A Cure For Alzheimer's ?

[Atherosclerosis]

Just received this email from Case:

Breaking News from Case Western Reserve School of Medicine
*
We wanted to be sure the Case Western Reserve University School of Medicine community is among the first to hear about a dramatic breakthrough in the battle against Alzheimer’s disease from our neuroscience faculty.
*
Tomorrow’s edition of the journal Science will report on how Professor Gary Landreth and his team discovered that a cancer drug can quickly reverse Alzheimer’s symptoms in animal models. Within 72 hours of administration, the medication halved the number of plaque deposits closely associated with this degenerative brain disease.* Additionally, the signs of cognitive and memory deficits disappeared within that same brief time period.
*
The potential of this research to assist the 5.4 million Americans living with Alzheimer’s disease is immense. These remarkable findings represent what each member of the Case Western Reserve School of Medicine community is a part of everyday—moving medical science forward, from discoveries to cures. Please join us in congratulating this team.*
*
For more details, please see the release below or click on this link, http://www.youtube.com/user/case#p/a/u/0/HdYdYeNAYpU, to watch a brief video.

---

Members don't see this ad.

 

[ppfizenm]

Just received this email from Case:

Breaking News from Case Western Reserve School of Medicine
*
We wanted to be sure the Case Western Reserve University School of Medicine community is among the first to hear about a dramatic breakthrough in the battle against Alzheimer’s disease from our neuroscience faculty.
*
Tomorrow’s edition of the journal Science will report on how Professor Gary Landreth and his team discovered that a cancer drug can quickly reverse Alzheimer’s symptoms in animal models. Within 72 hours of administration, the medication halved the number of plaque deposits closely associated with this degenerative brain disease.* Additionally, the signs of cognitive and memory deficits disappeared within that same brief time period.
*
The potential of this research to assist the 5.4 million Americans living with Alzheimer’s disease is immense. These remarkable findings represent what each member of the Case Western Reserve School of Medicine community is a part of everyday—moving medical science forward, from discoveries to cures. Please join us in congratulating this team.*
*
For more details, please see the release below or click on this link, http://www.youtube.com/user/case#p/a/u/0/HdYdYeNAYpU, to watch a brief video.

doubtful. (note i have not read the article or watched the Youtube video but the title really tells me all I need to know)
1. animal models aren't indicative of the actual disease process. This is especially true for many brain diseases. Usually the model just presents a symptom of the disease. In this case I would guess and AB plaques.
2. Last time I perused the research it was the soluble plaques, not insoluble, that were responsible for toxicity.
3. Alzheimer's is characterized by a loss of neurons. A cancer drug designed to kill cells will not be doing your neurons any favors.
4. Even if this drug is able to improve cognition, I would imagine it would be like many drugs out there today. Slow the development leading to a steep decline later. Without treating the underlying cause which is still unknown, all you are doing is masking the symptoms.

 

[Wombat Hunter]

anecdotal awesomeness


"...Over the next year, the dementia continued to reverse itself: he is able to run again, his reading comprehension has improved dramatically, and his short-term memory is improving—he often brings up events that happened days to weeks earlier and relays telephone conversations with accurate detail. A recent MRI shows that the brain atrophy has been completely halted..."

 

[Atherosclerosis]

doubtful. (note i have not read the article or watched the Youtube video but the title really tells me all I need to know)
1. animal models aren't indicative of the actual disease process. This is especially true for many brain diseases. Usually the model just presents a symptom of the disease. In this case I would guess and AB plaques.
2. Last time I perused the research it was the soluble plaques, not insoluble, that were responsible for toxicity.
3. Alzheimer's is characterized by a loss of neurons. A cancer drug designed to kill cells will not be doing your neurons any favors.
4. Even if this drug is able to improve cognition, I would imagine it would be like many drugs out there today. Slow the development leading to a steep decline later. Without treating the underlying cause which is still unknown, all you are doing is masking the symptoms.

Your response is so typical of an SDN pre-med that it borders on self-parody.

 

[Drrrrrr. Celty]

Your response is so typical of an SDN pre-med that it borders on self-parody.

I don't think she's bordering on self-parody, my friend is a graduate student doing research on Alzheimer treatments and more than half the time her treatments which work on a cellular level fail on organism level. How can you be sure that a drug done on a different organism completely would work on humans?

Alzheimer's is characterized by a few things, such as the pro-oxidative environment and inability to direct blood flow to get rid of plaques from the CNS. Drugs like chealators and zinc have been experimentally used to treat this now.

The drug seemingly just dissolves and gets rid of plaques, it does nothing to alter the conditions in the CNS, which likely caused them, i.e the pro-oxidative environment. I'm curious to see what this drug will lead to, and maybe it will have positive affects, but I am skeptical.

 

[North12]

Sure, Im skeptical too. But this is also SO EXCITING!

The drug was effective in 3 different mouse models, where most drugs are particular to a single model. This will also pour funding into this disease so its a win/win situation for Alzheimers all around.

 

[elblackwell]

Your response is so typical of an SDN pre-med that it borders on self-parody.

I agree. Maybe what they are saying is true but one can at least read the article before posting these comments.

 

[SpecterGT260]

animal models are just fine for these issues. otherwise I still have my doubts that we have an Alzheimers breakthrough....

in animal models we arent just finding something that looks similar and go play with it. animals are generated which lack specific genes that have been targeted as disease-causing suspects, and then attempts are made to save the gene function. we can even generate animals with human variant genes in them. The difference between animals and humans is what dictates the very deliberate process going from animal to human testing and the stages of human testing - but there IS a reason we start with animals. The models are valid

 

[ppfizenm]

I agree. Maybe what they are saying is true but one can at least read the article before posting these comments.

I don't need to read the article. I know what it's going to say. I've done researched neuronal degeneration for years. I wrote a thesis on it. But go ahead, surprise me. Tell me how this is a cure.

 

[ppfizenm]

animal models are just fine for these issues. otherwise I still have my doubts that we have an Alzheimers breakthrough....

in animal models we arent just finding something that looks similar and go play with it. animals are generated which lack specific genes that have been targeted as disease-causing suspects, and then attempts are made to save the gene function. we can even generate animals with human variant genes in them. The difference between animals and humans is what dictates the very deliberate process going from animal to human testing and the stages of human testing - but there IS a reason we start with animals. The models are valid

The animal models are not fine for this type of research. The animals are provoked into showing one trait of Alzheimer's. They don't develop it naturally, therefore the underlying cause isn't there. We don't know what the underlying cause is; there probably isn't even a single cause. It likely has to do with a confluence of factors including oxidative damage and ER stress.

Something like less than 10% of Alzheimer's cases are genetic so even using a transgenic model isn't the best way to go.

The problem that needs to be solved in this case and most examples of brain diseases (PD, ischemia, TBI, Huntington's, ect) that cause neuronal degeneration is how to prevent the neurons from dying. Earlier tests would be good also so treatment can begin before symptoms show, but you need to stop the neuronal degeneration.

 

[SpecterGT260]

I don't need to read the article. I know what it's going to say. I've done researched neuronal degeneration for years. I wrote a thesis on it. But go ahead, surprise me. Tell me how this is a cure.

often a paper is coming out which represents progress, but the layman gets ahold of it, slaps the phrase "possible cure" on the home page, and publicizes the crap out of it.

(this is me agreeing with you lol)

 

[SpecterGT260]

The animal models are not fine for this type of research. The animals are provoked into showing one trait of Alzheimer's. They don't develop it naturally, therefore the underlying cause isn't there. We don't know what the underlying cause is; there probably isn't even a single cause. It likely has to do with a confluence of factors including oxidative damage and ER stress.

Something like less than 10% of Alzheimer's cases are genetic so even using a transgenic model isn't the best way to go.

The problem that needs to be solved in this case and most examples of brain diseases (PD, ischemia, TBI, Huntington's, ect) that cause neuronal degeneration is how to prevent the neurons from dying. Earlier tests would be good also so treatment can begin before symptoms show, but you need to stop the neuronal degeneration.

i wasnt necessarily restricting my comment to alzheimers. just the possible implication that animal models should be rejected as invalid. and the genetic component of neuro diseases is growing in the literature as bioinformatics gets ahold of the data.

and alzheimers may be a good example of a situation where animal models are hard to come by (although I would still argue that their value in target gene identification is still quite high), but this doesn't apply to brain diseases in general. epilepsy is a good one. There are also genetic components identified in schizophrenia. This doesnt mean we will wipe out these conditions - as my understanding is they can have multiple causes - but a good many neurological/psych diseases are defined by the symptoms so induction of symptoms in a mouse is a perfectly fine model for exploring individual pathways.


would you mind explaining a little more on your research? undergrad lab tech? or are you PhD non-trad coming into medicine?

 

[gmcguitar4]

Don't you guys think the doctors and phd students working on this project thought of all of our skepticisms while working on this project? If they and the university are excited about it, it must be for good reason..it's not like this is a CNN article were they claim we found the cure for cancer every 3 months when new research emerges. On the other hand, they could just be looking for attention. We just have to wait for human trials to be sure about anything.

 

[crprep23]

I cringe when I hear the word "cure". I agree that this is interesting research, but I tend to side with the sentiments that the effects are likely overstated.

 

[Atherosclerosis]

I don't need to read the article. I know what it's going to say. I've done researched neuronal degeneration for years. I wrote a thesis on it. But go ahead, surprise me. Tell me how this is a cure.

Well, at least we've shaken that pesky border.

 

[CoolWhipp]

Don't you guys think the doctors and phd students working on this project thought of all of our skepticisms while working on this project? If they and the university are excited about it, it must be for good reason..it's not like this is a CNN article were they claim we found the cure for cancer every 3 months when new research emerges. On the other hand, they could just be looking for attention. We just have to wait for human trials to be sure about anything.

Researchers have to make it seem to the public like they are on the verge of a discovery. It's what has to be done for PR purposes, and it works. It brings in the money.

I can't help but to respond to these announcements like ppfizenm did. How many articles have you seen that said "breaking discovery, one step closer to the cure." I mean seriously, count the cures, they aren't raining down on us like the media suggests.

 

[ppfizenm]

i wasnt necessarily restricting my comment to alzheimers. just the possible implication that animal models should be rejected as invalid. and the genetic component of neuro diseases is growing in the literature as bioinformatics gets ahold of the data.

and alzheimers may be a good example of a situation where animal models are hard to come by (although I would still argue that their value in target gene identification is still quite high), but this doesn't apply to brain diseases in general. epilepsy is a good one. There are also genetic components identified in schizophrenia. This doesnt mean we will wipe out these conditions - as my understanding is they can have multiple causes - but a good many neurological/psych diseases are defined by the symptoms so induction of symptoms in a mouse is a perfectly fine model for exploring individual pathways.


would you mind explaining a little more on your research? undergrad lab tech? or are you PhD non-trad coming into medicine?

It was undergrad research but I applied to/was funded by the howard hughes medical institute. I worked with a 6-OHDA model of PD in rats but my research involved trying to prevent the neuronal degeneration caused by the neurotoxin i was injecting. The models are ok, but that depends on the model. The plaque model isn't the most reliable simply b/c we aren't entirely sure what if any role the plaques play.

 

[sliceofbread136]

Cure is thrown around so loosely. If every article stating that there has been a "cure" was actually true, cancer would have been cured like a billion times. We don't even know what causes alzheimers, I kinda doubt this group just stumbled into a complete cure for the disease.

 

[ppfizenm]

Don't you guys think the doctors and phd students working on this project thought of all of our skepticisms while working on this project? If they and the university are excited about it, it must be for good reason..it's not like this is a CNN article were they claim we found the cure for cancer every 3 months when new research emerges. On the other hand, they could just be looking for attention. We just have to wait for human trials to be sure about anything.

The are already treatments in human trials the remove the plaques. There is one the uses antibodies targeted against the plaques. But the plaques aren't the cause of Alzheimer's, they are a bi-product. Removing them may temporarily improve cognition because you are freeing up synapses for signalling however neurons are still dying. Eventually that will catch up to you.

 

[ppfizenm]

cure is thrown around so loosely. If every article stating that there has been a "cure" was actually true, cancer would have been cured like a billion times. We don't even know what causes alzheimers, i kinda doubt this group just stumbled into a complete cure for the disease.

+1.

 

[Atherosclerosis]

Cure is thrown around so loosely. If every article stating that there has been a "cure" was actually true, cancer would have been cured like a billion times. We don't even know what causes alzheimers, I kinda doubt this group just stumbled into a complete cure for the disease.

I heard they were throwing quarters into "hypothesis hats" from across the room.

 

[sliceofbread136]

I heard they were throwing quarters into "hypothesis hats" from across the room.

Very clever. Anyone with any experience in Alzheimer's research (or any medical research for that matter) would know to be very skeptical of this "cure". Even if by some miracle this actually is a cure (chances of this are astronomically small), it'll be almost another 10 years of clinical trails and approval procedures before it is available to anyone. So let's not get ahead of ourselves.

 

[elblackwell]

They never said cure. If anyone took the time to read the excerpt Case provided or you can read the article in Science when it is released, they say it's a promising breakthrough. I don't know as much about this area, but if something is published in a highly regarded peer-reviewed journal, it would seem like more than just hype and PR to me.

 

[Atherosclerosis]

Very clever. Anyone with any experience in Alzheimer's research (or any medical research for that matter) would know to be very skeptical of this "cure". Even if by some miracle this actually is a cure (chances of this are astronomically small), it'll be almost another 10 years of clinical trails and approval procedures before it is available to anyone. So let's not get ahead of ourselves.

Thank you.

Obviously, I'm not hailing this paper because it doesn't even come out until tomorrow. Of course we should take these headlines in with a shovel of salt.

I'm just tired of the mentatlity of pre-med SNDers like our friend, ppfizenm--students who have done a little bit of undergrad research and then proceed to spew opinions well beyond their depth.

PhD? Science publication? BFD... I know how to use a PCR machine, properly grow cell cultures, not to mention the 20+ papers I read on the subject. So yeah, I think I can tell you this research is bullsh*t.

 

[sliceofbread136]

Thank you.

Obviously, I'm not hailing this paper because it doesn't even come out until tomorrow. Of course we should take these headlines in with a shovel of salt.

I'm just tired of the mentatlity of pre-med SNDers like our friend, ppfizenm--students who have done a little bit of undergrad research and then proceed to spew opinions well beyond their depth.

PhD? Science publication? BFD... I know how to use a PCR machine, properly grow cell cultures, not to mention the 20+ papers I read on the subject. So yeah, I think I can tell you this research is bullsh*t.

Ya but I think it's better for us to be overly skeptical instead of naive. ppfizenm isn't claiming to know more than these scientist, he (she?) is just being skeptical of a relatively outlandish claim.

 

[Atherosclerosis]

Ya but I think it's better for us to be overly skeptical instead of naive. ppfizenm isn't claiming to know more than these scientist, he (she?) is just being skeptical of a relatively outlandish claim.

It's a he. And you tell me...

I don't need to read the article. I know what it's going to say. I've done researched neuronal degeneration for years. I wrote a thesis on it. But go ahead, surprise me. Tell me how this is a cure.

Years, I tell you! Years!

 

[ppfizenm]

Ya but I think it's better for us to be overly skeptical instead of naive. ppfizenm isn't claiming to know more than these scientist, he (she?) is just being skeptical of a relatively outlandish claim.

If I (a he) knew more, I would have come up with a suitable treatment to prevent degeneration. I wouldn't claim to know as much either because I have little experience with cancer drugs besides a semester of a cancer class and knowing the general mode of action but I know enough to figure out what they did from the title of the article. There is only so much a cancer drug could be doing to augment Alzheimer's, I picked the most likely.

I'll even propose a mechanism. Cancer drugs usually integrate into the DNA and prevent replication. Something you would want to do if you have cells that replicating uncontrollably in the body. The drug is probably making its way into the aggregate plaques and disrupting the inter-molecular interactions allowing the astrocytes and other maintenance glia to remove the smaller fragments.

 

[Whatyousay]

Case Western researchers reading this thread...

"What the hell did I ever do to warrant people taking giant s*** on my life's work?"

 

[Atherosclerosis]

If I (a he) knew more, I would have come up with a suitable treatment to prevent degeneration. I wouldn't claim to know as much either because I have little experience with cancer drugs besides a semester of a cancer class and knowing the general mode of action but I know enough to figure out what they did from the title of the article. There is only so much a cancer drug could be doing to augment Alzheimer's, I picked the most likely.

I'll even propose a mechanism. Cancer drugs usually integrate into the DNA and prevent replication. Something you would want to do if you have cells that replicating uncontrollably in the body. The drug is probably making its way into the aggregate plaques and disrupting the inter-molecular interactions allowing the astrocytes and other maintenance glia to remove the smaller fragments.

ppfizenm is quickly becoming my very favorite poster. You do all the hard work of parodying yourself, so I don't have to.

 

[ppfizenm]

It's a he. And you tell me...



Years, I tell you! Years!

Funny, if I didn't have a large amount of experience you would be denigrating me for not knowing enough. Perhaps try interjecting an opinion on the issue that isn't colored with a personal attack.

 

[sliceofbread136]

Funny, if I didn't have a large amount of experience you would be denigrating me for not knowing enough. Perhaps try interjecting an opinion on the issue that isn't colored with a personal attack.

You obviously don't know the rules of SDN. If someone disagrees with your opinion, then they are obligated to personally attack you.

 

[Atherosclerosis]

Funny, if I didn't have a large amount of experience you would be denigrating me for not knowing enough. Perhaps try interjecting an opinion on the issue that isn't colored with a personal attack.

And the party don't stop. Pubs or it didn't happen. **copyright**


But that's kind of my point, isn't it? I'm not taking weak sh*ts on research I haven't read.

 

[Atherosclerosis]

You obviously don't know the rules of SDN. If someone disagrees with your opinion, then they are obligated to personally attack you.

Come on now, no personal attacks needed. It's not like ppfizenm is the only poster who does this. He was just unfortunate enough to post on my thread whilst I am feeling snarky.

But really, I would love nothing more than to see some of ppfizenm's pubs so I can be assured that he doesn't fit this stereotype that I am unfairly assigning to him.

 

[ppfizenm]

And the party don't stop. Pubs or it didn't happen. **copyright**


But that's kind of my point, isn't it? I'm not taking weak sh*ts on research I haven't read.

If they put out research on dbagging I'm sure you wouldn't need to read it. But hey, we all have our areas of expertise.

 

[Atherosclerosis]

If they put out research on dbagging I'm sure you wouldn't need to read it. But hey, we all have our areas of expertise.

Annnnnd we have a live one.

 

[ppfizenm]

Come on now, no personal attacks needed. It's not like ppfizenm is the only poster who does this. He was just unfortunate enough to post on my thread whilst I am feeling snarky.

But really, I would love nothing more than to see some of ppfizenm's pubs so I can be assured that he doesn't fit this stereotype that I am unfairly assigning to him.

Because I've claimed to have them? I wrote a thesis.

here is the poster i did of itView attachment edited for sdn idiot.pptx

enjoy

 

[Atherosclerosis]

Because I've claimed to have them? I wrote a thesis.

here is the poster i did of itView attachment 18534

enjoy

A good friend of mine once said, "i have not read the article... but the title really tells me all I need to know."

 

[sector9]

Indeed, personal attacks are not allowed on SDN. Please continue this conversation respectfully or use the "ignore" feature for users you disagree with.

 

[ppfizenm]

A good friend of mine once said, "i have not read the article... but the title really tells me all I need to know."

yup. good thing it's titled it "edited for sdn idiot" then. I was scared you thought it was referring to someone else. Now that we've cleared that up you can get back to you're blind optimism in the land where people believe everything they are told. Just remember not to get your kids vaccinated, that one study published years ago linked it to autism.....

 

[Wombat Hunter]

Quit your bickering, please. I'm pulling the 'I watched my grandpa deteriorate and die from Alzheimer's' card, so seriously, please stop muddying the thread.

A sober analysis of the story I posted earlier.
Someone needs to bang out a 1-year double-blind on this ASAP.

 

[sliceofbread136]

Quit your bickering, please. I'm pulling the 'I watched my grandpa deteriorate and die from Alzheimer’s' card, so seriously, please stop muddying the thread.

A sober analysis of the story I posted earlier.
Someone needs to bang out a 1-year double-blind on this ASAP.

This story is pretty cool, but once again I doubt this does much more than delay symptoms (and long term ketosis is really bad for you). Hopefully I'm wrong, but I think we are some time away from a real cure. The good news is we are making some progress though.

 

[Wombat Hunter]

This story is pretty cool, but once again I doubt this does much more than delay symptoms (and long term ketosis is really bad for you). Hopefully I'm wrong, but I think we are some time away from a real cure. The good news is we are making some progress though.

1 year of symptom reversal is a far cry from symptom delay. [Is the story true? Representative of a larger population?]

I'm assuming that ingesting ketones is healthfully sustainable, unlike forcing the body into ketosis. No knowledge to back that up.

 

[Double Trouble]

The animal models are not fine for this type of research. The animals are provoked into showing one trait of Alzheimer's. They don't develop it naturally, therefore the underlying cause isn't there. We don't know what the underlying cause is; there probably isn't even a single cause. It likely has to do with a confluence of factors including oxidative damage and ER stress.

Something like less than 10% of Alzheimer's cases are genetic so even using a transgenic model isn't the best way to go.

The problem that needs to be solved in this case and most examples of brain diseases (PD, ischemia, TBI, Huntington's, ect) that cause neuronal degeneration is how to prevent the neurons from dying. Earlier tests would be good also so treatment can begin before symptoms show, but you need to stop the neuronal degeneration.

Right, the ***** Phds at CWRU must have overlooked that fact when they started the research and applied for grant money.

 

[Cinclus]

Right, the ***** Phds at CWRU must have overlooked that fact when they started the research and applied for grant money.

I don't know about this particular case, but researchers use completely incorrect animal models all the time. I was a fellow grad student of some very smart people using flies for entirely inappropriate studies. I've also heard anecdotal reports from profs of some hilariously improper uses for C. elegans.

 

[ppfizenm]

Well according to the CNN promo I just heard it "erases Alzheimer's". will add more later.

 

[ppfizenm]

I don't know about this particular case, but researchers use completely incorrect animal models all the time. I was a fellow grad student of some very smart people using flies for entirely inappropriate studies. I've also heard anecdotal reports from profs of some hilariously improper uses for C. elegans.

Certain models for diseases are very good. For example, we know the exact genes that cause Huntington's. You can create transgenic animals expressing these variants to study HD and be working with applicable model.You must keep in mind it is still an animal model and their are differences between it and humans. Some models just aren't so good though like you said. There are supposed "breakthroughs" all the time, and how much has actually changed.

In the best case here all we are is a new drug that address the some of the symptoms of Alzheimer's until the neuronal loss becomes so great a steep decline ensues.

Also, remember this is a cancer drug. Cancer drugs do not play nicely with bodily organs and cells.

 

[gmcguitar4]

cancer drug[/B]. Cancer drugs do not play nicely with bodily organs and cells.

Depends on the type of cancer drug used, you are thinking older chemotherapeutic drugs which don't have too much specificity. Now a days a cancer drug could mean a whole variety of things such as antiangiogenic or immuno activating. They could produce side effects as well but are much more controlled, especially with new forms of drug delivery.It probably isn't one of these examples but they need to give more detail because speculation is a waste of time until that.

 

[SpecterGT260]

Thank you.

Obviously, I'm not hailing this paper because it doesn't even come out until tomorrow. Of course we should take these headlines in with a shovel of salt.

I'm just tired of the mentatlity of pre-med SNDers like our friend, ppfizenm--students who have done a little bit of undergrad research and then proceed to spew opinions well beyond their depth.

PhD? Science publication? BFD... I know how to use a PCR machine, properly grow cell cultures, not to mention the 20+ papers I read on the subject. So yeah, I think I can tell you this research is bullsh*t.

Undergrad research doesn't account to much. You are prone to the same problems as laymen which is adapting specific facts inappropriately across a broad range. Without having really studied the systems you are likely to come to false conclusions

 

[SpecterGT260]

If I (a he) knew more, I would have come up with a suitable treatment to prevent degeneration. I wouldn't claim to know as much either because I have little experience with cancer drugs besides a semester of a cancer class and knowing the general mode of action but I know enough to figure out what they did from the title of the article. There is only so much a cancer drug could be doing to augment Alzheimer's, I picked the most likely.

I'll even propose a mechanism. Cancer drugs usually integrate into the DNA and prevent replication. Something you would want to do if you have cells that replicating uncontrollably in the body. The drug is probably making its way into the aggregate plaques and disrupting the inter-molecular interactions allowing the astrocytes and other maintenance glia to remove the smaller fragments.

Watch the link. They show increased expression of ApoE with the drug which down regulates the protein which, in Alzheimer's, cannot be cleared and leads to neuronal damage. This isn't a cure, but they are hoping to delay symptoms. If this works in humans and we can improve early detection this could potentially be awesome therapy.


But again, your opinions were formed via a narrow view of animal models and cancer drug action. When u get into med school you will likely see tamoxifen as your first cancer drug. Go look it up and you may get an appreciation for the non-genetic approaches that docs (both md and phd) are using to treat disease with genetic origins (and cancer has genetic origin even if the individual has a normal genome). You are thinking chemo. And yes chemo is often nasty. It is also ONLY 1 type of drug for cancer

 

[ppfizenm]

Depends on the type of cancer drug used, you are thinking older chemotherapeutic drugs which don't have too much specificity. Now a days a cancer drug could mean a whole variety of things such as antiangiogenic or immuno activating. They could produce side effects as well but are much more controlled, especially with new forms of drug delivery.It probably isn't one of these examples but they need to give more detail because speculation is a waste of time until that.

Some modern chemo drugs have some pretty nasty side effects. Besides the negative side effects of antiangiogenic or immuno activating drugs these are almost always used in conjunction with other classes to hit multiple points of development.

http://www.cnn.com/2012/02/09/health/us-cancer-drug-alzheimers/index.html

"mega-doses of bexarotene"

The drug is bexarotene. It interferes with replication by effecting transcription regulation. It also targets the liver, kidney's, and visceral organs.