does adding "of" really make you that angry?

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).

I just completed an intensive undergraduate course on cancer with a focus on genetics at UC Berkeley. We spent a significant amount of time on cancer genomes, and I have to say this announcement doesn't mean that much unfortunately. Cancers are genetically very unstable, and any given tumor you sequence will have many mutations that are completely unrelated to the cancer's survival and proliferation. they are known as passenger mutations, and need to be separated from the causative 'driver' mutations. sequencing many tumors of the same type and applying statistical analysis has been useful in this area, but considering that there are potentially millions of different combinations of active and inactive genes that lead to tumor formation, this approach has its limitations. this is especially true given that some genes are both tumor suppressors and tumor activators in different contexts (eg the TGF-b pathway). even if you identify a genetic locus as highly associated with a particular cancer, it is hard to go from there to understanding the molecular biology behind that association.

we have a long way to go before we defeat cancer, and sequencing can only take us so far.

I'm sure the paper is fine if it's in PNAS, I haven't had the chance to read it myself. But if you read the press release, it makes it seem as if this represents the discovery of p16. In fact, they make it seem as if p16 is unique to mole rats. I'd agree with you that a transformation of a more accepted cell line like NIH 3T3 or some human line would be more convincing. I imagine they are working on it.

really? how do you explain how those species overcome the end replication problem? we agree that aging is more complex than just telomeres... nobody thinks that. perhaps in the mainstream media.

i never said that telomeres were the answer to aging. but i did say that highly active telomerase is a characteristic trait among immortal cell lines. and that they are deeply involved in the aging process, especially in humans (which is the species in question). yes, many (not all) of those lines are messed up in one way or another. the point stands though: if there is a possibility of extending human lifespans through biotechnology, you can be sure that telomeres will be involved. i mean, just think of cancer. telomeres and telomerase are a key component of how cancer manages to sustain such explosive growth. if we had a good telomerase RT inhibitor, it would help greatly against cancer. once we do, average human age will necessarily increase, ergo biochemical control of telomeres is intimately related to aging.

that's a little silly to say. are you suggesting that telomeres evolved to place an upper limit on an organism's lifespan? I doubt you believe that.

telomerase is expressed at very low levels in adult somatic cells -> telomeres shorten, eventually get lost -> genes get lost. in what way is this not a large part of aging?

telomeres can be thought of as one part of the aging process. if the person you responded to had talked about DNA methylation or mutations, you could have responded by saying "well what about telomeres!" my point is that its involved, and from what I have been taught they play quite a large role in aging.

This is not strictly true. There are cell lines that are so-called 'immortalized', and have been dividing continuously for many years with no signs of slowing down. They typically have very high expression of telomerase and other protective factors. Cancer can be thought of as an immortalized cell line in a living body.

I am an undergraduate at UC Berkeley and am currently taking a class on cancer, especially the genetic basis for its development. One of the professors is Steve Martin, a famous cancer researcher. Even if I wasn't in this class, I would know that p16 is a well-known gene. They definitely did not discover it in this study. This article is very misleading. Humans definitely have p16, is it vital to the normal cell cycle. It is also frequently mutated in melanomas, one of the most vicious cancers. It is most likely that this group has found that naked mole rat cells use p16 in a unique way as it relates to certain types of cancer transformation pathways. Bear in mind that this sounds like this was a completely in vitro study, and so there is no proof this this gene behaves this way in wild mole rats.

All that being said, this could still turn out to be a big discovery. If they can identify the molecular mechanism behind the improved cancer suppression, it could lead to novel treatments.

Gyre never made it as far as chortle or galumph, but if it had crossed into proper english it would most certainly be a verb.

this is only slightly removed from one of those horrible child leashes. No child needs GPS tracking.

if you are that worried about your child's safety, move to a nicer neighborhood. you'll make up the cost difference with years of therapy averted in the future.

I do grunt work research in the ucb astro department, and I overheard some professors in the hall today complaining about these fiber cuts. apparently it affected their ability to download images from the keck telescopes in hawaii.