In the interests of balance, if you wish to investigate Peter Duesberg’s views from his own side of the argument, you should google for his website. However, the sources listed above address all of the issues raised and resoundly defend the mainstream scientific consensus. In the case of denying that HIV causes AIDS, his claims are incredibly harmful in the face of evidence.

Notice that virtually all cancers are aneuploid. If cells with a new, different set of chromosomes appears, that is a new species of life. That happens in cancers and even explains sudden resistance to chemotherapeutic agents.

Mostly the aneuploidy is not about changing the code for one gene though that can happen with random recombination of broken chromosomes. On the other hand losing or gaining an extra copy of an entire chromosome in one blow changes the use of hundreds or thousands of genes. Most such radical changes are harmful to those cells, but sometimes a more effective cell line is born.

How do we disagree here?

Lack of funding might be because there is no monopoly profit to be made. The high expense of conducting an FDA clinical trial serves to preclude approving any treatment other than a new patented drug. No supplements or dietary arrangements need apply. Indeed, it could be valuable to our health to address methods for making much cheaper clinical trials possible.

Your turn.

To start with, chromosome aberrations are a form of mutation. They are important in some forms of cancer, especially leukemias, but haven’t been implicated in any other types of cancer as far as I know. I’m going to be working with leukemia for the next five months (starting Monday, I’m very excited!), with a specific chromosome fusion event that creates the fusion protein AML1-ETO so there will be at least one post dedicated to this type of mutation, as well as another on leukemia in general. On this note – and I’m aware that you may take this the wrong way and decide that I’m being evasive – I’m busy packing and making arrangements to move to Frankfurt tomorrow so I don’t have time to find indesputable sources for everything I’m going to say here, or to follow up the work you’ve cited. The next week is going to be fairly hectic, but I’ll try to get back and give you some sources – I don’t want you to simply ‘take my word for it’.

Assuming that when you say ‘mutations’ you mean ‘point mutations’ (a single base change – a single letter of the DNA code being substituted for something else, deleted, or inserted) I would be extremely interested to find out why you think that they’ve never been shown to cause cancer, and why you think they’re rare. There is no question whatsoever that mutations cause cancer. None at all. Anyone who was able to show otherwise would be heralded as a hero by the scientific community. The fact that cancers evolve is also not under review by any legitimate researchers. The first example that springs to mind is that the progression from a benign neoplasia (a tumour that doesn’t invade neighbouring tissues) to a malignant one. That step requires an additional mutation (often in pathways that regulate the extra-cellular material, so the cells can ‘chew’ their way through tissues) that allows the cells that have it to escape their compartment and replicate further in other parts of the body: a form of evolution. This is not a ‘failed theory’, it’s a fact that is useful to bear in mind when thinking about cancer.

The only ‘cancers’ that I can think of that do not result from mutations are warts. These are benign neoplasias (which don’t count: no-one would really call a wart ‘cancer’) caused by a virus, HPV, a virus that may be familiar as other strains cause cervical cancer. For the non-invasive mass to become cancer, though, further mutations are needed, and these are common in cervical cells infected with HPV strains 16 and 18 – hence cervical cancer. Again, there will be a post later on viral causes of cancer.

You are correct in saying that asbestos doesn’t cause mutations, yet causes cancer. Here’s a simplified version of asbestos carcinogenesis (yet again, I may write a post explaining this a little better, especially since one of my lecturers last year died of mesothelioma, a type of cancer that is almost always caused by asbestos): asbestos in the lung consists of small particles that cause a certain degree of damage. The immune system sees this and tries to destroy the ‘invading’ particles but cant. The variety of weapons used by the immune cells causes further damage to neighbouring cells and you enter a vicious cycle. This results in a structure called a granuloma – asbestos particle in the middle, surrounded by dead, dying, and angry immune cells, and a wall of cells and extra-cellular proteins grows around it to stop the damage from spreading (as well as barricading the pathogens that the body thinks are invading). There are lots of growth factors and other signalling molecules floating around thick and fast, and you create an environment where some of the hallmarks (mentioned in the post) are not required to the same extent as usual. Thus it becomes easier for cancer to develop, and given several years, you end up with a vastly increased chance of getting cancer.

Getting approval for a clinical trial is not difficult as long as you can show that it is safe. If the ladies and gentlemen of Wake Forest cannot get support (i.e. funding, I assume), it is probably because they lack both the evidence that cancer resistance exists, or any kind of plausibility for such a phenomenon, and more importantly, evidence that if one were resistant to one’s own cancer, you could transfer that resistance to anyone else. You must remember that every cancer is unique and is descended from a different source.

You may not see much research on neutrophils with regard to cancer because they aren’t involved. Neutrophils are immune cells that respond very quickly to acute inflammation. If you get a cut, neutrophils will congregate there within minutes to phagocytose (’eat’) particles/bacteria/viruses that have entered, and to signal to the rest of the immune system that there is a problem. Other types of immune cell, such as NK and Cytotoxic T cells are much more important in defending against cancer, because they find cells that have a problem (i.e. they are cancerous or are infected with a virus) and they tell it to commit suicide (apoptosis). Furthermore, neutrophils are part of the innate immune system: they have no mechanism of resistance or memory. They will respond in the same manner, no matter how many times the problem has occured before.

I appreciate your comment, because it has helped to highlight certain areas that I want to focus on, and if you have any more queries, I’d be glad to help. From next week, I may even be able to consult bona fide cancer experts, and I will take a look at the work you’ve alluded to when I have the chance

Pay more attention to the insightful Peter Duesberg. He has explained in some detail how aneuploidy (loss, gain, or rearrangement of whole chromosomes) does the job, but can take decades to develop from the initial genetic instability of an aneuploid cell into a life threatening aggressive metastasizing cancer.

What I don’t understand is why a highly effective treatment via transfusion of white blood cells from cancer resistant people into patients with cancer can’t get support to carry out an already approved clinical trial at Wake Forest.

Where are the major studies of how neutrophil mediated cancer resistance works? Why do we not see in vitro experiments with many kinds of cancer cells with blood from cancer resistant people? Dr. Zheng Cui at Wake Forest Baptist Medical Center can explain how to screen blood donors for cancer resistance.