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dannzter t1_izybdyh wrote

Yes, in going to need an ELI15 in this one. Same as ELI5 without the baby talk.

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moistiest_dangles t1_izz29x9 wrote

Yeah so basically when DNA makes a copy it's transcribed into rna which is called a transcript. This paper shows evidence that something is impacting transcript length on a global scale over time which may be a trigger to aging.

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dannzter t1_j03ybto wrote

So making the transcript lose information?

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Mokebe890 t1_iztbdq8 wrote

Hm yes, but artificial longering telomeres results in rapid cancer growth. Where is the missing catch then?

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Anasthasia218 t1_iztfuw9 wrote

I don't think there is any catch and the article says nothing new. We knew about the shortening of the telomeres as we age a very long time ago.

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Mokebe890 t1_iztgemx wrote

Yes I know but I meant the catch how to work around creation of teratomas.

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wiga_nut t1_izviee8 wrote

This article isn't focused on telomeres its about RNA transcript length

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MRSN4P t1_izu01n3 wrote

Do you know of any good articles that describe this rapid cancer trend? I would like to learn more.

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freebytes t1_j006cjd wrote

An interesting discovery has been that telomerase activation has been shown to decrease cancers early in life. Once cancer begins, that is when telomerase is dangerous. But, many cancers begin because of the damage originating from short telomeres. However, the results of studies can vary, and while it seems like we may have researched such things to death, we need to keep studying it to know more.

  1. https://pubmed.ncbi.nlm.nih.gov/23468462/
  2. https://pubmed.ncbi.nlm.nih.gov/15746160/
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Gu1l7y5p4rk t1_izz1m59 wrote

>We recognize that our study holds a far-reaching implication on how RNA-seq studies are analyzed and interpreted. Technical biases in RNA-seq studies, which affect gene-specific readouts according to their length, have been reported widely, and several tools have been subsequently deployed to computationally counter the effects of this length association40,41,42,43.

>Jointly, these observations invite the unsupported hypotheses that during aging there may not be a single origin for the length-associated transcriptome imbalance and that the length-associated transcriptome imbalance in aging instead represents an intermediate step within a ‘bowtie structure’ through which multiple environmental and internal conditions simultaneously affect multiple downstream outputs55,56,57.

Above and below and between is much talk and mention of methods and incidents supporting the above quoted/mentioned.

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