@swamidass: Have you noticed this recent post at ENV addressing your arguments in Biologos ?
Based on your understanding, @Ashwin_s, what do you think about Well’s article? What points do you think are good? Which parts seen to miss the point?
I don’t think I understand enough to make a valid critique.
I got the larger point that cancer is not usually a constructive process as opposed to evolution. Hence it might tnot be a valid comparison.
Edit: I shared the OP mainly as information.
If cancer is innovating functions that are virtually impossible to expect… is it God ? Or Satan doing the designing?
@swamidass - You’re now DI’s favorite target. Well you have the entire scientific community backing you on this one. Have at it. It should be an easy rebuttal scientifically but remember this is public theater and the front line in the boarder culture war. Please don’t make it another Nye-Ham debate.
Perhaps this will help you:
Can cancer innovate?
Yup. Using the same definitions used by ID, it can innovate.
I am not familiar with the definitions… can you clarify.
If i remember your Biologos article correctly, you mentioned the cancerous cell finding ways to bypass the bodies defences and spread.
I don’t see how that is significant … end of the day the cancerous cell kills the organism… and itself.
Sounds like an innovative way to die.
Edit: To me that is exactly what I would expect from a stochastic process of change in a complex system… death.
No one is suggesting that cancer isn’t ultimately bad for the organism or the cancer cells. What Joshua and others mean is that in the development of a cancer, the cancer cells evolve, becoming more invasive and resistant. Within the ecosystem of a body, the cancer cells are undergoing adaptive evolution (and neutral evolution), leading to their proliferation and infiltration.
What happens in most cancers is that the cancerous cells acquire the means of proliferating and evading ‘stop-growing’ signals. Over time, the cells can also acquire the ability to invade other tissues, and redirect blood vessel growth to tumors, further supporting the cancerous mass. These things can vary between different types of cancers.
What we have seen is that in the process, new functional proteins can be generated (often from gene fusions), regulatory processes altered and/or bypassed, and step-wise accumulation of adaptive mutations that support the spread of the cancer cells. Cancer cells can also acquire resistance to treatments which is why remissions are often temporary. Many cancers exhibit a microcosm of evolutionary mechanisms.
In many multicellular organisms, the typical cellular response to unregulated replication is death. That’s because it’s often critical that the ‘right’ cells stay in the right places and are not disrupted by the presence of other cells. In fact, there are many apoptotic (cell suicide), triggers present that ensure this happens the majority of the time. There can also be other system defenses that target aberrant cell growth.
What you find with senescence (deterioration over time), or most cell-killing errors, is accumulation of missing cells. Over time, as these cells can no longer be replaced, the system or organ can ultimately fail, leading to death. For example, some types of diabetes occur this way. Probably some forms of dementia too.
Cancer is a different beast. It’s the opposite of senescence and single-cell death. Cancer cells escape apoptotic triggers. They can accumulate mutations that allow the cells to invade other tissues and migrate through the body. In a sense, they behave more like an invading organism or pathogen that adapts increasingly well to its host. Researchers have even found transmissible cancers that can move to different hosts.
I agree with you here. I think we can define cancer with loss of genetic information. Loss of genetic information is easy to explain by mutation. Gain of genetic information is the challenge.
Actually, it is an increase of genetic information. We can empirically measure this using metrics like CSI and ASC (@EricMH) .
Honestly, I’m not going to take many questions on this thread, and will likely close it soon.
I invited Wells to engage on this on Jun 1 and he did not have time. The fact is that he ignored most of the substance of the article. I’d be happy to engage with him here if he comes. I will send him another email. If he does not have the time to defend his article, I don’t have the time to rebut it.
@colewd perhaps ask Wells to make time to engage on this. For now the original article is a strong rebuttal:
Yep. Duplications and new gene fusions have been identified.
If a gain of information is causing dis regulation of a system there is a problem with the definition. I agree with you this should be something they are working on.
I don’t know Wells and my only contact would be through Gauger, Bagley, Nelson, Behe or Axe, however based on his article his knowledge of cancer is limited. I have never seen Wells post so he is understandably reluctant. Maybe @pnelson or @Agauger would participate.
It is critical in these discussions that “information” be well defined and applied consistently. Otherwise one can fall into the confusion that Lee Spetner did. (1), (2) That is, it seems one can frame any change as a ‘loss of information’ depending on what definition one chooses. Whether that definition is correct is what really matters.
No one is working on this from what I can tell. Invitation was resent to Wells. The information in my article was having a large effect, so I think they needed a public pushback. It will take them time and a lot of work to retool based on the new information I am drawing attention to here.
In the end, I’m honored he chose my work as one of his new “icons of evolution.” It points a new generation of students to the central importance of evolution in understanding biology. That is good news for science education.
I think that they are not ready to take on the whole definition of functional information argument. So I agree closing this up is the right call.