Heisenberg
Well-Known Member
Many people have found this helpful over at the Facebook page I run. Written by my co-admin.
Cancer quackery (along with charlatanism surrounding HIV/AIDs) has to be one of the most noxious of all pseudoscience-based enterprises. The enormous prevalence of cancer represents immensely fertile ground for scammers, and 'alternative treatments' for cancer are sought by millions, supporting a sickeningly steady cash-flow in the direction of fakes, charlatans, and otherwise ignorant followers of charismatic nasties. As well as fostering generalised distrust in science and burning holes in wallets, cancer pseudoscience often steers patients away from their one and only shot at survival.
The Internet is abuzz with 'natural remedies' and 'holistic measures' against cancer, and a quick trawl through some of the websites spouting these false claims reveals that the nature and extent of the 'errors' (lies?) upon which they are based are as varied as they are pernicious. However, two hallmarks crop up invariably: 1, a gross de-emphasis of the complexity and diversity of cancer, and 2, a blurring of the (extremely important) distinction between cancer prevention and cancer cure. Equipped with a basic understanding of how cancer works, cancer pseudoscientists’ lack thereof becomes painfully obvious. They chronically demonstrate ignorance of the most elementary aspects of oncology which, when combined with a total lack of legal regulation (not to mention endorsement by certain celebrities), enables them to claim, smilingly, that they know the secret to curing cancer. In this note, I offer a basic explanation of how cancer works, focusing on the not-widely-enough-appreciated role that evolution, by means of natural selection, plays in tumour growth and development. Above all, I aim to facilitate your feeling more confident, in any future debates you might have, that 'cancer cure' pedlars, whether through malice or misguidance, are full of shit.
Some necessary background information
I think the best place to start is to consider normal body cells. Unlike free-living cells, such as bacteria, the cells of our body do not compete with each other for their own ‘selfish’ genetic propagation. On the contrary, they co-operate on a huge scale, through a vast network of elaborate communication mechanisms, dividing and assuming designated roles in adherence to instruction and signals, and even committing suicide, on cue, for the interests of the aggregate. This non-rebellious behaviour is of course explained by the fact that body cells are a collection of clones. Co-operative behaviour contributes to the propagation of their genes.
In each somatic cell (that means all cells except sperms and eggs), there is a copy of the body’s genome. Your genome is the sum of all your body’s genetic information, which is organised into 46 chromosomes – 22 pairs of 'autosomes' and one pair of sex chromosomes (‘XX’ or ‘XY’, depending on whether you are a boy or a girl). Far from being an inaccessible ‘blueprint’, as it is often dubbed, each cell’s genome is a dynamically active factory, churning out myriad different proteins in response to incoming demands, which are communicated via precise chemical signals that either come from within the cell, or originate somewhere else in the body. These signals work by selecting specific stretches of gene sequence (‘written’ in DNA) to be read off and converted into corresponding protein sequences (which are ‘written’ in amino acids). There are an enormous number of different proteins, each of which coils, bends and folds into its own unique shape. Some of these shapes act as building blocks for making structures such as muscle and skin, whereas others function as tools for breaking things apart, or putting things together. Some act as vehicles, carrying important stuff around the body, while others work to neutralise germs and viruses that get into us. Yet another class of proteins work in communication, as chemical signals (like those mentioned above), to trigger the production of yet more proteins, perhaps in cells some distance away from the ones in which they themselves were put together. In some cases, a protein’s communication errand entails recognising a certain sequence on a certain chromosome, and sticking to it in order to deactivate a gene, or perhaps cause it to go into programmed hyperactivity, which would result in a concentrated outflow of a specific protein. So, as we can see, each copy of the genome (in every cell) acts like a mini-factory, and The Genome, in its singlular, more abstract sense, is responsible for matching supply and demand in a vast supersystem of interconnected production, maintenance, communication, and transport subsystems.
The growth and maintenance of this supersystem depends on cells’ ability to make copies of themselves, which is itself based on DNA’s ability to self-duplicate, since every new cell needs its own copy of The Genome. As with any copying system, DNA replication has an inherent, unavoidable error-rate. In the course of a human lifetime, some 10,000,000,000,000,000, (yep, that’s ten thousand million million) cell divisions take place. It is estimated that the probability of an error being made is approximately 0.000001 per gene, per cell division, under normal circumstances (i.e. in the absence of mutagens– substances which promote mutation). It follows that any given gene in The Genome can be expected to have experienced mutation around one million times in one lifetime. Unsurprisingly, evolution has stumbled across a number of mechanisms to fix errors as they arise. Occasionally, however, things do slip through the net. And it is at these moments of accidental neglect that cancer has its chance to begin laying the groundwork for infiltration.
So, what is cancer?
Cancer is the product of a collection of genetic alterations that promote ‘selfish’ behaviour in cells, at the expense of the body in which they live. A situation is set up in which natural selection, fuelled by a building momentum of newly-acquired mutations, works (unintentionally, of course), to cultivate an increasingly deviant population of cells that “compete” with their neighbours to proliferate their own mutant genotypes, a phenomenon which begins to manifest as a tumour. In the sense that they are subject to natural selection, tumour cells have started to look quite like unicellular organisms such as bacteria, which, as we know all-too-well, can evolve extremely quickly, thanks to the exponentiating speed with which a cell population can multiply. So, in the case of cancer, what kind of accidentally-acquired traits could flip a perfectly respectable, law-abiding body cell into the realms of cancerous activity? And what skills might then be useful for it in its selfish accrual of control?
The most obvious power that must be acquired by a somatic (body) cell, via a change in its copy of the genome, is that of overcoming restraints on cell division. Cells that begin breaking the rules like this are, in most cases, eventually detected by patrolling immune surveillance mechanisms and sentenced to death by “apoptosis”, which consists in a signal that commands the cell to digest itself. By the time detection occurs, therefore, for the trajectory of cancer development to continue, another ‘ability’ must have been acquired: the faculty to evade such a signal. A mutation conferring this ability may arise before or after uncontrolled cell division was allowed to begin, but of course one of the numerical implications of increased division is that the absolute rate of copying errors is increased, so it follows that an already-illegitimately-dividing cell lineage has an enhanced likelihood of chancing upon a signal-evasion mutation.
Now, any additional increase in tendency toward DNA mutation represents another advantageous trait for a cancer cell in-the-making and, therefore, any mutation that deactivates DNA repair mechanisms, or tampers with DNA copying mechanisms themselves, become favoured. (As a quick aside, when we talk of a “favoured” mutation, what do we mean, in this context? Well, simply one that boosts a cell’s probability of reproducing more prolifically, relative to cells lacking the mutation – a condition whichresults in it being replicated more than its un-mutated counterpart, and thus becoming increasingly proportionately well-represented in the population, as this population grows.)
The next barrier a potential cancer cell in a growing mass must overcome is the ability to colonise other parts of the body. This feat necessitates breaking free from the stringy matrix of proteins that surrounds all cells, keeping them stationary. Without away to do this, a cell can spawn a mass of abnormal offspring, but this localised tumour can be easily surgically removed. Such a tumour is considered ‘benign’. Conversely, a tumour whose cells have undergone mutations that allow them to invade surrounding tissues is considered malignant. Fugitive cells are said to have metastasised, escaping through blood or lymphatic vessels to form secondary tumours, or metastases, in other parts of the body. Once this has happened, it can be very difficult, and often impossible, to eradicate the disease.
A 'Miracle Cure' for cancer?
Now, in case it hasn’t already become clear that no amount of Chinese herbs or mango juice, or religious adherence to a macrobiotic diet could possibly 'cure cancer', I want to discuss this now. 'Cancer' is in fact not a disease, but a category of highly diverse diseases, the exact causes of which, both ultimate and proximate, are different in every patient. At this point, I want to distinguish between ultimate and proximate causes. Ultimate causes are things like smoking, drinking, exposure to radiation or UV, inherited predisposition, diet, lack of physical activity, and a whole load of other things that are yet to be identified. Proximate causes are the specific mutations, conferring the specific traits discussed above, that allow cancer to begin and progress. Everyone knows that cancers have a lot of different, interacting ultimate causes. What a lot of people don’t know is that cancers have an extraordinarily diverse set of proximate causes, too.
It is thought that, in most cases, between 5 and 10 mutations, contributing towards the selfish powers outlined above, are needed to create the conditions for full-blown cancer. However, (and crucial for our purposes of winning in a debate in which somebody says that cancer can be cured with megadoses of vitamin C, ginseng tea and bloodroot extract), these mutations may appear in any of thousands of candidate genes. A “favourable” cancer-enabling trait like genetic instability could be achieved through disruption of any of a huge number of possible cellular systems, at any of a huge number of potential stages along the biochemical pathway making up such a system. Since so many genes, and such an immense number of genetic interactions and systems are involved in the regulation of cell behaviour, in any given case, a unique profile of mutations (and therefore a unique set of cellular malfunctions) can give rise to the same cancerous symptoms in cells. This can be seen by looking at the genetic mutations found in tumours from different people suffering from the same form of cancer. While there are some genes that present mutations in a considerable number of cases, most mutations harboured in a cancer cell genome are ones that have never been seen before. In fact, if you compare cells taken from different areas of the same tumour, you find that there is considerable diversity in terms of what has mutated. Also, the more genetically diverse a tumour cell population is, the better its odds, by chance, of harbouring mutations that protect it from potential treatments, so the more likely it is to survive and recoup after an attack from a course of radiotherapy, chemotherapy, or individually-targeted drugs. Particularly sinister here is that, since the survivors of such an attack become the genetic founders of the subsequently regenerated tumour cell population, any mutations which played a role in allowing the surviving cells to live through such an attack will now be ubiquitous. By the time the tumour has grown back, it will therefore be extra-robust: more resistant to future attacks of the same kind, and sporting a whole load of new mutations to boot. This is just one of the reasons why choosing the right treatment, at the right dosage, is absolutely critical.
At the centre of cancer are not ‘cancer genes’, but an interdependent, and massively complex network of biochemical pathways, all of which are potentially disturbed by mutations in any of the genes involved in making them work. An effective cancer drug therefore needs a very specific mode of action – it needs to attack individual components of a faulty biochemical pathway. In the absence of knowledge of which biochemical pathways have been mutated, there is no ‘way in’. We are far from understanding all cellular biochemical pathways, and even further from understanding the precise ways in which each gene is involved in those pathways. What we do know is that it is monstrously and mind-bogglingly convoluted. I hope it’s becoming clear by now just how impossible it is for someone who has not examined the genetic aberrations within a specific tumour, and who does not understand cell biology, to make it go away.
Even if we did have a full documentation and understanding of all the biochemistry going on in cells, the idea of a comprehensive, all-round “Cure for Cancer” is implausible, due to the sheer number of different genetic and chemical components involved in different types of ‘the disease’.
Current cancer treatments take advantage of the properties that define cancer cells as distinct from normal cells. For example, some exploit their genetic instability. Ionising radiation, for instance, damages DNA. Both normal and abnormal cells get zapped, but whilst normal cells will arrest their cell cycles until they have repaired it, cancer cells, characterised by their ‘ability’ to ignore damage to their DNA and continue dividing, continue to multiply, and therefore die as a result of the catastrophic DNA damage they experience when they attempt to divide with defective chromosomes.
The main defining feature of CAM cancer 'treatments', as compared with science-based cancer treatments (apart from the simple fact that the former do not work, of course
) is that, unlike science-based cancer treatments, they are not targeted. Drug targets emerge from what is known about cell biochemistry. Biochemical pathways that can be seen to have been disrupted by mutation in a significant number of cancer cases represent places to look for such targets. Their various stages each represent a sort of window through which cellular behaviour might be modulated. Herceptin provides a good illustration. The 'HER2' gene, which mediates the 'HER2' pathway, is mutated in 20-30% of breast cancers, causing the production of too much of a certain protein which, through a cascade of cellular communication events, triggers cell proliferation. Herceptin intersects at one of these stages, and can in some cases halt tumour growth. The success of the treatment depends on perfect specificity between the drug and the drug target.
'Complementary' and 'Alternative' medicine (CAM) providers’ claims that alkaline water, or juice-fasting, or coffee enemas can 'cure cancer', apart from anything else, makes the erroneous assumption that cancer is a single disease, entirely overlooking the diversity that characterises cancer as a disease category, and directs research in oncology. These cancer cure claims can often also be easily identified by their appearance in CAM (or general) advice on cancer prevention. There are indeed various lifestyle changes that can be made to reduce risk of cancer onset, but once cancer has begun, none of these changes are capable of targeting an already-growing mass of cells. Reducing risk of cancer involves minimising risk of genetic mutation before the event. Incidentally, many phoney cancer-cure claimants invoke the 'power of antioxidants' to destroy tumours. This presumably stems from the suggestion that antioxidants can help reduce the risk of cancers developing in the first place. Notwithstanding the fact that the antioxidant hypothesis has now been called into question (see http://extremelongevity.net/wp-content/uploads/antioxidants.pdf), the reasoning that says “since antioxidants help prevent cancer, flooding already-present cancer with them must help to cure it too” is fallacious, and in some cases, antioxidants can actually help protect cancer cells that have broken away from their surrounding mesh of protein and would otherwise have died as a result.
While some of the big cheeses in CAM are no doubt ignorant rather than just callous, I'm not sure the distinction is particularly pertinent, since their ignorance is elective. All the information is out there, and making the active decision not to study cancer before taking cancer patients' lives into one's hands is shamelessly unethical. Hardly surprising though, since being an oncologist means years of training and difficult exams. CAM practitioners seem to want it all: to avoid ever putting in any effort to really understand cancer pathology, yet reap the rewards of being looked up to as experts; to earn the money and the reputation, yet circumvent the academic scrutiny that legitimises it. To achieve all this, they cheat, lie and manipulate, unconditionally dismissing all evidence against the efficacy of their methods. They cash in on oncologists’ deeply-held responsibility to be absolutely realistic about what can and cannot be expected from available treatment in any given case, offering failsafe cures where doctors could not. As Science-Based Medicine’sDavid Gorski puts it: “It is ironic that CAM proponents often simultaneously tout how individualized their treatment approach is, but then claim that one product or treatment can cure all cancer. Meanwhile they criticize the alleged cookie-cutter approach of mainstream medicine, which is actually producing a more and more individualized (and evidence-based) approach to such things as cancer.”
Our only weapon against CAM’s Crimes Against Humanity is education. Next time someone casually mentions that cancer can be cured "from within", or that “acid degradation of cells” is what causes cancer, don’t let it slide!
– E. R. Eastop
Cancer quackery (along with charlatanism surrounding HIV/AIDs) has to be one of the most noxious of all pseudoscience-based enterprises. The enormous prevalence of cancer represents immensely fertile ground for scammers, and 'alternative treatments' for cancer are sought by millions, supporting a sickeningly steady cash-flow in the direction of fakes, charlatans, and otherwise ignorant followers of charismatic nasties. As well as fostering generalised distrust in science and burning holes in wallets, cancer pseudoscience often steers patients away from their one and only shot at survival.
The Internet is abuzz with 'natural remedies' and 'holistic measures' against cancer, and a quick trawl through some of the websites spouting these false claims reveals that the nature and extent of the 'errors' (lies?) upon which they are based are as varied as they are pernicious. However, two hallmarks crop up invariably: 1, a gross de-emphasis of the complexity and diversity of cancer, and 2, a blurring of the (extremely important) distinction between cancer prevention and cancer cure. Equipped with a basic understanding of how cancer works, cancer pseudoscientists’ lack thereof becomes painfully obvious. They chronically demonstrate ignorance of the most elementary aspects of oncology which, when combined with a total lack of legal regulation (not to mention endorsement by certain celebrities), enables them to claim, smilingly, that they know the secret to curing cancer. In this note, I offer a basic explanation of how cancer works, focusing on the not-widely-enough-appreciated role that evolution, by means of natural selection, plays in tumour growth and development. Above all, I aim to facilitate your feeling more confident, in any future debates you might have, that 'cancer cure' pedlars, whether through malice or misguidance, are full of shit.
Some necessary background information
I think the best place to start is to consider normal body cells. Unlike free-living cells, such as bacteria, the cells of our body do not compete with each other for their own ‘selfish’ genetic propagation. On the contrary, they co-operate on a huge scale, through a vast network of elaborate communication mechanisms, dividing and assuming designated roles in adherence to instruction and signals, and even committing suicide, on cue, for the interests of the aggregate. This non-rebellious behaviour is of course explained by the fact that body cells are a collection of clones. Co-operative behaviour contributes to the propagation of their genes.
In each somatic cell (that means all cells except sperms and eggs), there is a copy of the body’s genome. Your genome is the sum of all your body’s genetic information, which is organised into 46 chromosomes – 22 pairs of 'autosomes' and one pair of sex chromosomes (‘XX’ or ‘XY’, depending on whether you are a boy or a girl). Far from being an inaccessible ‘blueprint’, as it is often dubbed, each cell’s genome is a dynamically active factory, churning out myriad different proteins in response to incoming demands, which are communicated via precise chemical signals that either come from within the cell, or originate somewhere else in the body. These signals work by selecting specific stretches of gene sequence (‘written’ in DNA) to be read off and converted into corresponding protein sequences (which are ‘written’ in amino acids). There are an enormous number of different proteins, each of which coils, bends and folds into its own unique shape. Some of these shapes act as building blocks for making structures such as muscle and skin, whereas others function as tools for breaking things apart, or putting things together. Some act as vehicles, carrying important stuff around the body, while others work to neutralise germs and viruses that get into us. Yet another class of proteins work in communication, as chemical signals (like those mentioned above), to trigger the production of yet more proteins, perhaps in cells some distance away from the ones in which they themselves were put together. In some cases, a protein’s communication errand entails recognising a certain sequence on a certain chromosome, and sticking to it in order to deactivate a gene, or perhaps cause it to go into programmed hyperactivity, which would result in a concentrated outflow of a specific protein. So, as we can see, each copy of the genome (in every cell) acts like a mini-factory, and The Genome, in its singlular, more abstract sense, is responsible for matching supply and demand in a vast supersystem of interconnected production, maintenance, communication, and transport subsystems.
The growth and maintenance of this supersystem depends on cells’ ability to make copies of themselves, which is itself based on DNA’s ability to self-duplicate, since every new cell needs its own copy of The Genome. As with any copying system, DNA replication has an inherent, unavoidable error-rate. In the course of a human lifetime, some 10,000,000,000,000,000, (yep, that’s ten thousand million million) cell divisions take place. It is estimated that the probability of an error being made is approximately 0.000001 per gene, per cell division, under normal circumstances (i.e. in the absence of mutagens– substances which promote mutation). It follows that any given gene in The Genome can be expected to have experienced mutation around one million times in one lifetime. Unsurprisingly, evolution has stumbled across a number of mechanisms to fix errors as they arise. Occasionally, however, things do slip through the net. And it is at these moments of accidental neglect that cancer has its chance to begin laying the groundwork for infiltration.
So, what is cancer?
Cancer is the product of a collection of genetic alterations that promote ‘selfish’ behaviour in cells, at the expense of the body in which they live. A situation is set up in which natural selection, fuelled by a building momentum of newly-acquired mutations, works (unintentionally, of course), to cultivate an increasingly deviant population of cells that “compete” with their neighbours to proliferate their own mutant genotypes, a phenomenon which begins to manifest as a tumour. In the sense that they are subject to natural selection, tumour cells have started to look quite like unicellular organisms such as bacteria, which, as we know all-too-well, can evolve extremely quickly, thanks to the exponentiating speed with which a cell population can multiply. So, in the case of cancer, what kind of accidentally-acquired traits could flip a perfectly respectable, law-abiding body cell into the realms of cancerous activity? And what skills might then be useful for it in its selfish accrual of control?
The most obvious power that must be acquired by a somatic (body) cell, via a change in its copy of the genome, is that of overcoming restraints on cell division. Cells that begin breaking the rules like this are, in most cases, eventually detected by patrolling immune surveillance mechanisms and sentenced to death by “apoptosis”, which consists in a signal that commands the cell to digest itself. By the time detection occurs, therefore, for the trajectory of cancer development to continue, another ‘ability’ must have been acquired: the faculty to evade such a signal. A mutation conferring this ability may arise before or after uncontrolled cell division was allowed to begin, but of course one of the numerical implications of increased division is that the absolute rate of copying errors is increased, so it follows that an already-illegitimately-dividing cell lineage has an enhanced likelihood of chancing upon a signal-evasion mutation.
Now, any additional increase in tendency toward DNA mutation represents another advantageous trait for a cancer cell in-the-making and, therefore, any mutation that deactivates DNA repair mechanisms, or tampers with DNA copying mechanisms themselves, become favoured. (As a quick aside, when we talk of a “favoured” mutation, what do we mean, in this context? Well, simply one that boosts a cell’s probability of reproducing more prolifically, relative to cells lacking the mutation – a condition whichresults in it being replicated more than its un-mutated counterpart, and thus becoming increasingly proportionately well-represented in the population, as this population grows.)
The next barrier a potential cancer cell in a growing mass must overcome is the ability to colonise other parts of the body. This feat necessitates breaking free from the stringy matrix of proteins that surrounds all cells, keeping them stationary. Without away to do this, a cell can spawn a mass of abnormal offspring, but this localised tumour can be easily surgically removed. Such a tumour is considered ‘benign’. Conversely, a tumour whose cells have undergone mutations that allow them to invade surrounding tissues is considered malignant. Fugitive cells are said to have metastasised, escaping through blood or lymphatic vessels to form secondary tumours, or metastases, in other parts of the body. Once this has happened, it can be very difficult, and often impossible, to eradicate the disease.
A 'Miracle Cure' for cancer?
Now, in case it hasn’t already become clear that no amount of Chinese herbs or mango juice, or religious adherence to a macrobiotic diet could possibly 'cure cancer', I want to discuss this now. 'Cancer' is in fact not a disease, but a category of highly diverse diseases, the exact causes of which, both ultimate and proximate, are different in every patient. At this point, I want to distinguish between ultimate and proximate causes. Ultimate causes are things like smoking, drinking, exposure to radiation or UV, inherited predisposition, diet, lack of physical activity, and a whole load of other things that are yet to be identified. Proximate causes are the specific mutations, conferring the specific traits discussed above, that allow cancer to begin and progress. Everyone knows that cancers have a lot of different, interacting ultimate causes. What a lot of people don’t know is that cancers have an extraordinarily diverse set of proximate causes, too.
It is thought that, in most cases, between 5 and 10 mutations, contributing towards the selfish powers outlined above, are needed to create the conditions for full-blown cancer. However, (and crucial for our purposes of winning in a debate in which somebody says that cancer can be cured with megadoses of vitamin C, ginseng tea and bloodroot extract), these mutations may appear in any of thousands of candidate genes. A “favourable” cancer-enabling trait like genetic instability could be achieved through disruption of any of a huge number of possible cellular systems, at any of a huge number of potential stages along the biochemical pathway making up such a system. Since so many genes, and such an immense number of genetic interactions and systems are involved in the regulation of cell behaviour, in any given case, a unique profile of mutations (and therefore a unique set of cellular malfunctions) can give rise to the same cancerous symptoms in cells. This can be seen by looking at the genetic mutations found in tumours from different people suffering from the same form of cancer. While there are some genes that present mutations in a considerable number of cases, most mutations harboured in a cancer cell genome are ones that have never been seen before. In fact, if you compare cells taken from different areas of the same tumour, you find that there is considerable diversity in terms of what has mutated. Also, the more genetically diverse a tumour cell population is, the better its odds, by chance, of harbouring mutations that protect it from potential treatments, so the more likely it is to survive and recoup after an attack from a course of radiotherapy, chemotherapy, or individually-targeted drugs. Particularly sinister here is that, since the survivors of such an attack become the genetic founders of the subsequently regenerated tumour cell population, any mutations which played a role in allowing the surviving cells to live through such an attack will now be ubiquitous. By the time the tumour has grown back, it will therefore be extra-robust: more resistant to future attacks of the same kind, and sporting a whole load of new mutations to boot. This is just one of the reasons why choosing the right treatment, at the right dosage, is absolutely critical.
At the centre of cancer are not ‘cancer genes’, but an interdependent, and massively complex network of biochemical pathways, all of which are potentially disturbed by mutations in any of the genes involved in making them work. An effective cancer drug therefore needs a very specific mode of action – it needs to attack individual components of a faulty biochemical pathway. In the absence of knowledge of which biochemical pathways have been mutated, there is no ‘way in’. We are far from understanding all cellular biochemical pathways, and even further from understanding the precise ways in which each gene is involved in those pathways. What we do know is that it is monstrously and mind-bogglingly convoluted. I hope it’s becoming clear by now just how impossible it is for someone who has not examined the genetic aberrations within a specific tumour, and who does not understand cell biology, to make it go away.
Even if we did have a full documentation and understanding of all the biochemistry going on in cells, the idea of a comprehensive, all-round “Cure for Cancer” is implausible, due to the sheer number of different genetic and chemical components involved in different types of ‘the disease’.
Current cancer treatments take advantage of the properties that define cancer cells as distinct from normal cells. For example, some exploit their genetic instability. Ionising radiation, for instance, damages DNA. Both normal and abnormal cells get zapped, but whilst normal cells will arrest their cell cycles until they have repaired it, cancer cells, characterised by their ‘ability’ to ignore damage to their DNA and continue dividing, continue to multiply, and therefore die as a result of the catastrophic DNA damage they experience when they attempt to divide with defective chromosomes.
The main defining feature of CAM cancer 'treatments', as compared with science-based cancer treatments (apart from the simple fact that the former do not work, of course
) is that, unlike science-based cancer treatments, they are not targeted. Drug targets emerge from what is known about cell biochemistry. Biochemical pathways that can be seen to have been disrupted by mutation in a significant number of cancer cases represent places to look for such targets. Their various stages each represent a sort of window through which cellular behaviour might be modulated. Herceptin provides a good illustration. The 'HER2' gene, which mediates the 'HER2' pathway, is mutated in 20-30% of breast cancers, causing the production of too much of a certain protein which, through a cascade of cellular communication events, triggers cell proliferation. Herceptin intersects at one of these stages, and can in some cases halt tumour growth. The success of the treatment depends on perfect specificity between the drug and the drug target.'Complementary' and 'Alternative' medicine (CAM) providers’ claims that alkaline water, or juice-fasting, or coffee enemas can 'cure cancer', apart from anything else, makes the erroneous assumption that cancer is a single disease, entirely overlooking the diversity that characterises cancer as a disease category, and directs research in oncology. These cancer cure claims can often also be easily identified by their appearance in CAM (or general) advice on cancer prevention. There are indeed various lifestyle changes that can be made to reduce risk of cancer onset, but once cancer has begun, none of these changes are capable of targeting an already-growing mass of cells. Reducing risk of cancer involves minimising risk of genetic mutation before the event. Incidentally, many phoney cancer-cure claimants invoke the 'power of antioxidants' to destroy tumours. This presumably stems from the suggestion that antioxidants can help reduce the risk of cancers developing in the first place. Notwithstanding the fact that the antioxidant hypothesis has now been called into question (see http://extremelongevity.net/wp-content/uploads/antioxidants.pdf), the reasoning that says “since antioxidants help prevent cancer, flooding already-present cancer with them must help to cure it too” is fallacious, and in some cases, antioxidants can actually help protect cancer cells that have broken away from their surrounding mesh of protein and would otherwise have died as a result.
While some of the big cheeses in CAM are no doubt ignorant rather than just callous, I'm not sure the distinction is particularly pertinent, since their ignorance is elective. All the information is out there, and making the active decision not to study cancer before taking cancer patients' lives into one's hands is shamelessly unethical. Hardly surprising though, since being an oncologist means years of training and difficult exams. CAM practitioners seem to want it all: to avoid ever putting in any effort to really understand cancer pathology, yet reap the rewards of being looked up to as experts; to earn the money and the reputation, yet circumvent the academic scrutiny that legitimises it. To achieve all this, they cheat, lie and manipulate, unconditionally dismissing all evidence against the efficacy of their methods. They cash in on oncologists’ deeply-held responsibility to be absolutely realistic about what can and cannot be expected from available treatment in any given case, offering failsafe cures where doctors could not. As Science-Based Medicine’sDavid Gorski puts it: “It is ironic that CAM proponents often simultaneously tout how individualized their treatment approach is, but then claim that one product or treatment can cure all cancer. Meanwhile they criticize the alleged cookie-cutter approach of mainstream medicine, which is actually producing a more and more individualized (and evidence-based) approach to such things as cancer.”
Our only weapon against CAM’s Crimes Against Humanity is education. Next time someone casually mentions that cancer can be cured "from within", or that “acid degradation of cells” is what causes cancer, don’t let it slide!
– E. R. Eastop