> There is a relatively new theory saying that malignant, metastatic cancer cells behave like single cell organisms, and that cancer basically represents an unwanted return to our genetic roots
It's not close to even 'relatively' being new. I was giving cancer talks that made mention of it back when I worked in cancer bio, just about 16 years ago now. I didn't come up with it, and it wasn't new then. I used it in talks to laymen, to give a very abstract idea of how cancer worked. But it fell into the category of "lies we tell children," because it was only true in the most abstract way, and utterly incorrect once you dug into any details.
The reason cancer bio people dislike it is because it's only true at the 10,000-foot, highly abstracted level. When you start digging into the granular level, its testable predictions rank between 'falsified' and 'irrelevant'. It doesn't produce any alternative lines for thinking about treatment, causality, etc. Especially given that the progress of a single cancer tends to be all about their interaction with the multicellular milieu - e.g., developing immune evasion, which isn't at all an "atavistic" trait, although it's one of the core hextad that defines malignant development. (On the contrary, it comes built-in for normal cells - they're now developing a novel immune evasion, to hide their newly altered antigens from the immune system).
e.g., "Cannot help but switch to previous single-celled metabolism" doesn't follow in any meaningful way from the thesis of atavistic traits. In fact, it doesn't predict at all the relationship between tumor size, distance from vascular supply, and anaerobic metabolism. "Cells without controlled growth will outgrow their vascular supply, requiring a transition to anerobic metabolism" does, however, and predicted the relationships we see. It's not "cannot help but engage with less efficient metabolism", it's "transition to relying on the only metabolism afforded to a highly-dysregulated cell that is not responsive to environmental signals that normally trigger or withhold growth." Normal unicellular organisms are responsive to those signals.
Yeah, I don't hate it - it's a cute metaphor. It's a nice way of thinking of cancer at the 10K-foot level. It's just also wrong at any closer level of inspection than that, which is why people whose job is to be elbow-deep in all of the nitty-gritty details of cancer can't help but look at it and go "please stop wasting my time."
It's not close to even 'relatively' being new. I was giving cancer talks that made mention of it back when I worked in cancer bio, just about 16 years ago now. I didn't come up with it, and it wasn't new then. I used it in talks to laymen, to give a very abstract idea of how cancer worked. But it fell into the category of "lies we tell children," because it was only true in the most abstract way, and utterly incorrect once you dug into any details.
The reason cancer bio people dislike it is because it's only true at the 10,000-foot, highly abstracted level. When you start digging into the granular level, its testable predictions rank between 'falsified' and 'irrelevant'. It doesn't produce any alternative lines for thinking about treatment, causality, etc. Especially given that the progress of a single cancer tends to be all about their interaction with the multicellular milieu - e.g., developing immune evasion, which isn't at all an "atavistic" trait, although it's one of the core hextad that defines malignant development. (On the contrary, it comes built-in for normal cells - they're now developing a novel immune evasion, to hide their newly altered antigens from the immune system).
e.g., "Cannot help but switch to previous single-celled metabolism" doesn't follow in any meaningful way from the thesis of atavistic traits. In fact, it doesn't predict at all the relationship between tumor size, distance from vascular supply, and anaerobic metabolism. "Cells without controlled growth will outgrow their vascular supply, requiring a transition to anerobic metabolism" does, however, and predicted the relationships we see. It's not "cannot help but engage with less efficient metabolism", it's "transition to relying on the only metabolism afforded to a highly-dysregulated cell that is not responsive to environmental signals that normally trigger or withhold growth." Normal unicellular organisms are responsive to those signals.
Yeah, I don't hate it - it's a cute metaphor. It's a nice way of thinking of cancer at the 10K-foot level. It's just also wrong at any closer level of inspection than that, which is why people whose job is to be elbow-deep in all of the nitty-gritty details of cancer can't help but look at it and go "please stop wasting my time."