Re: Challenging Conventional Wisdom on Cancer

From: janice matchett <>
Date: Sat Aug 20 2005 - 12:30:35 EDT

Thanks for your comments and the link. Very interesting. ~ Janice

At 09:54 PM 8/19/2005, Tim wrote:
>Genomic rearrangements, of which aneuploidy represents one subclass, have
>the attention of cancer researchers*. Well, one group of many mechanism
>being studied. It is known that the development of many cancers may
>involve stepwise progression from precancerous to malignant stages**.
>There is also discussion of cancer 'stem cells'. Unfortunately, it is
>difficult at this time to prevent progression in most cases: We can find
>that abnormal cells exist (sometimes, although even this is not always
>easy) in somebody, but that is a separate issue from being able to do
>something about it. There is some work that is examining how to block
>progression to more malignant states but in this regard the safety of
>treatments becomes a terribly important factor. Cancer drugs are not easy
>on the body. Agents that disrupt critical cell functions necessary for
>cancer cell growth can hit other pathways in non-cancerous cells and
>produce serious side effects. These effects are acceptable for patients
>with active cancers, but the risk/benefit ratio is much worse for treating
>the much larger population of *potential* cancer progressors. Preventive
>treatments must be well tolerated, efficacious and cost effective. Safety
>is a big concern because treatments would be long-term and given to a
>group of people where most might not otherwise develop the particular
>cancer. Efficacy is particularly difficult to assess and would require
>long (read: expensive and large) clinical trails. It's not clear how the
>FDA approval process will work.
>Meanwhile, developing treatments for "active" cancers will continue to be
>a major focus (prevention is never 100%). I have read some criticisms of
>"one-gene" approaches to treatment, but I think those tend to be
>overstated for the sake of trying to create a contrast with an "alternate"
>theory. For cancer cells to replicate, they have to evade many of the
>normal and common signal pathways that would otherwise cause improperly
>dividing cells to halt and/or suicide (apoptosis). It does not matter if
>cancer cells have 1, 2, 3, or 4 times the normal complement of genes; they
>*all* still have to get around growth checkpoints. Cancers can often be
>grouped by which pathways they use to circumvent replication blocks. Thus
>it is possible to attack cancer cells by targeting specific pathways or
>classes of regulators. The success rate of treatments is varied but some,
>like Lance Armstrong are finding benefit. It is likely that multidrug
>treatment regimes tailored to specific pathways will be required to
>increase efficacy. But these are hard evaluations to perform. In many
>instances, there are not enough patients to run trials of various combinations.
>Interestingly, if we do consider what early-stage treatments would be
>required to prevent progression to cancer, a very similar approach will
>probably be used. Once again, mechanisms that allow aberrant chromosomal
>segregation and instability tend to follow common paths. The same is true
>for mechanisms that could induce apoptosis in cells with these defects.
>These pathways will be targeted in similar way. And we'd better hope this
>is the case because having a limited set of causes at least provides a
>reasonable chance for some success.
>* Abnormal chromosome segregation is another mechanism for creating
>genetic variation which can be exploited in evolutionary processes. It
>also plays a role in some forms of speciation.
>** Interesting paper here. Note Dr. Frank's department:
>Tim I
Received on Sat Aug 20 12:30:38 2005

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