lab continued looking at CD47. They found that blocking CD47 with an antibody removed the do not eat sign and cured some cases of lymphomas and leukemias in mice by stimulating the immune system to recognize the cancer cells as invaders. Now, he and colleagues have shown that the CD47-blocking antibody may have a far wider impact than just blood cancers.
“What we’ve shown is that CD47 isn’t just important on leukemias and lymphomas,” says Weissman. “It’s on every single human primary tumor that we tested.” Moreover, Weissman’s lab found that cancer cells always had higher levels of CD47 than did healthy cells. How much CD47 a tumor made could predict the survival odds of a patient.
The lab then looked at whether blocking CD47 was beneficial. They then exposed tumor cells in a petri dish to macrophages , a type of immune cell, and anti-CD47 molecules. Without the protein, the macrophages ignored the cancerous cells, however when the CD47 was present in the petri dish, the macrophages engulfed and destroyed cancer cells from all tumor types.
Next, the lab moved their experiments to an animal model. They transplanted human tumors into the feet of mice (NOT HUMANS), where tumors can be easily monitored. When they treated the mice with anti-CD47, the tumors shrank and did not spread to the rest of the body. In mice given human bladder cancer tumors, for example, 10 of 10 untreated mice had cancer that spread to their lymph nodes. Only one of 10 mice treated with anti-CD47 had a lymph node with signs of cancer. Moreover, the implanted tumor often got smaller after treatment — colon cancers transplanted into the mice shrank to less than one-third of their original size, on average. And in five mice with breast cancer tumors, anti-CD47 eliminated all signs of the cancer cells, and the animals remained cancer-free 4 months after the treatment stopped.
“We showed that even after the tumor has taken hold, the antibody can either cure the tumor or slow its growth and prevent metastasis,” said Weissman.
Cancer researcher Tyler Jacks of the Massachusetts Institute of Technology in Cambridge described the study as promising, more research is needed to see whether the results hold true in humans. “The microenvironment of a real tumor is quite a bit more complicated than the microenvironment of a transplanted tumor,” he notes, “and it’s possible that a real tumor has additional immune suppressing effects.”
Another important question, Jacks says, is how CD47 antibodies would complement existing treatments. “In what ways might they work together and in what ways might they be antagonistic?” Using anti-CD47 in addition to chemotherapy, for example, could be counterproductive if the stress from chemotherapy causes normal cells to produce more CD47 than usual.
Bottom line, we are still a long way from a cure, or a magic bullet. Mice and humans are very different. This is not to say that I am not looking forward to the next step, a phase I trial with humans. I am very sure we will see this trial, and I will guess that we will see it in breast cancer, as the petri dish experiments seemed to have dramatic results.
Joel T Nowak, M.A., M.S.W.
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