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Cancer Resistant Mice

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For those looking to see if ID returns false positives (ASSUMING that indeed there is additional CSI involved in this immunity, which is apparently unknown at this time).


Spontaneous regression/complete resistance (SR/CR) mice resist very high doses of cancer cells that are lethal to WT mice even at low doses. In this study, we show that this resistance is mediated by rapid infiltration of leukocytes, mostly of innate immunity, in both primary and repeated challenges. Formation of rosettes with infiltrating natural killer cells, neutrophils, and macrophages was required for the subsequent destruction of cancer cells through rapid cytolysis. Highly purified natural killer cells, macrophages, and neutrophils from the SR/CR mice independently killed cancer cells in vitro. The independent killing activity by each subset of effector cells is consistent with the observation that the resistance was abolished by depleting total infiltrating leukocytes but not by depleting only one or two subsets of leukocytes. The resistance was completely transferable to WT recipient mice through SR/CR splenocytes, bone marrow cells, or enriched peritoneal macrophages, either for prevention against subsequent cancer challenges or eradication of established malignancy at distant sites.


Most research involving mice uses one of a large number of inbred strains, which have been bred for generations so that each mouse within a strain should be genetically identical to all others. This limits the potential confounding effects of genetic background on things like drug studies, and also means that tissues can be transplanted between individuals of a strain without immune rejection. That’s the idea, at least. In reality, there is nothing that keeps the forces that work on wild populations, such as random mutation and selective pressures, from acting on mice in cages.

That’s the background for a paper that appears in the latest PNAS, and is summarized in the New York Times, which also provides some historical information on the topic. Back in 1999, a lab received some mice of the BALB/c strain. These mice were to be injected with cancerous cells in order to study the spread of cancer, which should ultimately result in the death of the mice. This worked out as expected in most cases, but a single mouse refused to go along with the program: repeated injections failed to kill it. It’s often said that the most interesting scientific results are met with the phrase, “huh, strange,” and this was no exception.

The researchers gave up on injections, and started breeding the mouse, discovering that its resistance to tumor growth was heritable. In the latest paper, they identify the mediator of the resistance as being the white blood cells of the immune system. In these mice, a combination of natural killer cells, neutrophils, and macrophages quickly homed in on tumor cells and caused them to lyse, or explode. Intriguingly, transplanting the immune cells to other mice via a bone marrow transplant transferred the cancer immunity as well, indicating that it’s the immune cells themselves, rather than some context information, that provide the resistance.

It’s important to note that this revved-up immune system may not be generally healthy for mice; after all, in humans, overactive immune systems cause things like diabetes, multiple sclerosis, and lupus. But understanding the mechanism by which these mice wipe out tumor cells may allow the process to be replicated in a controlled manner. A temporarily hyperactive immune system may be able to stop or slow cancer without causing many more problems than many current forms of chemotherapy.

Haven’t had time to read the full PNAS article myself but I think it’s interesting that the author automatically jumps to assuming RM+NS as the mechanism without any evidence either way. But as pointed out the immunity “might” be due to a failure in the immune system by which the immune cells are overactive and attack things it normally would not. In short, there was a loss of information in the controlling mechanisms that provides a benefit under certain circumstances but is a negative in most others.


Very interesting stuff. Since the mice seem to have knock-out genes and similiar immune system to humans. A lot of current research in cancer, such as breast cancer, study these immunological effects. One in particular is Tak Mak of the University of Toronto. In his lab you will find very common type of research with mouse immunity and studying designed systems. In the medical biophysics department, they are currently designing medicines for diseases such as cancer. There seem to be an instant connection with design and cancer research.

Is there an official ID stance on inbreeding? Natural selection seems to be at odds with itself on this. Inbreeding can preserve positive traits, but at the same time introducing eventually lethal genetic drift (copy of a copy ...). So lethal that not even cancer survives in such a creature (such as the one mentioned in this article) Perhaps 'random mutations' are not so random after all, but rather the result of breeding methods which are outside of the 'design model'. Perhaps these mutations don't foster new traits, but simply retard the expression of the designed traits (such as immuno-response?) ID would seek to express itself in intelligent breeding activities, which might have the goal of avoiding in-breeding completely. Collin DuCrâne

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