Cancer Vaccines

[Alex_Krycek]

Recently I read an article in The Guardian about cancer vaccines.

Do you think these vaccines are likely to be on the market available for patients within this decade?

Cancer and heart disease vaccines ‘ready by end of the decade’

Exclusive: Pharmaceutical firm says groundbreaking jabs could save millions of lives

https://www.theguardian.com/society/2023/apr/07/cancer-and-heart-disease-vaccines-ready-by-end-of-the-decade

[Agent Smith]

Why can't we just present the tumor antigens to the immune system, that's the way a normal vaccine works. No extra step involving genetic engineering is necessary.

When we make a vaccine against microbes, we kill them and extract the immunogenic antigens and inoculate the patient, simply stimulating the immune system to mount a response. 

Of late I'm inclined to believe Paul W. Ewald's every disease is an infection hypothesis. So, at the root of cancer is also either a known/unknown infection. If so we can create vaccines much easier and safer than interfering with genes. The catch though is to identify the offending organism. 

[CharonY]

Cancer cells are our own cells. Antibodies against them would target healthy cells, too. Only some cancers are associated with e.g. viruses and there are vaccines against e.g HPV.

[CharonY]

9 hours ago, Agent Smith said:

every disease is an infection hypothesis

I don't think that he postulated it as aggressively (in part because it is trivially false). What I believe he has argued (and it does align to some level with what my line of thinking) that a) the role of prior infections in disease development are often overlooked and the the current paradigm of looking for current active infections might be too limiting and related to that that b) especially for chronic diseases, folks assume a too elevated role of genetic factors.

It is a while back where I read a little a bit about those arguments and I do think that the research field has moved a bit along based on data of the last two decades. But again, the quote above is clearly inaccurate. 

 

[Agent Smith]

18 hours ago, CharonY said:

I don't think that he postulated it as aggressively (in part because it is trivially false). What I believe he has argued (and it does align to some level with what my line of thinking) that a) the role of prior infections in disease development are often overlooked and the the current paradigm of looking for current active infections might be too limiting and related to that that b) especially for chronic diseases, folks assume a too elevated role of genetic factors.

It is a while back where I read a little a bit about those arguments and I do think that the research field has moved a bit along based on data of the last two decades. But again, the quote above is clearly inaccurate. 

 

My interest in Paul W. Ewald's hypothesis piqued when Covid-19 researchers discovered the virus was binding to ACE II receptors (hypertension). Could hypertension be caused by an infection? was the question that crossed my mind. Very unlikely, but you never know. That's the most recent update to my Paul W. Ewald file. 

Too, I'm a bit suspicious about so-called autoimmune disorders - maybe the immune system's attacking infected tissue and there's always collateral in a war, which it is, oui? 

Je ne sais pas.

[CharonY]

16 minutes ago, Agent Smith said:

Could hypertension be caused by an infection? was the question that crossed my mind. Very unlikely,

Not unlikely, infection-associated inflammation is known to be associated with hypertension. You just cannot make the assumption that ll hypertension is related to infection.

19 minutes ago, Agent Smith said:

Too, I'm a bit suspicious about so-called autoimmune disorders - maybe the immune system's attacking infected tissue and there's always collateral in a war, which it is, oui? 

It is unfortunately way more complicated than that.

[Agent Smith]

7 hours ago, CharonY said:

Not unlikely, infection-associated inflammation is known to be associated with hypertension. You just cannot make the assumption that ll hypertension is related to infection.

Glad that we see eye to eye on the issue, even if half-heartedly. This isn't an assumption (re: Covid-ACE II receptor link).

 

7 hours ago, CharonY said:

It is unfortunately way more complicated than that.

How so? Anyway, mine is just a weak hypothesis, relatively speaking. A few cases where we see even a shadow of a link (between infection and so-called autoimmune disorders) should provide us a something to work on. 

[CharonY]

1 hour ago, Agent Smith said:

Glad that we see eye to eye on the issue, even if half-heartedly. This isn't an assumption (re: Covid-ACE II receptor link).

 

How so? Anyway, mine is just a weak hypothesis, relatively speaking. A few cases where we see even a shadow of a link (between infection and so-called autoimmune disorders) should provide us a something to work on. 

What I meant is the link is established, and not unlikely as per your post. But hypertension also has many other non-infection related causes, so the reverse is not true.

For imune response, the underlying mechanism are too complex for this forum. Infections can push the system to a state that triggers an autoimmune response, but so can for example prolonged stress and metabolic syndroms.

Simplified generalized explanations of  complex biological processes tend to be only applicable in a very narrow way, if at all.

[Agent Smith]

On 7/29/2024 at 7:18 AM, CharonY said:

What I meant is the link is established, and not unlikely as per your post. But hypertension also has many other non-infection related causes, so the reverse is not true.

Si, I'm painfully reminded of the multifactorial nature of etiology. 

 

On 7/29/2024 at 7:18 AM, CharonY said:

For imune response, the underlying mechanism are too complex for this forum. Infections can push the system to a state that triggers an autoimmune response, but so can for example prolonged stress and metabolic syndroms.

Do you know how viral illnesses are handled by the immune system? One way is to trigger apoptosis so that virion load is reduced. Another way is to go "autoimmune", let the WBCs destroy (infected) cells, Both? Come to think of it a viral infection is uncannily similar to malignancies (in both cases, we have a genetic problem and in both cases, there's serial mutations, and in both cases we have to attack rogue cells)

 

On 7/29/2024 at 7:18 AM, CharonY said:

Simplified generalized explanations of  complex biological processes tend to be only applicable in a very narrow way, if at all.

There's no harm in discussing the question on fora like this; we're not submitting a paper for publication where being right is crucial.

Edited July 30 by Agent Smith

[CharonY]

10 minutes ago, Agent Smith said:

There's no harm in discussing the question on fora like this; we're not submitting a paper for publication where being right is crucial.

There is some harm as simplifications are inherently more attractive than the more accurate, but far more complicated answers. If phrases carelessly, folks might actually come to wrong conclusion and challenge existing (and effective) treatments. Especially in the area of vaccinations misleading information have shown the impact of how poor science has led to real harm

The issue here is that there are common but also very different pathways involved in antiviral responses and certain auto-immune diseases. The latter are incredibly varied and at best superficially similar. Yet, infections are known triggers for many autoimmune diseases with different manifestations. Now, the important bit are really these differences, but despite having a background in infectious diseases, I wouldn't be able to draw up the involved pathways without significant time investment on my end. And even for the same diseases, viruses can have different routes. The viruses HTLV and EBV have both been associated with rheumatoid arthritis, for example. But while the former seems might impact it via proinflammatory responses at synovial cells, EBC seems to mess up something with T cells. 

27 minutes ago, Agent Smith said:

Do you know how viral illnesses are handled by the immune system? One way is to trigger apoptosis so that virion load is reduced. Another way is to go "autoimmune", let the WBCs destroy (infected) cells, Both? Come to think of it a viral infection is uncannily similar to malignancies (in both cases, we have a genetic problem and in both cases, there's serial mutations, and in both cases we have to attack rogue cells)

I am not quite sure what you mean here, the non-immune driven apoptosis has multiple triggers, including the presence of certain dsRNAs intracellular, others via detection of viral RNA extracellularly via receptors (and more). Immune-induced activation of killer cells relies on detection of viral antigens. So at least at that point does not mess with self-recognition.

[Agent Smith]

@CharonY, verum, there's that risk, with dangerous consequences, of oversimplifying an actually complex process. I was just checking if there's any link between infections and 1) all diseases in general, 2) cancer and 3) autoimmune disorders. You will agree that there's at least an association. it'd be fabulous if all diseases were infections. All we'd need to do is develop more antibiotics, they'd be the magic bullet - the Holy Grail of pharmacology. 

[CharonY]

This is a good example how erroneous and/or simplified assumptions invariably lead to wrong conclusions. As mentioned above, there is a difference between link and active causative agent. Infections can trigger certain (long-term) issues down stream, but there are two things that are important and you seem to have missed. Especially the loose use of all (i.e. generalization) is very problematic here).

a) just because infections can trigger some potentially unrecognized issues, it does not mean that all of these issues are in fact triggered by them. So while it may be fabulous that all diseases are caused by infections, we know that it isn't the case. 

b) you confuse trigger with the active cause. The reason why some folks (myself included) think that some chronic issues are related to infection but have not recognized as such is because certain symptoms manifest after the infection is cleared. You need to read Ewald in the context of Koch's postulate more carefully. If there was an ongoing infection the link would be far more trivial to establish. However, we are aware of conditions like post-viral syndromes (such as long-COVID).

Just based on this, the argument of antibiotics does not make sense. First, depending on the pathogen and their interaction with the immune city, the trigger for later issues can arise early on in the infection process or at symptom onset. Therefore, antibiotics would be too late to the game. 

Second, even if they weren't some of the best understood interferences with the human immune system are viral (some bacteria also do odd things, mostly intracellular ones, but they seem to be fairly different as a whole). Antibiotics don't work on viruses.

Third, your argument that we just need to develop new antibiotics itself is problematic. We are  running out of them as resistant bacteria (which again as a whole are likely  not that relevant to the current discussion), are taking over. In the last ten years only 20 or so antibiotics have been approved and they have been very long in the development pipeline. In some cases, within months, resistant bacteria against  new drugs have been detected. Far from being a panacea, we are increasingly unable to treat simple infections.