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Scientists Crack 'Entire Genetic Code' of Cancer 235

Entropy98 writes "Scientists have unlocked the entire genetic code of skin and lung cancer. From the article: 'Not only will the cancer maps pave the way for blood tests to spot tumors far earlier, they will also yield new drug targets, say the Wellcome Trust team. The scientists found the DNA code for a skin cancer called melanoma contained more than 30,000 errors almost entirely caused by too much sun exposure. The lung cancer DNA code had more than 23,000 errors largely triggered by cigarette smoke exposure. From this, the experts estimate a typical smoker acquires one new mutation for every 15 cigarettes they smoke. Although many of these mutations will be harmless, some will trigger cancer.' Yet another step towards curing cancer. Though it will probably take many years to study so many mutations."
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Scientists Crack 'Entire Genetic Code' of Cancer

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  • Better yet (Score:4, Interesting)

    by MrEricSir ( 398214 ) on Wednesday December 16, 2009 @08:23PM (#30467018) Homepage

    Maybe we can make cigarettes that don't cause cancer.

  • by Meshach ( 578918 ) on Wednesday December 16, 2009 @08:26PM (#30467040)
    Interestingly the article seems to only reference "preventable" cancers:

    The scientists found the DNA code for a skin cancer called melanoma contained more than 30,000 errors almost entirely caused by too much sun exposure. The lung cancer DNA code had more than 23,000 errors largely triggered by cigarette smoke exposure.

    Hopefully this will lead to treatments for other cancers as well.

  • by Anonymous Coward on Wednesday December 16, 2009 @08:27PM (#30467050)

    The breakthrough isn't in the results, it's in the technique. They're developing new methods and software to perform this sort of analysis faster and faster. That's what's big about this work. They can now do a very difficult task much more rapidly than before.

  • by johncadengo ( 940343 ) on Wednesday December 16, 2009 @08:33PM (#30467096) Homepage

    I have very little background in this area. But I'm curious. If skin cancer is caused by exposure to the sun, then it must be different for each patient? Because it's cause isn't inherited it seems to me that each patient with skin cancer has a unique and individual genetic cause to their skin cancer. Something akin to snow flakes. Perhaps once they find the absolute minimum change within the genes of an otherwise healthy human to having skin cancer, headlines can claim that scientists "crack entire genetic code of cancer."

  • by AdmiralXyz ( 1378985 ) on Wednesday December 16, 2009 @08:48PM (#30467244)
    Not necessarily. If they can find a protein corresponding to one of these mutations that is not produced in a healthy cell: presto, instant cancer test.
  • Re:Patent? (Score:5, Interesting)

    by AdmiralXyz ( 1378985 ) on Wednesday December 16, 2009 @08:59PM (#30467358)

    Why are patents allowed on naturally occurring phenomena like genes anyway?

    I've read interviews with multiple government and legal officials, whose basic point seems to be that patents on genes are a "necessary evil", because research into genomics is really, really, really expensive, and without patents + licensing fees giving biotech firms some way to recover some of their investment now (as opposed to ten years down, when drugs based on their discoveries could conceivably come to market), no businessperson would even think of throwing his money at that kind of research. According to them, without patents, there would be no research and progress in this field whatsoever.

    I'm not saying whether or not I agree with that, but that's the way it is.

  • by scapermoya ( 769847 ) on Wednesday December 16, 2009 @09:24PM (#30467600) Homepage
    it's not quite that simple. there are many many many events that are required, and it can't really be boiled down to those three categories. there are some key players that are almost always inactivated in some way or another across any cancer types (eg p53 or Rb), but many are unique to particular cancers (eg GSK-3b).
  • by xrayspx ( 13127 ) on Wednesday December 16, 2009 @09:40PM (#30467740) Homepage
    One of the things driving me when I began the quitting process was that my back of the napkin math showed I had smoked in the area of 148,000 cigarettes. I had a hard time putting that in terms of anything else. I couldn't compare it to any other non-reflexive thing. I haven't signed my name 148,000 times, or tied my shoes. What have I done 20+ times per day for 20 years?

    Now I learn that that means I have 10,000 cell mutations on top of that. Neato. Of course, 10,000 cells is kind of a drop in the bucket compared to the inner surface of my airway.

    To smokers: Please note his does not mean that I'm not still hopefully addicted to nicotine. Now it just comes in the form of Cherry Commit Lozenges [commitlozenge.com]. They work pretty OK. I've had maybe 1 cigarette per month for the last 5 months.

    On the other hand, I miss that I no longer look cool.
  • Misleading title... (Score:5, Interesting)

    by hahn ( 101816 ) on Wednesday December 16, 2009 @10:10PM (#30468044) Homepage
    Saying they've "cracked" the code to these two cancers (skin and lung) is not really as big a step as the title implies. They've found the genetic mutations associated with the cancers. That's probably the easy part (and it wasn't so easy). The problem in studying cancer is that the function of genes is often dynamic and interdependent. Think of a room with 30,000 light switches. Sometimes light switch #5 will turn on the light bulb, but sometimes it won't. It depends on whether light switch # 7, 100, and 10542 are all on simultaneously or not. And if switch #2742 is on, the light, if it's on, will be very dim. This why even though we give a cancer a single name - e.g. "melanoma" - there are often very different mutations present, any one or multiple ones which can affect the person's survival, but not necessarily all the time. There are cancers which reliably result from single mutations, but the most common ones are due to mutations in many many different genes. To the point that most cases of cancer can or should be considered unique.

    IMHO, where I think the results of these studies may be most helpful with regards to treating people successfully is figuring out which mutations cause the cancer to spontaneously regress [nih.gov], whether it's by self-destruction or immune mechanisms. Even then, maybe it's not even because of a cancer mutation. Maybe some people possess some genetic trait in their immune system that allows them to destroy cancers. In which case, too many people would be looking in the wrong haystack for a needle.
  • Re:Patent? (Score:3, Interesting)

    by tg123 ( 1409503 ) on Wednesday December 16, 2009 @10:31PM (#30468212)

    Why are patents allowed on naturally occurring phenomena like genes anyway?

    .......no businessperson would even think of throwing his money at that kind of research. According to them, without patents, there would be no research and progress in this field whatsoever.
    I'm not saying whether or not I agree with that, but that's the way it is.

    The reality is business people / drug companies do not invest in drug research period.

    Business investment tends to goes into marketing the drug its the university's and research institutes that do the drug research.

    http://www.uab.edu/reynolds/MajMedFigs/Index.htm [uab.edu]

  • by protein folder ( 228881 ) on Wednesday December 16, 2009 @10:41PM (#30468264)

    More importantly, since they've shown that they can apply this technique (it's not really specified, but I'm assuming it's whole genome sequencing) and applied it to one patient, there's nothing stopping them (except money) from applying this to other patients with the same condition. Maybe a different patient has 25,000 mutations, maybe another has 27,000, etc. Chances are these mutations are not all going to be affecting the same sequence positions in all the different patients. If they can find mutations that are more common than others or genes that are mutated more often than others, then they can perhaps discover new genes which, when mutated drive the development and progression of the tumor. If you can discover which genes are important you can perhaps design treatments for that.

    That said, the title ought to be more like: "Scientists crack 'Entire Genetic Code' of one melanoma patient's tumor and one lung cancer patient's tumor. This is definitely a very impressive achievement in its own right, and the technology that has made this possible is pretty amazing, but it's a bit premature to say "we've cracked the genetic code of cancer" full stop.

  • by DebateG ( 1001165 ) on Wednesday December 16, 2009 @11:26PM (#30468572)

    So I work in biological sciences, and I have the special privilege of having the guy who sequenced the first cancer genome working down the hall from me (he's also my thesis committee).

    There is now technology to sequence entire genomes very quickly using massive parallel sequencing. Ideally, if you were sequencing a tumor from a single person, you would get tissue from the tumor and also from the non-tumor (usually skin) and sequence them at the same time. Then you compare the two to distinguish what is simply variation in each person's genetics and what is acquired by the tumor. In my opinion, that's the best way to do things and probably the most informative because you're looking a tumor in a real person that is subject to all the selective evolutionary pressures that occur in people.

    These groups didn't take that approach for reasons unclear to me. Instead, they sequenced cancer cell lines. If you cut out a person's tumor and stick it in a test tube with various growth factors, it will almost certainly die within a week or so. However, you occasionally get some cells that can grow in this situation because they've acquired some mutation that lets them grow in tissue culture. You then expand and passage these cells until they grow rapidly in culture. The problem here is that you're no longer dealing with a normal human tumor; you're selecting for tumor cells that grow in the artificial tissue culture environment. The second problem is that you're not sure what to compare the tumor sequence with. Due to privacy concerns, you almost never know who actually gave the tumor that was made into a cell line (as an aside, look up the HeLa cell line and its sordid history) so you have to compare to the human genome project. The problem here is that there are differences between people and you can't tell whether the "mutation" you see is just a normal variation or actually something in the tumor.

    These are the important limitations you have to consider when evaluating these papers.

    Now, on to your question. They have 30,000 changes in the DNA compared to their reference "normal" genome. Nearly all of those are in "junk" DNA: as far as we know, they don't code any genes or anything else that regulates genes. Of the ones that are in interesting regions, the vast majority of them are called synonymous mutations which means the DNA is changed but due to the way it is interpreted, the protein that it makes is identical (to use a computer analogy, imagine that an the opcode for JMP was changed from 01 to 02 but both 01 and 02 are translated by the computer as JMP).

    Now, a certain number of mutations aren't like that. They either lead to truncated proteins, alter the amino acid sequence of proteins, alter mRNA splicing, etc. There are also other genetic changes such as duplications where the gene sequence is unchanged but may be copied several times to increase the gene dose. These are really the interesting things because they alter protein function or gene dose. From a brief reading, it looks like there are around 100 of these.

    Now, it's really difficult to tell whether these mutations are really relevant to cancer progression. Some of them might just happen due to tumors just mutating really fast and not really affect the cancer progression one way or another; they are so called "passenger" mutations that just come along for the ride. You can introduce these mutations into cells in lab to see if they do anything, but the real test is to sequence a bunch of human cancers and see if certain mutations are recurrent. This work is currently underway and will prove very informative about how genetically heterogeneous tumors really are.

    So, in short, there are about 100 haystacks. Further sequencing of other tumors will show if these are relevant to cancer in general. In my personal opinion, I think that further sequencing will identify very few common mutations and everyone's cancer will be essentially unique in the mutations it acquires. That will force us to completely rethink how we view cancer on a broader scale as not a single disease but a collection of highly related diseases that need to be treated individually.

  • Michael Chin (Score:2, Interesting)

    by mikorangester ( 1702164 ) on Wednesday December 16, 2009 @11:44PM (#30468712)
    One of the reasons why slashdot is good is because its readers tend to be aware of the state of the technology. Thanks commenters for precise answers to some very stupid genetic advertising. And yes, skin cancer grows on you....:D
  • Common damage (Score:5, Interesting)

    by AlpineR ( 32307 ) <wagnerr@umich.edu> on Thursday December 17, 2009 @08:27AM (#30472124) Homepage

    If you fire a rifle at a running car, it might survive several shots and still keep running. Some of the shots go through the windows, some through the doors, and some just bounce off the pillars. But some shots could poke holes in the body and leave underlying parts exposed. Then further shots might puncture the gas tank or the radiator. A little less likely, shots might break the fuel pump or electric distributor. And just maybe a shot will interrupt the ignition circuit.

    Even though any particular car's damage will be unique, the damage that made cars stop running will be common. Most will involve the gas tank or radiator. And a few will involve smaller parts.

    A study like this is looking for those major parts which are likely to be damaged in cancer cells. It might also reveal common patterns of damage which disabled protective mechanisms and left those key part vulnerable. Then you might have an idea of how to detect critical damage, how to repair subcritical damage, how to armor critical areas, and how to completely disable malfunctioning cells.

  • by nbauman ( 624611 ) on Thursday December 17, 2009 @02:19PM (#30476286) Homepage Journal

    Actually, cigarette smoking lowers public expenditures. Cigarette smokers are likely to die younger.

    The main savings is in pensions, social security, and health care for the aged.

    An Eastern European country required a cigarette company to submit data on the costs of cigarettes. The company handed the job over to their usual health economists and PR guys, who came up with a report that cigarette smoking would save the country money for those reasons.

    It was nice to see such refreshing candor from a cigarette company. Or maybe I should say, I'm glad they didn't stop to think about it before they released the report.

    Sorry I don't have a citation.

  • by Anonymous Coward on Friday December 18, 2009 @04:06PM (#30492214)

    Yours is the clearest response yet. Thank You! Try reading "walkking Between Walls" by Greg Bradden! its about filling out the DNA mapping. Creative and spiritual aspects considered into scheme of things as well! BRJP 12 18 2009

To write good code is a worthy challenge, and a source of civilized delight. -- stolen and paraphrased from William Safire