Betty - Re: Colon Cancer

[Guest guest]

Hi Betty,

> But this doctor (onc) we met w/at the initial consultation, spoke

> with him maybe a whole 10- 12minutes, then we were set up to get the

> chemo treatments at the hosp.instead of at his office, and we never

> see him. I have called him in this last 6 weeks, probably 3 - 4times

> to ask questions,(first time was to find out stage!and prognosis to

> refill pain meds, ect.)He has never called us, or set up another

> meeting

>I had heard our onc. cancer docs was one of the best in the area,

>and I am sadly disappointed in his " bedside manner " and

>communication side.

>We are still going to the local appts for the chemo, and will tell

>this first doc about the second, when he calls - or when it is time

> to do the removals.

Unfortunately the " lack of personal attention from oncologist " seems

to be a common problem...I've gotten the feeling of being just

another number a lot more often than I would have thought or hoped

would happen. Some doctors seem much worse than others with this.

If you are dealing with a local onc to administer the treatments, it

may help to look around a bit locally to see if there is another

doctor who is easier to talk to.

> Having read up on this and calling other c.c centers, it seems that

> what Bob has, it spreading to the abdomen area is somewhat unusual.

> Only 16% of cc patients get spread to there(? anyone hear different)

> and nowhere else like liver or lungs, etc.

Yes, it is pretty unusual...but if things aren't too extensive when

they go for the " cytoreductive surgery " , there really is a chance

of " cure " with Intraperitoneal Chemo, no question about that (e.g.

the Sugarbaker paper). The IPC can kill surface micromets MUCH

better than systemic chemo, but it can only reach a few cell layers

deep & therefore can only get areas that are more or less " visible "

during the surgery.

> If one goes thru all this chemo, to reduce tumor (s) and all of a

> sudden chemo stops working, surgery is done to remove, then after

> surgery wait a bit - a start up chemo again to kill any other mets,

> (not old chemo that quit working ??) so experiment to find another

> good one. Does this mean that 1) all the chemo gone thru prior was

> for not much of anything - if it stopped working and only way to be

> able to tell this was return of asistis swelling up the belly and

> feeling it? 2) the chemo that was working, now cc has built

> resistance to it -- did this ruin a better chance of the future

Ø chemo from killing more cells??

<<Does this mean that 1) all the chemo gone thru prior was for not

much of anything>>

Shouldn't view it that way. . .he may or may not get " cured " from the

current things he's doing (followed by surgery), but he is clearly

getting immediate benefit from chemo in terms of treating the

ascites. That's something, isn't it? Gotta take this one step at a

time, don't ask for everything at once ;o)

I don't think they consider a chemo to have " stopped working " unless

known tumors grow, new tumors appear, or CEA rises significantly

while ON the chemo, so if Camptosar is working well for your husband

pre surgery my GUESS is they would continue that post surgery as

well. Hopefully following the surgery your husband is CURED so that

after x number of months post surgery chemo he is finished with chemo

forever! If he has a recurrence after surgery (such as in the liver

for example), what they do depends on the situation (e.g. a few small

liver/lung mets could be surgically resected or RF ablated), and in

that case should he decide to have more chemo he would probably be

switching to Oxaliplatin or Xeloda/Celebrex (assuming he's not in a

clinical trial). The question of whether recurrent cancer from a NED

patient means the patient is chemoresistant is not clear to me.

Chemo has a pretty hard time of killing every last cancer cell in a

patient with no VISIBLE (on scan/exploratory surgery) disease, this

may be because chemo can only kill fast growing cancer cells but some

of them are in a " dormant no growth " state and escape. Does that

mean those cells are " chemoresistant " or would they have been killed

if they had been in their " growth phase " when chemo was previously

administered? I dunno, this is tricky. . .

The " clearcut " chemoresistance occurs when a chemo has been working

on (scan) visible tumors, then at some point (assuming no surgery or

ablative techniques such as RFA or stereotactic ablation are done),

it stops working and tumors grow. In such a case, it appears that

not only is the cancer resistant to whatever chemo the patient has

been getting, it is resistant to other chemos as well. This is the

reason that Oxaliplatin, for example, when given as a first line

therapy has a pretty high " tumor response rate " - approaches 50% or

so. But if you give Oxaliplatin following Camptosar failure (tumors

growing after responding to Camptosar), the response rate drops to

around 9% (as was discussed in the WSJ articles I mentioned in

another post). It is also the reason that most of the " good "

clinical trials (Phase III's) only want chemo naive (never received

chemo) patients - they know that chemo has the best chance of working

right away and the more chemos a patient has failed the harder it is

to find anything which will " work " , and as you know the trial sponsor

MUST show tumor response and increased survival time to get FDA

approval for their new drug.

NOTE: From the patient perspective, it would also follow that stage

IV's hoping for a " cure " by using chemo prior to surgery should

consider enrolling in Phase III clinical trials which typically add

on an experimental drug to " standard therapy " , meaning there is

nothing to lose and maybe something to gain if the patient is

randomized into the experimental arm. In other words,

use " everything up front " to get a cure immediately, as the

probability for that happening declines with each failed therapy.

Best Wishes,