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Why has a cure for cancer/hiv/aids not been found yet?


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I have read some where that if such permanent cures were to be found than pharmaceutical companies would lose alot of profit from there temporary cures for these diseases...

 

but out of curiosity what is so difficult about finding a cure for cancer, I have a resonable knowledge with biology as I am currently studying it, just curious..

 

*I'm not saying that it should be easy to find one, just wondering why it is so hard to find one:p

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Fundamentally it is because the human body and indeed any organism is a very complex system. There are lots of things to take care of and small changes in something can lead to big effects and changes elsewhere.

 

I am sounding like Dr Ian Malcolm now! Chaos theory anyone?

 

I am sure others here can give you a better idea of specifics here.

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Cancer is more the end result of a number of mutations occurring within your own cells.

 

To some degree each cancer type and even individual cells are different. If even one is missed or has evolved some means of evading the cancer can start up again.

 

We've only just started finding focused techniques to attack cancer. Previously it was all broad methods that killed as many good cells as bad, and were not 100% effective at removing all traces of the malfunctioning cells.

 

HIV/AIDS is somewhat similar, though in this case a virus is hijacking one of our own immune responses to spread.

 

Anything that can react via evolution is going to be a long uphill battle for human medicine techniques.

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As mentioned, cancer is essentially not a disease per se, but rather a systemic issue with the way our cells propagate themselves. There will be no simple cure just a hope that we will find something that kills those cells more efficiently than others. Even today, more focused approaches are not that selective and have mostly been shown to be effective in cultures. In whole organisms or even tissues it will be quite difficult and is likely to cause severe damage (but hopefully less than full-blown chemo).

In addition to cell-type specificity there is also the issue of delivery, for example.

 

HIV has the issue that the parts being identified by our immune system change a lot so that vaccinations generally do not work. I have heard of some progress in that area, though.

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  • 2 weeks later...

There is some semantic innuendo to do with your question. The problem with finding a cure for cancer is that there probably isn't one. "Cancer" encompasses many diseases each with their own complications to the respective region they affect, i.e. no universal cure -- so even if one were to cure a particular kind of cancer, that does not guarantee any immediate success for the other kinds.

 

Simplistically, cancer results from a group of cells stuck in perpetual mitosis. At first, I thought a universal cure would be realistic as long as we focus on fixing that perpetual mitosis. However, one quickly realizes that a botched cell cycle has many potential causes, each with its own complicated mechanism. Nonetheless, your question still stands. Even with teams of scientists focusing on those specific mechanisms, why have none of them found a cure for just one of all the many different types of cancer?

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Determinate Individualism: Each cell is its own individual. This also applies to particles. As well as DNA/RNA. Everything that exists! While a cell may look , act, seem alike, it is not. It is its own individual. Space, Time, Mass makes sure this is self evident. As no single cell is ever in the same place, or at the same time. To be able to stop a free radical you must prevent it from forming. Which can be done by breaking it down to its individual source. Which realistically is very difficult.

 

Determinate Individualism is also the reason we cannot cure the common cold. As each of the many billions and trillions of cells in a organism is its own individual. It is equivalent of searching for a needle in a haystack that is a mile high and a mile wide.

 

Also consider. as each cell, particle is its own individual, it reacts( Causal/Effect) due to the other individual particles/cells in its environ. It is not random, rather the effect is based on the outcome of that interaction with other objects. As well as space,time. mass! One of the main factors is the state of each individual always in a form of movement. This applies to everything that exists. So, yes it is a very difficult endeavor for a scientist or researcher to find a cure.

Edited by jduff
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  • 3 weeks later...

Cannabinoids like cannabidiol have been proven to catalyse rogue cell death and protect healthy cells. Not a cure but preventive measure.

 

I only heard this from a documentory though

Edited by DevilSolution
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Isn't cancer just mutated cells?

 

Wouldn't a strong immune system with a lot of immune system cells, the mobile cells, be able to invoke apoptosis on the mutated cells?

 

Just seems pretty deluded to think that the human body cant defend itself as a whole when it receives the proper nutrition.

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Isn't cancer just mutated cells?

 

Wouldn't a strong immune system with a lot of immune system cells, the mobile cells, be able to invoke apoptosis on the mutated cells?

 

Just seems pretty deluded to think that the human body cant defend itself as a whole when it receives the proper nutrition.

 

 

The pathway for apoptosis itself can suffer from mutations.

 

There might actually be nutrition based preventative measures. Neither of the two sugars I know of are in anyone's normal diet though.

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The problem with cancer is a problem of heterogeneity. To begin with, there are various different types of cancer depending on the tissue from which the cancer arises. Then, the same type of cancer will be different for different people because our genomes, proteomes and metabolomes are not identical - and because different people are exposed to different environmental conditions throughout their lifetime - which will affect the nature of the individual's cancer. And then, even within an individual tumour there will be various different clumps of cells as a result of clonal expansion. And then, even within a given clone in a tumour, the individual cells will be different. And remember that all of these levels of differentiation are in constant dynamic flux: over time, individual humans grow and change, their cancer may grow and become invasive/metastatic, or may remain static or even spontaneously regress. These changes will be underpinned by changes in the tumour clones - those with activated potent oncogenes or suppression of key tumour suppressor genes may be selected and so the cancer may evolve; individual cells within the tumour clones may die, survive, differentiate or de-differentiate depending on the signalling pathways operating within the cells. So, this is a taste of the heterogeneity that pervades the cancer problem. Attempting to find a universal cure would therefore be very challenging - I will not say impossible. There is still much about the basic biology of cancer that is unknown, although Weinberg's 'hallmarks of cancer' has arguably given the field a sensible basis on which to expand our knowledge, by uniting the universal features of all cancers - and so preventing the field of cancer biology from stagnating under the weight of its own complexities. Classic chemotherapies are generally highly toxic or cytostatic and are usually delivered systemically so adversely affecting the patient's normal cells and causing side-effects. By comparison with the treatment (cure) of bacterial infections with antibiotics, there is not such a marked difference between normal human versus cancerous human cells as there obviously is between normal human versus bacterial cells. There are some rationally-designed therapeutic agents targeted against key oncoproteins (see, for example, the tyrosine kinase inhibitor Gleevec which has been approved for the treatment of chronic myelogenous leukaemia and certain gastrointestinal stromal tumours). Any differences between normal versus cancer cells (e.g. expression of a cell surface receptor) will usually not be shared by all of the cells in a tumour. Therefore, any rationally- designed treatments targeted against the cell surface receptor will necessarily leave certain tumour cells untouched - once the other tumour cells have died, the remaining (resistant) ones are free to clonally expand and so cause recurrence of the tumour. Combination therapies will hopefully reduce the capacity for cancers to develop resistance to drugs in this manner. I think further work needs to be done on investigating the heterogeneity at all levels (between humans, between cancer types, between tumour clones, and at the single cell level between individual cells within tumour clones) so that we can develop more nuanced therapies, delivery regimes, personalised doses etc. In order to get to this stage of progression biologically and clinically, the supporting technologies (high-throughput genome sequencing, proteomics/mass spec and metabolomics at the single-cell level) need to be developed and to be affordable for high-throughput usage. I should note that drug development is also a very expensive business, costing something like $2 billion to get a new drug to market; perhaps there is room here for improved efficiency. Political lobbying might also have an impact on affordability, by for example diverting funds at the Treasury from one Department or from one section of the Health Department to fund basic and translational research (1.7% and 2.7% of GDP was spent on Science in the UK and US, respectively, in 2011) as well as subsidising cancer drugs (Cameron has recently pledged £400 million to keep the Cancer Drugs Fund running in the UK); the passive option is to wait for drug patents to expire as with Gleevec, the patent protecting the active principle will expire on 4 January 2015 and the patent protecting the beta crystal form of the active principal ingredient will expire on 23 May 2019. We need inspired biologists such as yourself to join the field and hopefully revolutionise our understanding so that efficacious treatments can be brought to the market sooner. I will address your question on HIV/AIDS later, need a coffee wink.png

Edited by Tridimity
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Yum. Coffee.

 

So, the problem with HIV/AIDS can also be considered one of heterogeneity. Any attempt at an effective vaccine against HIV as prophylaxis would require that a highly conserved part of the virus be selected as antigenic epitope. The problem here is that HIV has a high mutation rate and so administration of a vaccine targeting an antigenic epitope on the virus that is subject to mutation would result in destruction of those virus particles expressing the target epitope but preservation of those virus particles that have undergone mutation in this region and so effectively evade the vaccine-induced immune response against the virus. As such, HIV would then rapidly evolve, not only on transmission between humans but even within individual humans (note the parallels here with cancer evolution). It's kind of like an arms race between the virus and the immune system, with the virus constantly shifting the goalposts. There is some interest in targeting (amongst other molecules) GP120, a glycoprotein of molecular weight 120 that is exposed on the surface of the HIV envelope and mediates fusion with the membrane of the host cell. GP120 is evolutionarily highly conserved and so represents a good candidate target. More here: http://evolution.berkeley.edu/evolibrary/news/070301_hiv and here: http://en.wikipedia.org/wiki/HIV_vaccines#Clinical_trials_to_date

 

I would add also, as a general point, that progress in any field of medical research tends to be, for the most part, slow and steady. It takes a considerable amount of time to prove with an acceptable degree of certainty that, first of all, a given molecule represents a promising target for intervention; secondly, that there are therapeutic agents capable of interacting specifically with the biological target; thirdly, that any in vitro data are confirmed in animal models; fourthly, that the therapy is safe in humans and has the desired effect and minimal side-effects; finally, that the therapy is sufficiently cost-effective as to be made available by the National Health Service (in the UK) or as part of private healthcare policies (in the US, UK and many other parts of the world). A career scientist is lucky to contribute to or fulfil even one of the aforementioned goals; the really lucky ones see target validation through to the clinic.

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Great thoughts so far in this thread.Then, there's all the root causes of cancer, where to begin? An individual has varying degrees of control over potential risks to cancer-causing agents. As has been said here, cancer cells, and how they grow, remain unpredictable and in some cases mysterious. Even after seemingly effective treatments, ''tricky'' cancer cells are able to sort of 'hide' in some patients and resurface at later dates. It's very terrifying in that sense, that doctors think they have the disease under control, but come to find out, they don't. I think there have been trememdous strides though, so at least progress is being made.

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  • 3 weeks later...

An update on potential treatment options for HIV:

A potential new HIV treatment has a "profound and unprecedented" impact on the virus, according to animal studies published in the journal Nature.

Potent antibodies were able to wipe a hybrid of human and monkey immunodeficiency viruses from the bloodstream of monkeys within days. The findings could "revolutionise" the search for an HIV cure, say experts. The US researchers said trials in patients with HIV now needed to take place. The immune system produces precisely targeted antibodies to take out HIV, but the virus is able to rapidly mutate to evade the immune assault. However, some antibodies have been discovered that target the "conserved" parts of HIV - those that the virus struggles to change because they are vital for it to function.

 

'Undetectable'

 

Two groups, from Harvard Medical School and the National Institute of Allergy and Infectious Diseases, performed the first trials of these antibodies. They used rhesus macaques that had been infected with simian-human immunodeficiency virus (SHIV), a blend of HIV and the monkey equivalent. Data from the Harvard team showed that injection of the antibodies drove SHIV from the bloodstream until it reached undetectable levels after three to seven days. The effect lasted for one to three months, but in three monkeys the virus did not return to the blood during the 250-day study. Prof Dan Barouch told the BBC: "The effect with these potent antibodies is profound and unprecedented. It's probably as large an antiviral therapeutic effect as has ever been seen. "But we have to make sure we don't overhype and the limitation is the study is in animals, not humans." The antibodies were also able to attack the virus in some tissues. Drugs can assault the virus in the blood during normal HIV treatment, but the virus can hide in other parts of the body. These early findings raise the prospect of using antibodies to clear these tissues as well. Similar results were produced by the team at the National Institute of Allergy and Infectious Diseases

'Revolutionise'

 

HIV infection is incurable, although taking a daily dose of medication can keep the virus in check, giving patients a near-normal life expectancy. The antibodies will be tested in human clinical trials and if successful they could be used alongside antiretroviral drugs as a treatment. It may also be possible to devise a vaccine that could train the immune system to produce these antibodies.

However, both these ideas are dependent on human trials being successful. Commenting on the findings, Prof Louis Picker and Prof Steven Deeks said: "The findings of these two papers could revolutionise efforts to cure HIV." However, they warned that HIV was so prone to mutation that it was "likely that some people will harbour viruses that are resistant to one or more" of the antibodies.

 

 

 

http://www.bbc.co.uk/news/health-24745611

Here is the Nature paper Abstract:

Human immunodeficiency virus type 1 (HIV-1)-specific monoclonal antibodies with extraordinary potency and breadth have recently been described. In humanized mice, combinations of monoclonal antibodies have been shown to suppress viraemia, but the therapeutic potential of these monoclonal antibodies has not yet been evaluated in primates with an intact immune system. Here we show that administration of a cocktail of HIV-1-specific monoclonal antibodies, as well as the single glycan-dependent monoclonal antibody PGT121, resulted in a rapid and precipitous decline of plasma viraemia to undetectable levels in rhesus monkeys chronically infected with the pathogenic simian–human immunodeficiency virus SHIV-SF162P3. A single monoclonal antibody infusion afforded up to a 3.1 log decline of plasma viral RNA in 7days and also reduced proviral DNA in peripheral blood, gastrointestinal mucosa and lymph nodes without the development of viral resistance. Moreover, after monoclonal antibody administration, host Gag-specific T-lymphocyte responses showed improved functionality. Virus rebounded in most animals after a median of 56days when serum monoclonal antibody titres had declined to undetectable levels, although, notably, a subset of animals maintained long-term virological control in the absence of further monoclonal antibody infusions. These data demonstrate a profound therapeutic effect of potent neutralizing HIV-1-specific monoclonal antibodies in SHIV-infected rhesus monkeys as well as an impact on host immune responses. Our findings strongly encourage the investigation of monoclonal antibody therapy for HIV-1 in humans.

 

 

http://www.nature.com/nature/journal/vaop/ncurrent/full/nature12744.html

Edited by Tridimity
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  • 1 month later...

Cancer is difficult to cure due to so many factors! Most cancers aren't even detectable until they are malignant (metastasised) and grown to a critical mass, by then the damage is already done. New techniques needs to be found in order to just discover cancer let alone cure it. Plus there are so many types of cancer, the word cancer is used to describe lung cancers, colorectal cancers and breast cancers etc. Within each of these organs the cancer categories can be subdivided into even more cancers depending on the cell type or location. For example lung cancer can be divided into - small cell and non small cell or it can be divided by location such as bronchogenic or alveolar. Also the cancerous cells may look nothing like the normal cells for that particular organ as the cancer cell will be poorly differentiated compared to the normal adult cell. Why is it so difficult to cure ? Because, I highly doubt one drug will cure all cancers etc. Say we even find a drug that cures all lung cancers this drug will have to also have minimal side effects and will have to take 10 years or so to be processed and brought to the market.

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