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I am a cancer research scientist - AMA!
Hi PC!
So some of you who know me might already know that I'm a (currently training) biologial scientist. Specifically, my interests are in molecular and cellular biology and my current research is on cell communication in cancer metastasis. Soon, I will be leaving my current lab and moving to another where my work will predominantly be on cell membrane trafficking. Since a number of people have been talking about AMAs in this section and since it'd be cool for us to have people who work in science talking about what they do, I discussed this with Team Fail and Tsutarja and we thought it'd be a good idea. In this thread, ask me: • About the general biology and biochemistry of cells and cell communication; • About cancer biology - what it is, how it develops, how we treat it, and why it's so difficult to cure; • About my work and the rationale behind it; • About my day-to-day job and what I'm actually doing in the lab; • About science as a career and (unfortunately) as a business; • Anything else! Please don't ask me: • About my present results - these are unpublished and are therefore confidential; • Questions about your own health which should be directed to a medical doctor; • Anything about trees. Go! |
What would you say are the biggest challenges facing workers in your industry? What, if anything, is being done to remedy these problems?
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How do you treat cancer? How? And why it is that dangerous?
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How many people work with you on the research? Does your lab have multiple research projects going on at once, or do you all work on the same one?
I find this all very interesting & think these threads are a great idea! Especially for those of us who don't work in a science field and like to learn more about it :) |
What brought you into the field? Did you have an inspirational moment or was it more of a continuation of things you worked on in school?
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Brolaire, I saw your post after I finished writing this one so I'll reply to it in my next post!
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This is not only a problem for the PIs because it's difficult to get money to do the work they want to do, but it's hard for the lab workers too; if you've got no funded project you've essentially got no job and no security. PhD students won't be able to get places at all if they don't have a project which has been allocated funding, meaning that applicants for PhDs are often left hanging until the last minute to find out if they will have a place or not. When you don't have funding, it makes problems for everybody and that's unfortunately a very common situation to be in. In the cancer field the situation's a little better because "curing" cancer is of enormous public interest, but for rarer or less severe diseases the funding often simply isn't there. If you're not researching diseases at all then that's a whole other layer of difficulty and restricted money that you've got to overcome. Really, it's not pretty all-round, haha. In terms of what's being done to help the situation, it's not entirely in our hands; it's up to funding agencies and governmental bodies to realise the importance of funding for research. A lot of effort on our part, though, is going into raising public awareness of our work and showing them the importance of it. Lots of people aren't aware, for example, that it's not the medical doctors who are working on finding cures for diseases - it's us. Science is an undeniably complex field which lots of people shy away from, but the issue is that this translates to a lack of public interest which ultimately results in our work being devalued and being considered "lesser" in the public eye. And, as I said earlier, no interest = no funding. So engaging the public more in science and explaining to them why it's important and why we do what we do will hopefully result in more money coming in via charities and government bodies. Quote:
The problem, though, is that all of the processes dysregulated in cancer are also present and functional in normal, healthy cells. With traditional treatment methods, you can't selectively kill cancer cells whilst leaving normal cells alone. If you admininister a drug which kills dividing cancer cells, you also end up killing dividing normal cells. Forcing apoptosis in cancer cells forces it in all cells. So while these drugs can work in killing cancers, the side-effects are pretty severe because they're able to target theoretically any cell in the body which makes use of the mechanism that the drug targets. Another way to treat cancer is radiotherapy - which works by inducing massive numbers of mutations in the DNA of cells so that they're unable to stay alive. This is pretty good for solid tumours which are difficult to operate on or to make sure that areas which have been operated on are completely free of remaining cancer cells, but has the nasty side-effect of also killing normal cells unspecifically if they're too close to the area being radiated. Additionally, cells which survive radiotherapy actually have a small chance of becoming cancerous themselves (bear in mind that cancer is a disease induced by genetic mutations), so it's really not ideal. Surgery is the last common method of cancer treatment, and it's actually pretty good against early-stage solid tumours. The danger arises when the tumour is in a sensitive location (such as the brain or the lung), or when it's a quite advanced tumour; tiny surgical mistakes can introduce cancer cells into the bloodstream which gives a massive risk of metastasis. Still, it's good for very early-stage cancers and often makes long-term chemo/radio unessecary. The best cancer therapies - some of which are being worked quite intensively on right now - will involve either the delivery of drugs specifically to the site of the tumour or will involve exploiting the features of cancer cells which are absent in normal cells, such as mutated versions of proteins. A big example of this which is becoming popular right now is the concept of a "vaccine" against cancer, where the immune system can be primed against mutant proteins found often in cancer. But for now, the therapies which we've got are mostly double-edged, unfortunately. Quote:
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What are the biggest misconceptions people have about 1) your job 2) cancer, as a disease?
Is a cure for cancer even possible? |
Where exactly do you see yourself in your field in like, 10 years or something? Give us your thoughts on the "science as a business" bit?
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So glad to see this up! :]
I'm not sure if you knew about this, but my mother passed away on New Year's Day this year after a near year-long battle with multiple myeloma, having been initially diagnosed at Stage 3. Do you have any experience in studying, researching, and/or working with this disease? |
Here's something a bit different.
Cancer is such a globally-affecting disease and one that is both connected through all of us (cancer donations and charities, cancer research, celebrities getting it, almost everyone knowing someone or of someone who has it, etc.) to how society exists, but in a world where cancer is completely curable and treatable like taking a vitamin or a flu shot to prevent it altogether, how do you feel society would change? More simply: what if cancer was easily curable? |
What would you say is the best and worst parts of working as a cancer research scientist (besides the possibility of curing cancer)?
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What are other diseases that you feel should have as much of a spotlight on as cancer?
Also, what are your typical day-to-day duties/tasks? Even in the same broad field scientists do different sorts of things to each other. |
Phew, that second answer took a while. I'll reply to the next four posts (Tsutarja, Klippy, KetsuekiR, bobandbill) when I've got time to.
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So up until this 16-year-old point I was never actually that into science. I mean, yes - I did enjoy it and I was pretty good at it - but it wasn't my 'thing' if you know what I mean. That was more about music and art and sport, which is what I was for sure known for at the time. However, as much as I enjoyed these, I never really wanted to try to make them into a long-term career (nor did I think it'd be feasible to do so - not that science is much better as it turns out, haha). So I found science quite interesting and knew I was generally good at it so I went with that. It wasn't until later that I figured out that biology had always been the obvious choice - whenever I learned anything to do with how biological things work I wanted more and more and more and more detail until I knew every single molecule behind the process which I was looking at. This is basically the curiosity which drives my whole field, so I'm really glad I decided to follow through with it. Quote:
There are also a lot of misconceptions about animals and animal experimentation - why we need animals (mostly on this point), what we do with them and how we treat them. But that's a whoooooole other topic which I'll go into more if anyone wants me to. Quote:
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All of this is just my opinion of course, but I don't think that we're ever going to find a definitive "cure" for cancer - partly because of what I said above about cancer being highly heterogenous, but moreover for another reason: cancer should be considered as an evolutionary disease. In evolution, members of the same species evolve certain traits which allow some individuals to outcompete others and to have better reproductive success, and this is also happening in cancer. Cells in a tumour more capable of destroying matrix surrounding the tumour to make more space to grow in, for example, are likely to survive better than those which can't. Cells which can detatch from the primary tumour and enter into the bloodstream are more likely to form metastases, while the others will get left behind. It's essentially cancer's own version of extremely rapid and aggressive natural selection. More importantly when we're talking about a cure, cells which can resist a drug treatment will overtake cells which cannot. This means that drug treatment can actually select more fit cancer cells to propigate future tumour growth; you can treat a paitent with a drug which seems to be working only to later find that cells start showing up which resist the drug. In fact, I watched a really interesting presentation recently where a group treated late-stage colorectal (iirc) cancer paitents with a drug which targeted a mutated version of a protein called EGFR (whose mutants are common in cancer, and are important in signalling for cell division) and observed that most of the cancer died, until three months later... when no fewer than six individual further mutations of EGFR showed up which highly specifically resisted the drug's mechanism of action. This really highlights to me just how able to resist treatment cancer can be and, no matter how well-targeted our drugs are, aggressive cancers will find ways around them. There's also another phenomenon called tumour dormancy, which is a big problem for "curing" cancer; following treatment, a cancer can visibly seem to be completely gone, but there could very well be "dormant" cancer cells left over - these are cells which have stopped dividing and invading like normal cancer cells, but which still harbour the basic cancer characteristics. The big problem here is that, when using drugs which target features of active cancer cells, these are very capable of slipping by unnoticed. A cell that's not dividing won't be harmed by a drug targeting cell division, for example. These cells can remain dormant for years, coming back as a secondary cancer anything up to decades following the "cure" of the original tumour. So it's very difficult to say usually whether or not a paitent's cancer truly has been beaten, or if it's just the active cells that have been removed. So the long and the short of it is that, no, I do not believe that we will find a definitive "cure" for cancer. It has too great a variation in possible mutations and it's too capable of evolving in real-time to find its way around drugs that we throw at it. When it seems like cancers are gone, there could well be dormant cancer cells still alive which can cause relapses later in life. It's not all this bleak, though; everything I've said here is characteristic of quite advanced cancers which have probably already reached the point where they've got virtually no control over their mutation rates and are able to spread easily. Early, more simple tumours are certainly very treatable, and I do believe that we'll get to the point where we're able to cure any cancer featuring a single solid tumour which was detected at an early stage. In fact, we're almost at that point now; 90% of cancer-related deaths come from cancers which are highly advanced (or, to be more specific, post-metastatic: it's the metastasis, not the primary tumour, which usually causes deaths), with only a minority of deaths being caused from non-metastatic early-stage tumours. It's just about finding it early and getting rid of it quickly. This, combined with preventative tactics (for example, blocking metastasis - which is a big part of my present work), will hopefully stop cancers being able to progress to such late stages, acting as a sort of "proxy" cure. We're a way off that but we'll get there, I hope. Quote:
Also, at least from what I've seen, if you try to go into cancer long-term too early you probably won't get far - it's such a hot topic and there's so much competition that there's no way you can really make yourself stand out. In my opinion, you should become proficient in some other field and then apply it to cancer if you really want to get somewhere, which is maybe what I'll do later down the line. I dunno. It's a hard thing to say since in science 10 years is a really long time and your research interests and ambitions can change dramatically over that time. But yeah, this is the direction I'm headed in now; go into working on EVs, with or without cancer, and see where it takes me. Quote:
There's also a lot of people trying to climb over each other, particularly in cancer. When someone makes an important discovery, you get 10 people jumping on them trying to get authorships on their work or even trying to take the credit for it when they, realistically, haven't done that much. There's a lot of drama over who gets published on whose papers and in what order and etc. and it's all a load of bullshit, honestly. Science does, unfortunately, often lack a lot of integrity when it comes to fairly crediting people for their work, with more "senior" people often taking the credit for the work of people "below" them based on seniority alone - despite having done nothing for the work themselves. It happens way too often and it's one of the few massively unfair things that's genuinely made me think about leaving science before. Even now just typing this I'm getting pretty irritated over it, so I'm gonna stop, haha. Quote:
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How much of an impact do cancer research charities actually have on your field, if at all? How much of the money do you (the researchers in general) actually see?
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How Cancer develops? Is Cancer can be prevented at all?
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Ahaha, these questions are coming in quickly and they're pretty good and I want to give them all the time that they deserve - so apologies for not answering them as soon as they appear. If your questions aren't answered in my post then assume that I'll do them in a future one instead.
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Interestingly, lots of advances in understanding in cell biology have been due to cancer. Cancer gives us a model whereby we have cells with dysregulated processes as a result of mutations in particular proteins - and these are cues for us to study those proteins and understand how they work and ultimately, how they link into cell behaviour. If there was no more cancer (and therefore, no more cancer research) this'd be stunted. I can imagine it being much tougher to get basic research funded because cancer is the driving force behind a lot of projects (i.e., "this protein has been identified to cause cancer and we want to study it more to understand why and to progress towards a cure"), so in that way an easy cure for cancer could actually be harmful to science - although this is all just speculation on my part. I'm certainly not saying that I'd rather cancer not be cured here, mind. Quote:
The bad, though, is pretty bad. The thing that probably bothers me most is what I wrote in my reply to Nah - about how business-like it can all be and how people try to climb over each others' work all the time. I do spend a good amount of my time just bluntly thinking "please just fuck off for a bit and let me do my work" and I know that many other scientists do too, haha. The work itself is very difficult and is probably not well-enough paid (this could go in my earlier "misconceptions" list, actually - we really aren't as well-paid as we're made out to be), but that's not such a big deterrent if as I say you're doing the work for the joy of it. The big problems are for sure the business aspects of science, for me anyway. Animal work is pretty draining too sometimes, and maybe I'll touch on that some more in my reply to Harley Quinn later on (unless anyone has more specific questions). Quote:
Another, more specific disease, is diabetes. Although the therapies which we have for Type 1 diabetes are reasonably effective and safe, they aren't completely ideal and furthermore there is no gold standard consensus medical treatment for Type 2 diabetes. Diabetes is perhaps the most common disease which impacts almost every single body system - almost the entire body is reliant on proper glucose homeostasis which is badly controlled in diabetes. The result is that, if the diabetic person for some reason is unable to access treatment or whatever, you end up with massive systemic issues that can cause an extremely broad range of problems. The impact that diabetes can have on the body is pretty underestimated and poorly-appreciated imo, even often by diabetics themselves who are told that it's a straightforward disease. Glucose metabolism and homeostasis is one of the most conserved, intricately regulated and all-round important processes in the body and in diabetes it's messed up - yet, in my view, diabetes doesn't recieve the attention or the research that it deserves. Particularly given that Type 2 diabetes is on the rise, more has to be done to research it and find more efficacious ways to combat it. There are a great number of ways to treat both conditions at present, but neither of them have been fully "cured" and the sheer number of ways that there are to treat the disease is an indicator of how hit-and-miss they can be. Finally, I guess you could give osteoporosis a mention. I feel like osteoporosis is kinda allowed to slip by because it's not a very severe disease and it is extremely common, but it can actually be quite damaging to quality of life and near-immobilising in severe cases. Furthermore, there are a lot of easily available treatments for osteoporosis which can both prevent its onset and alleviate some symptoms after its onset which people simply don't know about. I think this could use a bit more attention in the public eye since it doesn't have to be "just one of those old-age things" and is actually quite manageable. It's a fairly straightforward and well-understood disease too, so really it's just down to getting the treatments out there to the people who need them. Dunno if I'd say that any of these warrant "as much" of a spotlight as cancer does, but certainly, these warrant far more attention - as do hundreds of other diseases. Cancer is very much stealing the show with medical research and it's a bit of a pain for everyone with a problem that isn't cancer, haha. I could go ahead and name another fifty diseases which need more attention but I'll stop there; those are three things which in my mind could do with a bit more attention paid to them. Quote:
...I think that's what you were asking, anyway. If I didn't answer your question properly then just let me know. |
Why is it that certain types of lifestyle choices, such as smoking, increase the likelihood of getting cancer?
Adding onto my earlier cure question, would it be possible, in the future, to prevent cancer entirely? As in, be able to reduce the chances of these mutations occurring at all? Thanks for the in depth answers by the way, they're really insightful. |
Sorry, been busy with work. Lots of new data to collect and organise right now - exciting times!
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I guess the most important thing in my mind which I'd like to communicate is why animals are so neccessary for all of us. When you want to publish a bit of research (particularly if it's medical research), one of the critical questions is "does your idea actually work in living creatures?". If you've come up with a pathway which you think is dysregulated in a disease or if you've come up with a drug which you think could cure a disease, but you've only been able to show these things in vitro (in the lab - dishes of cells, reaction tubes, etc), you've got a huge problem. It's not at all uncommon that in vitro something works but when you put it in vivo (in a living animal) it doesn't work for some reason - this could be due to the idea itself being wrong in live animals or due to unknown / unexpected factors in the animals interfering with the idea, among other possibilities. Particularly given that we're publishing work here which we hope to one day translate to human health, we absolutely must be able to show that what we're doing has a role in a living animal. The medical research community cannot work off of "findings" and "treatments" which only apply to cells in plates in incubators. If we're going to build on a finding, we have to know that this finding is relevant to a living creature, and it's the medical community's duty make sure that ideas for application in humans which have not been tested in vivo don't make it into disease-focussed journals. Unfortunately, this does sometimes turn into a case of "we want to publish, so let's do things with animals until something happens and work backwards from there" which is a really bad mindset and one that I absolutely hate - animals should only be used when there is serious in vitro evidence to back the use up. This causes problems sometimes as I said before for some people who have done years of in vitro work only to find that when they go in vivo, nothing happens - but that's more often than not due to something which has been overlooked or which isn't properly explored yet and which, in the hands of the right researchers, could easily open up new routes of investigation. All in vivo data, including negative results, is extremely valuable and the animals which provide it are taken much more seriously than walking bags of cells. When an animal is sacrificed (and yes, that's legitimately term for it) at the end of an experiment, absolutely everything possible is collected from it - not just the tissues in question but all of the tissues, its weight, the weight of the tissues, the animal's fat distribution, tumours and other unexpected tissue structures, anything and everything which could be used later to provide data and to avoid having to re-do the experiments in further animals. Things like the animal's behaviour, sleeping, metabolic and mating habits may have been noted too if the animal is being used for any related studies. These are really goldmines of information and they aren't used lightly by good investigators. So the next question which I guess arises is what can be done to reduce the use of animals or to substitute them for something else altogether. I hear a lot of people who suggest using tissues taken from animals (the advantage here being that a single animal can provide many tissues) or donated from human patients to emulate the real thing and to an extent, it's a good idea which lots of people make use of. We, for example, can use slices of bone from donor paitents on which we culture cells to test the impact that a particular treatment or condition has on the ability of cells to degrade that bone. These sorts of things are called ex vivo (i.e., "out of the living") techniques and they're extremely useful to test basic hypotheses in more complex systems that dishes of cells. Artificial tissues and organs are also becoming popular too - although there is scepticism around how "realistic" they are and they don't truly satisfy the idea of an ex vivo experiment. However, neither of these systems alone is enough to draw meaningful conclusions from; as I said before, they can test basic hypotheses (and, if the hypothesis is incorrect then they can postpone or fully prevent progression to in vivo experiments), but if the results from these experiments are positive then the experiment will still have to progress to in vivo. There's only so much that a single tissue can tell you, even if that tissue is your tissue of interest, and when you need to know what your condition does beyond a single tissue then you need an animal to do that in. You could ask, "why not use more tissues?", but it's extremely difficult (if not impossible) to properly mimic the communication between these tissues ex vivo without adding even more tissues to the equation, and eventually you just end up asking the question "why not just use an animal?". Another important use is genetically modified animals. We can use animals to study the function of genes by methods such as disabling or overactivating that gene in animals - either systemwide or in specific tissues under certain conditions. This is possible (and far easier) in cells, too, but these methods do not give a systemwide overview of the gene's effects. For example, we could have some gene which we hypothesise inhibits the division of bone-forming cells (osteoblasts) in mice. We knock this gene out in mice and find that, yes, their osteoblasts divide more - but we might also see, for example, that mice which have lost this gene spontaneously develop lung cancer (or whatever). This tells us that this division-regulating gene which we thought functioned in bone may also have a role in the lung and, further to that, may be important for preventing cancer in the lung. This is a real wealth of information which we could never have obtained from a homogenous population of cells in culture, and it's not at all uncommon to see unexpected consequences such as this from modifying animal genetics. The last thing worth touching on would probably be in silico modelling - using computers to predict what would happen in animals instead of using the actual, real thing. However, most scientists agree that we do not currently have the knowledge to reliably predict large-scale biological processes on computers. While a few specific pathways or processes have been successfully emulated by computers, and while computers are great for target prediction (see later), we would need a comprehensive understanding of every single interaction going on between every single molecule in mammals to have a true in silico model of a living animal, at which point we'd be pretty much done with cell biology anyway, haha. So although the theory is nice and although some fairly basic things are possible already in silico, the in vivo models are still needed to verify these results and we're a long way off being able to faithfully extend in silico results to humans. Computers are, however, extremely useful right now for predicting interactions - for example, guessing where protein might bind DNA based on the DNA's sequence and the protein's structure, or how two nucleic acids could interact. These are applications definitely useful, but we can't scale them up to entire animals or draw sound conclusions with regards to the functional consequences of these interactions yet. This reply probably raises some more questions, so please do ask away. Quote:
With regards to how much of their money we actually see - this is a really interesting question, but unfortunately I don't have experience with enough charities to say for sure - nor am I able to see which other projects charities are funding. The trend that I see in general is that the smaller the public interest in the topic that the charity works on is, the greater the proportion of its money put into research is - probably due to lacks of funding not leaving them much to spend on themselves after investing into the work that they promise to support. One of our major funding bodies, for example, specifically funds rare diseases including rare cancers and puts an enormous amount of their finances into actually getting science done whereas one of the major UK charities for widespread diseases (I can't remember which) was found to be putting in only a tiny portion of its money. So I'd say that it depends on the charity and the nature of the work being funded (or in the case of your specific question, which cancers are being funded) but I'm honestly not fully-equipped to answer this question. |
To what extent do you collaborate with medical doctors in your work? Do you have a physician-scientist PI or perhaps have close ties with another lab that's more applied in nature? How often does your lab communicate with medical practitioners?
Do you mind giving a bit more detail about the project you're working on? Like a mini-abstract or something. |
Just a quick update, I'm completely bogged down with work right now - loads of stuff has come up at once which I need to do so I'll get to these this weekend. Sorry that this hasn't gone as smoothly as I'd have liked it to have, haha.
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To quickly cover DNA's structure, in case you don't already know it, DNA is basically a long chain of individual sugars attached to groups called bases, named adenine, cytosine, thymine and guanine (or A, C, T and G). The individual order of the bases is what determines what DNA codes for, and it's therefore important that the order is maintained properly and that the bases are not modified. To take your smoking example, as you probably know lots of chemicals in cigarette smoke are carcinogenic. Most of these chemicals, though, will have different mechanisms of action. A particularly well-known and highly carcinogenic one is called benzopyrene, which is a small, flat molecule made of cycles of carbon. It's a product not only of cigarette smoke but of pretty much any combustion process - burning coal, wood, etc. and on its own it's pretty much inert and safe. However, its metabolism in the cell converts it into another molecule which has an additional oxygen capable of reacting strongly with guanine, one of the four bases incorporated into DNA which I mentioned above. This binding distorts DNA's structure and induces replication errors, ultimately leading to an increase in mutations which can accumilate to cause cancer. This, taken together with the fact that cigarette smoke's tar buildup physically brings benzypyrene into close proximity of cells in the airways and in the lung, makes cigarette smoke a pretty effective delivery system for carcinogens (or, strictly speaking, procarcinogens - since benzypyrene is harmless before its metabolism). Additionally, in the lung, benzypyrene can diffuse into the bloodstream, explaining in part why smoking cigarettes increases cancer incidence in non-respiratory organs. This is just one of probably hundreds of carcinogens in cigarette smoke. Another example you could give is the use of sunbeds, which use UV radiation to give you a tan. UV radiation is actually pretty high-energy and exerts enough of that energy on DNA to physically change its structure - more specifically, it causes dimerisation of bases in DNA. This means that two ajacent bases in DNA, assuming that these are the correct bases (or more specifically, cytosine and thymine), can join together not only as part of the main DNA backbone but directly to each other as well when influenced by the excess of energy provided by UV radiation. This is actually a fairly common form of mutagenesis since the sun itself radiates UV, and there are ways for DNA repair machinery to correct it - although interestingly, mammals including humans lack a truly specific mechanism to repair this sort of damage (and are therefore more susceptible to it), instead having to rely on more general repair mechanisms such as cutting away and re-synthesising entire regions of DNA containing photodimers. However, depending on the environment that the dimerisation has occured in, sometimes this cannot be repaired and in this case, DNA replication errors are almost certain to occur when DNA polymerase is unable to "read" the two joined-together bases. Indeed, this is a major driving force in melanoma development, which is tightly linked to excessive exposure to harsh sunlight and the use of sunbeds. So tl;dr it's a pretty long story depending on which specific lifestyle choice and its respective mutagen you're looking at. Mutagens can be chemical like benzypyrene or physical like UV radiation, and there are loads of mechanisms behind them. The common theme, though, is that there is some process involved which messes with DNA or its maintenence and replication machinery, ultimately inducing mutations or increasing error rate, which leads to cancer. Quote:
So, yes, it's possible to reduce mutation rates but if it's feasible or desirable is another question, and the extent to which we could completely eliminate environmental cancer inducers is still a pretty tough question which I doubt we'll be answering any time soon. I do, though, need to point out one other thing - not all mutations are environmental. In fact, lots of them are caused by errors in DNA Polymerase itself. It's important to consider that, throughout all of life's existence on earth, the driving force for evolution itself is mutation. The same thing that drives cancer. Change in species is induced by the selection of members who have mutations which give them an advantage over other members; be it more toxic venom, more intimidating markings, or more suitable anatomies for getting food (see: giraffes). So for the progression of species, an inherent ability to mutate is actually necessary. This means that DNA Polymerase, by design, is imperfect; its error rate is fairly low absolutely speaking, estimated in humans at ~1/108 errors per base replicated (and many of these errors are then repaired anyway), but when you consider how many cells you have with how many DNA strands are being replicated at once, this is actually quite a significant chance of error. Iirc human DNA Polymerase is generally considered more error-prone than most, too. The problem for humans is that we no longer have much selection pressure in the developed world, so this "error by design" is largely redundant and backfires quite heavily against us - furthermore, we can't naturally select for people with more stable DNA Polymerase because cancer is typically an old-age disease, and therefore we've usually already had kids before we get cancer. So even if we were to remove all of the carcinogens in the world, we wouldn't be able to completely stop mutation - meaning that, given long enough, our own DNA replication machinery will give us cancer. This does represent a very interesting drug target, though; if we were somehow able to reduce DNA Polymerase's error rate with pharmeceuticals, we'd be able to dramatically reduce the number of "background" replication errors and probably sharply decrease the risk of cancer. How we'd do that, though, is beyond my knoweldge. Quote:
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Don't actually have a question, just wanted to say I'm glad there's still a lot of work being done by people like you. I'm about 4 years remission from my own cancer (Nasopharyngeal), and although I don't think anyone ever really says their cancer treatment wasn't that bad, mine was actually a lot better than it could have been due to results from a recent study that apparently reevaluated the treatment for my specific cancer. So I guess that even though I think anonymous thanks over the internet are a little weird, and you mentioned you are in training... Thanks.
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In school, the definition for cancer in my biology textbook was 'the uncontrolled growth of cells.' Now, for fear of sounding silly, what do cancer cells actually look like? Or, to be more specific, granted you've examined some samples, what have you seen cancer to ressemble with your own eyes. Do they in any way stand out from the structure of regular cells?
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Spoiler: MCF-10A, a healthy breast epithelial cell line
Spoiler: MCF-7, a cancerous but relatively unaggressive breast epithelial cell line
Spoiler: MDA-MB-231, a highly aggressive human breast cancer cell line
So really it depends a lot on which cell we're talking about and how aggressive it is; but almost always, cancer cells grow either inconsistent or completely incoherent tissues and often display features suggesting that they are more migratory than normal cells, and in some cases more invasive. If you're asking more about what a whole tumour looks like, while I'll spare your eyes by not posting the images here, in a word: messy. They're usually large growths with few clear defining features. They have a complex network of disordered blood vessels running through them which feed nutrients to the tumour; these vessels themselves grow because cancer cells can instruct the surrounding tissue to grow them themselves. Sometimes in particularly large tumours you can see smaller tumour-like structures or discrete sheets of cells on the original mass, indicating sub-populations of cancer cells which are genetically different to those in the main body. They can be pretty complex structures when quite advanced. Hope this answers your question! |
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