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Profil korisnika/ce PetrovADmitri
Dmitri Petrov
Dmitri Petrov
Dmitri Petrov
@PetrovADmitri

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Dmitri Petrov

@PetrovADmitri

Evolutionary biologist at Stanford. Rapid Evolution and Genomics. Open Science advocate. Immigrant.

petrov.stanford.edu
Vrijeme pridruživanja: ožujak 2013.

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    Dmitri Petrov‏ @PetrovADmitri 17. ruj 2019.
    • Prijavi Tweet

    I am extremely excited about this work on the way natural selection succeeds and crucially fails to weed out deleterious mutations in cancer due to the constraints posed by linkage and Hill-Robertson interference. https://www.biorxiv.org/content/10.1101/764340v2 … 1/n

    10:14 - 17. ruj 2019.
    • 88 proslijeđenih tweetova
    • 200 oznaka „sviđa mi se”
    • Hiba Ali Molecular Ecology Shyamsunder Buddh Lindy McBride Gregory Wickham Nicole Nova Tyler Kent Aaron Pomerantz Answers in Rocks
    6 replies 88 proslijeđenih tweetova 200 korisnika označava da im se sviđa
      1. Novi razgovor
      2. Dmitri Petrov‏ @PetrovADmitri 17. ruj 2019.
        • Prijavi Tweet

        The work was co-led by a fantastic grad student in my and @cncurtis lab @SusanneTilk and a truly stellar postdoc in my lab @cd_mcfarland. For me this work finally solved some troubling puzzles about how evolution works in cancer. We would really love to know what you think! 2/n

        2 proslijeđena tweeta 7 korisnika označava da im se sviđa
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      3. Dmitri Petrov‏ @PetrovADmitri 17. ruj 2019.
        • Prijavi Tweet

        Dmitri Petrov je proslijedio/a tweet korisnika/ceSusanne Tilk

        Note that @SusanneTilk posted a very clear description of the main results here: https://twitter.com/SusanneTilk/status/1173693668793831424?s=20 … I will just add some of my personal musings. 3/n

        Dmitri Petrov je dodan/na,

        Susanne Tilk @SusanneTilk
        Really excited to share the first chapter of my PhD on how genome-wide linkage in cancer reduces the efficacy of selection via Hill-Robertson interference (HRI), with mentors @cd_mcfarland, @PetrovADmitri and @cncurtis. https://bit.ly/2lTDQnT  (1/10)
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        3 proslijeđena tweeta 2 korisnika označavaju da im se sviđa
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      4. Dmitri Petrov‏ @PetrovADmitri 17. ruj 2019.
        • Prijavi Tweet

        This is our first foray into cancer genomics and evolution. Cancer biology has been a big focus for us but so far we have focused primarily on modeling cancer in genetically modified mouse models as part of a truly great collaboration with http://med.stanford.edu/winslowlab.html  4/n

        1 reply 1 proslijeđeni tweet 3 korisnika označavaju da im se sviđa
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      5. Dmitri Petrov‏ @PetrovADmitri 17. ruj 2019.
        • Prijavi Tweet

        That collaboration was also co-led by @cd_mcfarland, as well as Zoe Rogers and Ian Winters who all developed Tuba-seq: http://petrov.stanford.edu/pdfs/0136.pdf , http://petrov.stanford.edu/pdfs/0143.pdf , https://news.stanford.edu/2018/04/03/stanford-scientists-track-cancer-growth-crispr/ …. That work is still going strong but Chris and Susanne here opened a new chapter. 5/n

        1 reply 1 proslijeđeni tweet 2 korisnika označavaju da im se sviđa
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      6. Dmitri Petrov‏ @PetrovADmitri 17. ruj 2019.
        • Prijavi Tweet

        PSA: Chris McFarland is on the job market this year. Don’t miss your chance! 6/n

        1 reply 2 proslijeđena tweeta 5 korisnika označava da im se sviđa
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      7. Dmitri Petrov‏ @PetrovADmitri 17. ruj 2019.
        • Prijavi Tweet

        Ok, so what is the puzzle? First some background. Cancer sequencing showed that most cancers accumulate many mutations in many genes. Some of these mutations are likely to be advantageous for the tumors (they generated drivers) but many are thought to be mere passengers. 7/n

        1 reply 4 proslijeđena tweeta 9 korisnika označava da im se sviđa
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      8. Dmitri Petrov‏ @PetrovADmitri 17. ruj 2019.
        • Prijavi Tweet

        The word passenger is good here as it connotes hitching a ride with a driver. This is particularly appropriate in clonal, somatic growth without recombination. Once a mutation lands on the genome of an expanding clone it got it made, even it doesn't help the expansion. 8/n

        1 reply 1 proslijeđeni tweet 5 korisnika označava da im se sviđa
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      9. Dmitri Petrov‏ @PetrovADmitri 17. ruj 2019.
        • Prijavi Tweet

        Passenger mutations by definition can be either neutral or harmful. So what are they in cancer? The standard approach to test this is to ask whether natural selection weeds out putatively functional passengers at a higher rate than the mutations more likely to be neutral. 9/n

        1 reply 1 proslijeđeni tweet 1 korisnik označava da mu se sviđa
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      10. Dmitri Petrov‏ @PetrovADmitri 17. ruj 2019.
        • Prijavi Tweet

        These analyses suggested that almost none of the putatively functional, amino acid replacement mutations are weeded out by selection in cancer unlike in germ-line evolution where the majority (often vast majority) of replacement mutations are eliminated 10/n

        1 reply 2 proslijeđena tweeta 2 korisnika označavaju da im se sviđa
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      11. Dmitri Petrov‏ @PetrovADmitri 17. ruj 2019.
        • Prijavi Tweet

        These fantastic papers from 2017 by @imartincorena and colleagues as well as Donate Weghorn and colleagues established this pattern quite clearly: https://www.ncbi.nlm.nih.gov/pubmed/29056346  and https://www.ncbi.nlm.nih.gov/pubmed/29106416  11/n

        1 reply 1 proslijeđeni tweet 6 korisnika označava da im se sviđa
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      12. Dmitri Petrov‏ @PetrovADmitri 17. ruj 2019.
        • Prijavi Tweet

        Why would this be the case? There are two possibilities. One is that these replacement mutations are neutral. They do nothing at all possibly because most genes in humans are only important for multicellular function and development and dispensable in clonal growth. 12/n

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      13. Dmitri Petrov‏ @PetrovADmitri 17. ruj 2019.
        • Prijavi Tweet

        This is a fascinating hypothesis but never seemed likely to me because most selection against germ-line protein mutations is due to their effect on folding and unrelated to function. This was shown convincingly by @dallandrummond and colleagues https://www.pnas.org/content/102/40/14338 … 13/n

        1 reply 0 proslijeđenih tweetova 4 korisnika označavaju da im se sviđa
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      14. Dmitri Petrov‏ @PetrovADmitri 17. ruj 2019.
        • Prijavi Tweet

        I don't see a reason why somatic cells should escape the deleterious effects of protein misfolding as long as the putatively dispensable genes are expressed in cancer. And they are. So, something does not quite make sense here. 14/n

        1 reply 1 proslijeđeni tweet 2 korisnika označavaju da im se sviđa
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      15. Dmitri Petrov‏ @PetrovADmitri 17. ruj 2019.
        • Prijavi Tweet

        The other possibility is that passengers are often quite harmful but selection can't remove them. One key possibility is the lack of recombination allows deleterious passengers to hitchhike with the drivers as long as the drivers are stronger than the passengers. 15/n

        1 reply 0 proslijeđenih tweetova 5 korisnika označava da im se sviđa
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      16. Dmitri Petrov‏ @PetrovADmitri 17. ruj 2019.
        • Prijavi Tweet

        @cd_mcfarland and @SusanneTilk decided to test this possibility in a very clever way. It is known that selection is particularly inefficient in the absence of recombination when mutation rate is high. 16/n

        1 reply 0 proslijeđenih tweetova 3 korisnika označavaju da im se sviđa
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      17. Dmitri Petrov‏ @PetrovADmitri 17. ruj 2019.
        • Prijavi Tweet

        If mutations are rare then they also rarely end up being linked and selection can notice marginal effects of mutations quite easily. If mutation rate is high, marginal effects of mutations are less important. Both purifying and positive selection become inefficient. 17/n

        1 reply 1 proslijeđeni tweet 5 korisnika označava da im se sviđa
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      18. Dmitri Petrov‏ @PetrovADmitri 17. ruj 2019.
        • Prijavi Tweet

        Here @SusanneTilk and @cd_mcfarland show that these predictions hold. Cancers that have very low mutational burden show strong evidence of purifying selection against passengers (~60% of replacement mutations are eliminated) and very strong positive selection for drivers. 18/npic.twitter.com/Z5HkruXEnX

        1 reply 1 proslijeđeni tweet 6 korisnika označava da im se sviđa
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      19. Dmitri Petrov‏ @PetrovADmitri 17. ruj 2019.
        • Prijavi Tweet

        These patterns hold across multiple datasets, mutational calling algorithms, cancer types, and clonal and sub-clonal mutations. Similar patterns are seen in copy-number mutations. An aside - while the paper is short and readable it describes a ridiculous amount of work! 19/n

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      20. Dmitri Petrov‏ @PetrovADmitri 17. ruj 2019.
        • Prijavi Tweet

        Having established the pattern of attenuation of efficacy of selection in the high mutation burden tumors, @SusanneTilk and @cd_mcfarland used simulations to demonstrate consistency with predictions of simple models of clonal evolution and estimated some key parameters 20/n

        1 reply 0 proslijeđenih tweetova 3 korisnika označavaju da im se sviđa
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      21. Dmitri Petrov‏ @PetrovADmitri 17. ruj 2019.
        • Prijavi Tweet

        They showed that the data are consistent with drivers having on average ~20% advantage (which is roughly what we see in mouse models for Lkb1 loss http://petrov.stanford.edu/pdfs/0136.pdf ) and passengers having an average individual cost of ~1% and total cost of ~40%. 21/n

        1 reply 1 proslijeđeni tweet 2 korisnika označavaju da im se sviđa
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      22. Dmitri Petrov‏ @PetrovADmitri 17. ruj 2019.
        • Prijavi Tweet

        So it looks like the tumors carry a large deleterious load of many likely mis-folded proteins. How do they manage this? And does this generate a key vulnerability in tumors that can be exploited therapeutically as was suggested previously? https://www.ncbi.nlm.nih.gov/pubmed/23388632  22/n

        1 reply 1 proslijeđeni tweet 3 korisnika označavaju da im se sviđa
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      23. Dmitri Petrov‏ @PetrovADmitri 17. ruj 2019.
        • Prijavi Tweet

        I am very excited about this work and for the authors. It is particular fun that this work confirmed Chris's Ph.D. work with @leonidmirny where they did argue that cancer progression is the tug of war between advantageous drivers and deleterious passengers. 23/n

        1 reply 1 proslijeđeni tweet 4 korisnika označavaju da im se sviđa
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      24. Dmitri Petrov‏ @PetrovADmitri 17. ruj 2019.
        • Prijavi Tweet

        I would like to also thank @cncurtis and both of our labs for great discussions! Please do let us know what you think - we would love to know. n/n

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