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A way to Stop Mets?


Elaine

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John posted a link on another thread that I began to explore, and I found the following: (As a side note: I suffered for many years from almost daily headaches, which were often migraines; thus, I popped a lot of Exederin Migraine--oddly enough in the two years before DX, my headaches dropped to maybe one every two months or so--eek! so I stopped taking asprin, which is a blood thinner!). I wish I hadn't! Please note: I do know that my lung tumor was there long before two years ago--so I know that taking lots of aspirin did not prevent it from occuring.

"Tumors cells must stop in one location for 20 minutes to begin to colonize in another location. What would make tumor cells stop within the fast-moving circulatory system? A blood clot. The clot works like stickly fly-paper to catch tumor cells and start a new tumor-cell colony. Nearly all cancer patients exhibit a tendency towards thick blood. This is well documented in the medical literature, yet not one oncologist addresses this issue.

In 1979 a British researcher studied 532 of his patients taking blood-thinning medications for 12 years. Seventeen of these patients developed tumors, but none spread to another location, they remained local. Cancer patients should know that vitamin E, fish oil or flaxseed oil, magnesium and garlic are all natural agents that help to thin the blood and prevent the spread of tumors. A cure for the metastatic form of cancer was published in 1979, but the world missed it. "

here's the link. It's a good website, it seems.

http://www.askbillsardi.com/sdm.asp?pg=news&specific=83

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Hebbie has also posted a lot about fish oil (omega-3), etc

Also consider that a lot of research is based on drugs that are angiogenesis inhibitors, then this even fits with what drug companies are doing (I think)

The main problem would seem to be that it is a way to stabilze and not cure (not that this is completly bad).

Ultimately, the genetic defect has to be corrected or some how cause the cancer cells to self destruct (apoptosis)

Remember the main problem with cancer cells are that they are immortal.

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The weird thing is that I have been thinking with my admittedly layman mind about why mets occur and when they do why they occur where they occur--I wondered if they began to organize in weak spots and if so then besides taking anti oxidants then perhaps take supplements that strengthen the other commen places mets develop.

Couldn't hurt. Also this suggests keeping them moving, which could help.

Here are some natural angiogenesis inhibitors:

"A long list of dietary factors strongly inhibit blood vessel growth, among them resveratrol in red wine, as well as genistein in soya, catechins in green tea and brassinin in Chinese cabbage."

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Yes! Red wine!!

Interestingly, TBone had always suffered from headaches, and was prone to taking Goody powders fairly often (and for you uninitiated - Goody powders are basically just ground up aspirin and caffeine so it goes to your system more quickly. They're frequently associated with car racing and other redneck activities. And yes, it's gross to take, unless you've become a pro like TBone and me. Just gotta pour it way back in your throat and have a good chaser close by!) :lol: But I digress . . .

Anyway, TBone suffered a perforated ulcer in February 2001, a little less than three years prior to diagnosis. The doctor then made it clear that in addition to stress, the primary cause was his frequent use of the Goody powders, cause they basically just "sat there" in his stomach and ate holes in it. (Nice visual, huh?) Plus the fact that taking medications like this so often causes a rebound headache effect, so you get into a vicious cycle. You might say the doctor read him the riot act about his use of the things, and subsequently he read it to me. To be honest, I'm not sure Terry ever actually stopped his use of the powders, although I'm sure he at least curtailed it a little.

When we took him out to MD Anderson for the second opinion, the doctor had the CT scan taken in February 2001 (leading to the perforated ulcer diagnosis), and she said that the cancer DEFINITELY WAS NOT THERE AT THAT TIME.

So . . . did his stopping/curtailing his aspirin use lead to enough thickening of his blood that the cancer cells "slowed down" their journey and took ahold? We'll never know, but it's an interesting theory, to say the least.

Gotta go - a Goody powder and a glass of wine are awaiting me! :lol:

Praying for us all,

TeeTaa

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Hmmm

From what I have read, it NSCLC--adeno takes about 8-12 years to be come large enough to be seen on xray and squamous somewhat longer. (I am doing this totally by recall so I may be off a bit from what I read).

Hmmm John do you know how long they are there lurking before being able to be spotted?

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TBone's was adenocarcinoma, and it barely showed up on x-rays, even when he was diagnosed. But again, the doc at MDAnderson (who ran the dept) said it DID NOT show up on the abdomen/chest CT scan three years earlier. So maybe it was there but too small to be seen in ANY type of scan?

TeeTaa

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Katha

I found this in an article specifically about lung cancer so it does seem to apply:

"According to Dr. Black, lead time refers to the amount of time it takes for a tumor to grow from one cm to three cm, (2.3 years) at a constant doubling time of 180 days, which should add to survival time. Over-diagnosis is the detection of pseudodisease or false- positives, which can markedly increase reported survival rates. Tumor biology differences assume that there are only two types of lung cancer: aggressive and indolent. Aggressive tumors metastasize when they become 1 millimeter in size, but they remain hidden until they reach 1.5 cm. In contrast, indolent tumors do not metastasize until they reach over three cm in diameter. Under those assumptions, IA tumors might be either aggressive or indolent, depending on size, and curable or incurable, depending on metastases stage.

I also read a case history of a guy who had a 3mm lung tumor resected and within like 6 months of surgery, he had many mets. I think it has to do with how aggressive the pathology is.

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Katha,

I also found this:

Malignant nodules usually grow at a constant exponential rate, which can be expressed as the tumor's doubling time (ie, the interval required for it to double in size). An increase of 28% in nodule diameter indicates doubling (1). In malignant lesions, the doubling time is between 25 and 450 days in most cases, with a median of 120 days.

Benign lesions are usually stable (ie, show no growth). Sometimes they grow slowly (ie, doubling time exceeds 500 days), but occasionally their doubling time falls within the time frame typical of a malignant tumor. A long-standing surgical dictum states that a solitary pulmonary nodule is almost certainly benign if it is stable over a 2-year period (which implies a doubling time exceeding 730 days). Stability is determined by retrospective analysis of one or more chest films.

A doubling time of less than 20 days usually signifies that the nodule represents a nonmalignant, acute inflammatory process.

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Elaine, That's a lot of interesting information.I wonder why after surgery I had CTs every 2 months for 4 mos and all was clear.Then on the 3rd scan ( 6 mos after surgery) all of a sudden I have a 3cm tumor on and in the airway of my one & only remaining lung???.Unless it broke off during surgery and was moving around in there.(but you'd think it would have shown up on one of the earlier CTs.??).

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Just based on the doubling time and the size of a cell

being around 1X10-6 m you could use the doubling time at

www.yana.org and come of with a size of 2cm as detectable (on average)

3 cm for a x-ray

For a doubling time of 200 days it would take 21 times of doubling

200*21 = 4200 days to get to be 2cm which is about 11-12 years

http://jjco.oupjournals.org/cgi/content ... t/24/4/199

http://www.yana.org/doublingtime.htm

http://www.biology.arizona.edu/cell_bio ... ells2.html

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Frank,

That is pretty weird. I think the smallest thing a Cat Scan can pick up is about 2-3mm, fairly reliably (sometimes smaller, and sometimes larger depending on location (whether it's hiding behind some structure or not) so to grow that fast in two months is really fast.

Maybe John or Oncodoc can help if they see this.

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Just based on the doubling time and the size of a cell

being around 1X10-6 m you could use the doubling time at

www.yana.org and come of with a size of 2cm as detectable (on average)

3 cm for a x-ray

For a doubling time of 200 days it would take 21 times of doubling

200*21 = 4200 days to get to be 2cm which is about 11-12 years

http://jjco.oupjournals.org/cgi/content ... t/24/4/199

http://www.yana.org/doublingtime.htm

http://www.biology.arizona.edu/cell_bio ... ells2.html

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I was just thinking. A interesting point you made Elaine about when something metastasizes.

If a tumor does not adhere to itself very well and breaks off, it will not grow locally as fast and thus not be detected because it does not form a larger tumor.

So more aggressive tumors that start to met early will be smaller at the primary site?

Not sure if this is true but I think it makes sense.

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Elaine

I have been wondering this ever since my mothers dx....drs say it cant spread when undergoing chemo...but im not sure, especially after reading all this. No surgery for mom and one tumor was 1.5x2.5 on 11/2/02 same size for 2 yrs then 6/25/04 its 2.5x3.5, which is when they decided to tell us theres something there. I would not be surprised at all when they finally do another scan that we have mets. from june till late nov/early dec is alot of time in between scans, and time for things to grow. I wish they would scan her NOW.....

very interesting theory

Kim

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Elaine if you look at the data on yana.com and see where the doubling time makes the tumor about 2-3 cm, then you can guess at what point the lesion is detectable. I think spiral cat scans detect down to less than 1cm.

If the cancer doubled every 200 days it would take 11 times of doubling to be about 2cm, that is 2048 days to get to 2 cm which is 6 years

I actually miscalculated before.

An average cell is 10X10-6m so to get to a size of 2cm there have to be about 2,000 cancer cells

I think CHEMO is supposed to kill the cells not break the tumor apart.

Sometimes CHEMO does not work though and that is why it spreads, not because it *causes* the spread.

Kim, Drs usually look at if it is calcified/non-calcified and other factors (such as the border of the nodule) on a CT scan to determine if it is malignant. Contrast can be used to detemine vascularity

How often did they do a CT scan?

1.5X2.5 on 11/2/02 what scans did they do between 11/2/02 and

6/25/05 2.5x3.5

Is the size mm or cm?

http://www.emedicine.com/radio/topic782.htm

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John,

Yes I know, but it doesn't always kill the cells, right? But does often just kill some of them, which would then break the tumor down, right? I am not doubting you, just trying to understand.

I also did not think that it was impossible for mets to occur while undergoing chemo. It seems lots of people discover mets in between scans to see if chemo is working. Or is it just that those mets just so happened to become large enough to be visible--which also means that they are growing while chemo is being administered.

I kind of wish my onc would have been at least somewhat hopeful but I think he was being honest with what he told me. I also think he was wrong. I see others with large tumors that have not had mets. He swore I did, but they just weren't showing up and it was hard to tell because of my HPOA.

Then again I have no idea how long it takes for a met to present itself either.

Kim, hope you see John's questions to you and that you can answer.

Thanks

elaine

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I would think mets and the primary COULD grow while chemo is being administed, some tumors don't respond to chemo.

Chemo is supposed to target fast dividing cells, so if a tumor is slow growing then it won't work as well. That is why SCLC is responsive and carcinoids aren't as responsive (if at all)

You might have a point about the breakdown, but I am not sure. Metastasis happens because a series of events. Typically cells stick to one another because of cellular adhesion. (cell to cell adhesion)

Cancer cells have been found to have unusual surface carbohydrates. Maybe this makes them more "slippery". If you search the web for e-cadherin and "cell adhesion" you will get more references.

It is supposed to be difficult for a cancer cell to break off and metastasize according to what I have read.

Long article about metastasis at the link below

http://www.americanscientist.org/templa ... dPnUwqx_QE

http://wwwpe.mskcc.org/PatientEd/Course ... emotherapy

http://dragon.zoo.utoronto.ca/~B03T9902 ... uction.htm

http://lucchesi.org/ann/C640194710/E86240073/

http://www.findarticles.com/p/articles/ ... i_64771664

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