Fighting Cancer With The Common Cold?

Roland Piquepaille writes "After 30 years of work, Saint Louis University researchers have genetically engineered a common cold virus to fight cancerous cells while leaving unaffected healthy ones. They received a patent for this research and clinical tests on humans will start soon, according to this news release. Dr. William Wold, chair of the department of molecular microbiology and immunology, received the patent No. 6,627,190 for his work. Preclinical testing has already been done so clinical trials should start soon. We can only hope they will be successful. This overview contains many more details and references about this potential cure for all kinds of cancer. [Note: this is a very different project from the one mentioned by a previous Slashdot post.]"

Comments

Re:Must be Microsoft

[unixbum]

It must be really hard to genetically engineer out of nothing, something... very... common.. Hmm.

The point is not that they have geniticly engineered a common cold, the point is that they have engineered a common cold to only attack cancerous cells.

Natural Selection of Cancer Cells

[TheSync]

I think the biggest problem is that cancer undergoes natural selection rapidly, which is why it is so hard to fight. Since cancerous cells have a great deal of genetic mutation, populations of cancer cells can "evolve" to thwart treatments. Targetting almost any individual protein in cancer is bound to fail.

Re:Natural Selection of Cancer Cells

[Anonymous Coward]

What moron modded this as Informative? You wait 'til I Metamoderate! lol. The poster clearly doesn't understand what cancer is. (No offense to the poster, you're just confusing cancer with other diseases which do adapt)

Cancer does not "evolve." It is the natural mutation of our own cells. Nearly everyone over the age of 70 has some form of cancer -- just not often the deadly kind. (benign moles, colon polyps, etc. etc. are common)

Because of flaws in cell division due to age, exposure to radiation (including sunlight's UV and tanning beds), and chemical poisons such as food additives and drugs, our cells occasionally mutate. These mutations are often harmless & if the mutation lies in a part of the DNA that is not active (say a skin cell has damaged DNA that is only used in brain cells and isn't switched on), then the new, mutated cell may function as a normal cell instead of becoming "cancerous".

Occasionally, when cells mutate... they become cancerous by dividing rapidly to form tumors which starves surrounding tissue of vital nutrients. Even worse, cells can break free and start new tumors in other parts of the body which impedes normal functioning and multiplies the growth of cancerous cells while killing off healthy cells.

Cancerous cells are usually identical to each other genetically, and because they are so closely identical to the host's own cells, they are often not attacked by the immune system. If a cancerous cell were to spontaneously mutate to avoid a treatment -- which is VERY unlikely -- it might mutate enough for the body to notice the intruder and destroy it.

Viruses mutate because they often use RNA and a protien called reverse transcriptase which often makes errors in duplicating the RNA of the virus.

Bacteria mutate because they have plasmids which can swap bits of DNA with other bacteria... or, they have a less -evolved cellular structure which allows mutation as a norm -- not as something to be avoided in order to insure survival.

Cancer cells are simply human cells with damaged DNA. They do not mutate any more or less than a normal human cell... which means they're very unlikely to adapt to any treatment. Unfortunatly, it's difficult to prescribe treatments other than surgery and targeted radiation to remove cancer. Chemotherapy can help & the fact that cancer usually has a less guarded cell wall which allows larger molecules in (partly b/c it has to in order to feed and spread so rapidly), larger poisons tied to plastics can enter cancer cells, yet leave healthy cells alone. Viruses could detect cancerous cell walls and enter and infect cells with unusual cell walls, thus destroying them... yet leave healthy tissue alone. If treatments are specialized to attack the very nature of cancer which is different than normal tissue, I don't see how cancer could possibly survive

Re:Natural Selection of Cancer Cells

[terranlune]

Wow, that's a totally ignorant statement. I'm not even going to get into how you think cancer can evolve.. it's just not possible. Read some of the other posts.

As for treatment, almost all cancer research right now (especially that use viruses) attempt to target the very nature of cancer: uncontrolled cell growth. There are some very key protein pathways (conserved through almost every species we've bothered to look for them in) that are very related to this growth regulation. For example, p53 is a big one that actively prevents uncontrolled cell growth (so many cancers somehow mess up the creation of this protein, thereby increasing the propensity for uncontrolled cell growth). Another big one is the ras pathway, which is responsible for telling the cell when it should grow normally. If this pathway gets sped up or damaged, then you get uncontrolled cell growth.

The thrust of many cancer therapies right now is to use these properties to our advantage. The reovirus (previously covered), for example, is only able to infect cells with a messed up ras pathway (which only happens in tumor cells) so it will always be an effective treatment against cancer, unless the definition of cancer changes.

Makes sense

[teutonic_leech]

I did not RTFA, but from similar excerpts on the subject matter it is clear that they engineered the virus to only infect cancerous cells. The virus might be attracted to the increased level of telomerase that is being produced by cancer cells. Telomerase is used to replenish the expended telomeres on the end of the shoelaces-like DNA helixes. From what I know RNA attaches itself to the telomeres and starts recreating what it reads off. However, the place where it attaches itself does not get fully read, and therefore not re-created. Thus, the new molecule has a shorter telomere (the shiny end part on your shoelace). Now, when the end of the telomere is reached, the cell knows that it's time to commit senesence (suicide). Some guy called Hayflick figured that out in the 50's and that's why they call it the 'Hayflick limit', which is somewhere around 50 replications per cell (aka mitosis).
The problem is that cancer cells produce a lot more telomerase, which replenish their telomeres, so those suckers just won't die. If I would engineer a virus, I'd have it be attracted to that.
Anyway, just my 2 cents, maybe someone who really knows this stuff can elaborate on my layman explanation of this.

Re:Makes sense

[mattjb0010]

Senesence refers to cells that are no longer dividing but still metabolically active. Programmed cell death is apoptosis (from the Greek for falling leaves or something like that), "uncontrolled" cell death is necrosis. Telomerase (a protein with RNA) is a part of what cancer is about, but there are other things like genetic instability, lack of programmed cell death in general, increased replication rate, angiogenesis, etc.

Re:Makes sense

[pikayou]

I think it's unlikely that the recombinant adenovirus they created is attracked by the overproduction of telomerase. I read both the article and their lab's page....they are very vague as to exactly how they target the virus specifically to cancerous cells. There are lots of ways to artificially kill cell in vivo, but cancer cells are almost always impossible to distinguish from the untransformed type. After reading the patent itself, they apparently placed the ADP (adenovirus death protein...the 'smart bomb') under the control of telomerase regulatory elements. Thus, any cell constituitively expressing telomerase (i.e. cancer cells) will be lysed by this virus. A couple concerns spring to mind: 1) how to eliminate the virus after treatment? Just because it's not lysing non-cancerous cells doesn't mean it can't infect them. 2) cells susceptible to adenoviruses. Adenoviruses enter through mucus membranes in the lungs, etc. and initially infect the epithelial layers. I think you might have trouble targeting these recombinant viruses to, say, brain or other kinds of cancer located in remote regions.

Re:Must be Linux

[tepples]

Only a Linux zealot would make the claim that they genetically engineered something... when it's a replication of an already known common virus.

For the record, researchers didn't make the virus from scratch; rather, they took a cold virus and made it fight cancer. The "engineering" refers to the changes made to the virus to make it target cancer.

Re:So...

[Anonymous Coward]

What they do with other similar treatments is inject large quantities of the virus directly into the tumour. The cancer gets infected before the immune system has a chance to react. Then the immune system goes to full throttle, does some serious virus-slaughtering, and takes out a number of the virus-infected cancer cells while it's at it. Then the virus kills (or at least interferes with) most of the remaining infected cancer cells.

Not sure what these guys' stragtegy is, but this isn't exactly new science anymore, so they're probably doing something similar.

Adding two and two

[kimmop]

Altough this is a good achivement it's no scientific breakthrough. If you're interested please read the description section from the patent It's quite well written and understandable.

There's few things you have to know about viruses and cancer to understand this thing:

First: The viruses (adenoviruses to be specific) work by infecting the host (human) cell and by forcing the host to replicate the viral DNA and to produce the proteins coded in the DNA. After few days of this, a lot of new viruses form inside the host cell and the cell gets broken up (lysed) relasing a lot of new viruses to infect the nearby cells.

Second: Cancer is uncontrolled replication of cells. Actually quite many genes must be deactivated (like p53) and activated (like telomerase) to produce a bad type (neoplastic) tumor. The telomerase is needed in the cancer cells because it extends the ends of the chromosomes in the cell after each replication, thus allowing a cell to replicate more.

Prior art: Some people have taken the promoter (DNA sequence that activates a gene) from human telomerase and put it in an adenovirus (that was mutated to be non-replicating) together with cell-suicide inducing gene. By infecting a cancer cell with this virus, you can kill it nicely if the cell expresses telomerase (i.e. is replicated i.e. is a cancer cell)

The problem with the prior art is that producing non-replicating viruses is difficult and expensive and you have to infect all of the cells more or less individually.

Invention: Use the telomerase promoter to drive a gene required for the DNA replication in the virus. This way the virus will kill (by lysis) the cancer cells and infect the other cells nearby but will not lyse the healthy (telomerase-deactive) cells.

Even though this is not a major scientific breakthrough I still hope this works and think it's clearly worth a patent.

Re:Obligatory

[SEE]

Priorities?

Viagra was designed and developed in a research effort that was originally looking for anti-hypertension drugs, and was later refocused on anti-angina drugs. While the stage II clinical trial showed it was not as effective as hoped, it did discover a curious side effect. The priority was not to create an impotency drug; that was a foruitous side effect of what was otherwise seven years of wasted research and funding.