November 21, 2013 (This
is the last post of November. Happy
Thanksgiving!)
This week in AP Biology we began to look at the processes of
cell division, namely the cell cycle, mitosis and meiosis. Understanding of these processes is essential
and a hot topic in medical research.
Many human diseases can be traced to problems associated with the
regulation of the cell cycle. To that
end, in this week’s blog I would like you to read the linked article and then
pose one question that is generated having read the article on cell cycle
regulation.
Is there one specific fault in protein translation that can be located for every form of disease or cancer? If not, can the techniques that the researchers used work for every type of disorder, or will they have to be greatly adjusted for each one?
ReplyDeleteHave the scientists tried this ribosome profiling on any living organism? If so, where the results positive or negative? And if not, do the scientists have any idea as to when they can try this on a living organism?
ReplyDeleteMost treatments in place for cancer, like chemotherapy, simply kill cells that divide rapidly, if the cell-cycle mis-regulation is most often the cause of human disease, why don't researchers create a drug that can regulate the cell cycle to reduce human disease?
ReplyDeleteIs there a way to monitor levels of the protein RICTOR? If production of this protein "is constitutively turned on in cancer," would it be useful to measure RICTOR in cancer patients in remission? I wonder if these findings would be able to be used to screen patients for relapse, in addition to the experimental cancer therapies mentioned in the article.
ReplyDeleteIf the regulation of the translation of RNA by Ribosomes is so important why don't our body's have a back up regulation system for when Ribosomes fail? It seems as though are bodies should be able to prevent unregulated mutations and growths even with a Ribosome failure. Is it possible that we could evolve a back up?
ReplyDeleteBy observing and analyzing the activity of the different groups of proteins of the translation phase, will scientists be able locate the groups causing the cancer and just kill those individual proteins, or will it be likely that they will need to kill all the cells with the faulty proteins in order to rid the cancer?
ReplyDeleteResearchers discovered that different groups of protein were made in abundance at a particular phase, while other studies of the translation of RNA into a protein focused on a couple genes at a time. Why is this method going to be more helpful to researchers, and what are they going to do with it?
ReplyDeleteSince RICTOR helps cancer cells to continue their cell cycle, could a drug specifically target this protein to prevent cell division? If so, would other proteins produced previously during the cell cycle still be able to support the "immortality" of tumor cells?
ReplyDeleteAre there currently any ways to bring the irregular cell regulation back to normal? If not, how might scientists aim to combat this in the future?
ReplyDeleteSince scientists know the types of proteins that are present in normal cell division and the transcription and translation processes, could they target solely the faulty proteins that do not belong with a drug? This could potentially be helpful for patients with diseases associated with cell cycle malfunctions such as cancer.
ReplyDeleteAlthough the specific timing and coordination of protein production during the cell cycle appears to be mostly regulated by ribosomes, the first step in the production of proteins is the reception of a signal from somewhere that tells the cell to start making the proteins. If the pathway leading to excessive protein production was traced back far enough, could we figure out what is causing the cell to try to divide in the first place and intercept those signals?
ReplyDeleteWhat is the detailed process of 'ribosome profiling'? How did they come about this and what was the original use to profile ribosomes?
ReplyDeleteDo all cancer cells undergo these processes, or is it only the specific ones researched in the experiment? I am curious as to whether or not the scientists actually discovered a unifying trait that can help further our knowledge of all cancers, or just an anomaly in specific cells.
ReplyDeleteIs RICTOR the only protein that has the function of helping the cell cycle run? If not, what would be the side effect of removing all of it from a cell, with hopes of reducing the possibility of it becoming a cancer cell? Would the cell work fine with reduced levels of RICTOR or with none at all? And are there any other proteins that work similarly that don't have any risk of causing cancer?
ReplyDeleteI would be very interested to know just what “computational techniques” and “sophisticated computer algorithms” the scientists used to arrive precisely at these findings. I understand that the writer probably realized that, for most readers, these terms are better left unexplained, but I would personally be very interested to know at least a little more about how the whole process of making conclusions from ribosome profiling data (which seems very obscure, and much more difficult than the article made it sound) is gone about.
ReplyDeleteRuggero suggests that RICTOR is constitutively turned on in cancer. Is there a possibility that the RICTOR concentration could be reduced through therapeutically targeting these proteins as Ruggero mentioned? Could this reduced concentration reduce the likelihood of cancer or would the all the proteins have to be removed to make a big enough impact? While a treatment like this could help a patient fight or prevent cancer, would it also severely inhibit translation during the S phase?
ReplyDeleteIf scientists are able to determine which mRNA is translated into protein, is there way a to reverse this same process and determine which DNA segments encode which RNA strands and therefore specific proteins, like RICTOR? This would allow cancer researchers to try to target specific DNA strands rather than the RNA they create, and hopefully stop or slow RICTOR production to control the cancer.
ReplyDeleteWhat impact does the collective organization of the proteins -- being ramped up "all at once," as the article states -- occurring at the end of the cell cycle have for research into solutions? The cell clearly makes it so far in the cycle that most the cycle goes uninterrupted or faulty. Would an effective treatment target just that point, the last leg, in the cell cycle? Or would it be necessary / more effective/efficient to modify the way the entire cycle functions in the cell? This obviously has many evolutionary precautions to consider, though.
ReplyDeleteMany people commenting prior to myself have posed questions about lowering or attempting types of therapy that might control the production of RICTOR in the cell process. My question is how would this sort of therapy affect the cells of the organism and how would it latter affect the host? RICTOR seems to be an important enzyme in the cell cycle, without it would the organism still be able to survive?
ReplyDeleteTumors rapidly create proteins, and other proteins such as RICTOR could also play a role in cancer. These groups of proteins are made in abundance at different stages in the cell cycle, but what are scientists doing to stop the creation of these proteins? The article talks about how this could be another cause of cancer but nothing is said about any solutions to the issue.
ReplyDeleteTetrahydrocannabinol has been shown to reduce tumors in cancer patients in a 1986 double-blind study 2/5 of the patients who received Tetrahydrocannabinol, commonly known as THC. Would THC directly affect the RICTOR proteins produced by tumors?
ReplyDeleteMost comments here seemed to be centered around rather or not RICTOR protein production can be slowed or stopped based on what we know. What I'm wondering though, is could some of these aforementioned strategies be used to increase RICTOR production and increase cell growth and division? I'm not sure if there would really be a practical purpose to this, but rather or not we are able to do this is still an interesting question.
ReplyDelete"When this regulation falters, it wreaks havoc in the cell" - Like what? How does one such cell affect surrounding cells? Do certain mis-timings yield different results that distinguish a disease? What percentage of diseases can be attributed to errors in translation (only genetic ones)?
ReplyDelete-How important are translation errors in relation to genetic variation (evolution)? Didn't mean for that to rhyme!
Also, RICTOR is an acronym for 'rapamycin-insensitive companion of mTOR.' mTOR participates in TOR pathways, which regulate cellular growth.
ReplyDeleteIf the protein RICTOR is "constitutively turned on in cancer," as Ruggero says, does this mean that it is not as crucial in the events of a healthy cell's cell cycle? If so, would finding a way to turn the production of this protein off at least slow down the productions of cancer cells? Or would the absence of this protein have too detrimental of an effect on healthy cells for the host to continue healthy bodily functions?
ReplyDeleteWhat initiates increased production of the RICTOR initiation factor to closely coordinate production of so many different proteins during S1 and trigger them to gather together the translation initiation complex components: ribosome small and large subunits, mRNA and initiator tRNA?
ReplyDeleteThe article stated that RICTOR is part of a biochemical cascade, is it possible that something else is wrong with DNA translation, and should we be focusing on what exactly causes the start of this cascade and prevent it, thus possibly preventing the RICTOR to be turned on to such a degree?
ReplyDeleteRibosomes play a large role in the cell cycle. If it is possible to locate where and how the cell initiates the production of proteins, would it be possible to alter the ribosomes/other contributing factor(s) of these cancer cells and halt the production of proteins in these cells individually?
ReplyDeleteQuite simply, why had no prior scientists thought to look more closely into the role translation might play in diseases originating within the cell, seeing as translation is one of the most essential parts of healthy cell function and how translation is what converts the potentially flawed genetic code into an active protein to begin with?
ReplyDeleteHave scientists tried this ribosome profiling on any living organism? This seems like a quite important step to figure out which messenger RNA was being translated into protein by the ribosome during human cell division.
ReplyDeleteWhat effect does radiation have on ribosomes and mRNA during translation? Does it hurt or help protein manufacturing malfunctions, or does it have any impact on it at all?
ReplyDeleteHow was RICTOR isolated as a sole variable in the manufacturing of cancerous cells, and have other aspects of translation been as thoroughly evaluated?
ReplyDeleteIs there a way to artificially regulate proteins to control cell division in human disease? Could this be a cure for all human diseases?
ReplyDeleteDo these scientists think that eventually ribosome profiling could help cure cancer and other human diseases?
ReplyDeleteBeyond the scope of cancer, what other disease are caused by uncontrolled cell production and could scientists learn more about cancer by studying these other diseases? Is there any way we could harness this rapid cell growth for good, such as rapidly growing epithelial cells to create skin grafts for burn victims, etc.?
ReplyDeleteSince the RICTOR protein is believed to be the cause of cells rapidly reproducing and producing cancerous tumors, have any tests been done one organisms with cancer to try to prevent this protein form over producing? If so, what were the results?
ReplyDeleteHow exactly will the drug work that is supposed to decrease the amount of the protein RICTOR produced during translation? Also, what are some other cases where the amount of RICTOR produced is increased?
ReplyDeleteWhat other cures for diseases could benefit from this research besides cancer? Could the research behind this discovery be replicated to make new discoveries towards cancer research or other diseases?
ReplyDeleteWhat are the other common human diseases besides cancer are caused by misregulated cell cycle control?
ReplyDeleteAre there any other proteins similar to RICTOR in that incorrect regulation of its production and role in the cell cycle is directly linked to cancer?
ReplyDeleteWhy is the one of the first times that scientists are looking into the role of translation regarding disease and the health of the cell? Were they focusing only on what caused the disease and not how it spread?
ReplyDeleteDid RICTOR potentially have a positive role in the cell cycle before it was linked to causing tumor growth? Could it potentially have mutated?
ReplyDeleteWould therapies allowing RICTOR to be shut off keep tumors from growing, or is there another factor which would also have to be dealt with to eliminate any risk?
ReplyDeleteIf RICTOR causes increased translation in the S phase, that would produce more proteins. Do these proteins somehow speed up the cell cycle or cause it to repeat? Also, how does this affect the cell cycle in other, surrounding cells to form metastasizing tumers? Do they emit some chemical signals?
ReplyDeleteIf RICTOR is boosted due to increased translation during the S phase, then during what other phase does this production "quiet down," and how does this process occur?
ReplyDelete