Liver RFA vs surgical resection

[kk1]

You ladies were all so helpful last time, when I was trying to decide if I should have a mastectomy or not after 5 months of chemo as I was stage IV at primary diagnosis, that I thought I would seek your experiences and advice again this time in regard to my Liver met scar tissue.

In October I decided to have the radical mastectomy even though I was NED after someone on the board made the argument that I should think about “micro particles” that could still be active in the tissue but not visible in the scans. You were absolutely right!!! Turns out the pathology showed several regions in the breast tissue where there were active micro particles, and 4 of 59 nodes showed some evidence of past disease. I am so glad I decided to have the surgery. I am happy to report I am still NED currently doing 3-week maintenance Herceptin, Zoladex, and Aromasin (er+/pr+/Her+++ ).

My team and I are now having discussions in regard to removing what they believe is scar tissue remaining from my 3 small clustered liver mets. For background I appear to be oligometastatic meaning I have only ever shown a small met region in my liver none in my bones, lungs, or elsewhere. Given that we saw active micro particles in the breast the possibility exists that there could be small unresolved particles in the scar tissue in my liver too. So while unconventional for stage IV NED we are thinking about a liver resection if I remain NED after my next set of scans in late Feb. I know that some of you have had radio frequency ablation (RFA) rather than surgery and after research I find that very tempting. My surgeon however makes the argument that if we are concerned about micro particles then I would need a wide incision so they can visualize a bigger area and make sure they get everything, and that this would negate the main advantage of RFA which is done laproscopically and thus easier recovery. Of course from his prospective surgery is the “gold” standard but his argument about seeing a large area makes sense. Would love to hear your opinions or experience with either technique.

Thanks in advance
KK1

[al from canada]

Dear KK1,
I recall reading an article about cancer proliferation following routine or exploritory surgeries. It was suggested that surgical trauma and the healing process may activate the HER2 gene and result in uncontrolled cell proliferation (cancers). You may want to consider this or research it more before going under the knife.
Good luck,
Al

[Lolly]

I have to agree with Al, although I haven't done any research to back thism up. However, one of the reasons I've had no reconstruction on my bilateral mastectomies is because of my belief that additional surgery would put me at increased risk for another recurrence, as each of my previous recurrences was preceeded by physical stress from working, getting too tired and coming down with bad colds...Would be interesting to find any research on this theory.

Love, Lolly

[StephN]

Hi KK1 -
Nice to see you doing so well these days!

My sense would be DO NOT go in and do anything with those little scars.
You did not say what kinds of scans you have coming up in Feb.
Are you having a PET or CT/PET fusion??

I also had a raging liver that was about 60% involved with tumor not long after adjuvent therapy. (I am ER and PR -, but HER2+++.) I managed to kick out all the cancer with a very aggressive program of Taxol, Navelbine and Herceptin. I have been mainteined on Herceptin and Zometa for over 30 months now and clean as a whistle from my earlobes down, had PET in Dec and chest/ab Ct in Jan (you may not know I just had Gamma Knife for 2 brain mets last week, and doing fine from that - try to keep your brain monitored now.)

When my CT scans showed just two small spots left in liver, I had a PET to confirm no tumor activity - and was let off the chemo when none showed.
Within 6 months of getting off chemo one spot completely disappeared and the other has remained a 5mm scar right up to my last CT on Jan 4. My med onc says that no one would believe this is the same liver he saw 3 years ago! All functions have been normal and it has COMPLETELY regenerated.

Think about letting your body do its own work - you have the Herceptin going after any stray cancer cells that may be about. We know we have some - and the Zometa will help protect you bones.

And - take a look at the good news on Oleic acid and olive oil new research that shows a synergy with Herceptin! This is fantastic and is a way for us to help ourselves without a recovery period.

[kk1]

You all make good comments about the stress from surgery , problem is I have not really seen any scientific studies that support this. On the other hand it is hard to design an experiement that can measure the "stress" variable objectively.

What start me thinking about surgery was an article published in 2003 by doctors at MD Anderson showing a role for surgery in a very select pool of stage IV patients. I have attached a pdf file of the article (I think/hope?) to this message. Warning it does have some very graphic images of resections....not for the squimish. I also have another article along the same lines for an RFA like technique they are using in Europe but uses laser induced thermal heating instead of the RF. Both articles show really good overal long term survival statistics in oligo metastatic patients if these additional treatments are under taken, they even go as far as suggesting that it is close to a cure, which is of course really appealing but probably an overstatment by the authors---I can always hope.

I should probably talk to my onc again about Zometa---last time it was just in the context of bone loss due to being place in chemical menopause and the AI drugs, he suggested we wait until my bone density measurements started to actually show some bone loss. I had not realized that it had been shown to prevent bone mets. My Onc is somewhat hesitant to combine too many different drugs as he feels that alot of combo's have not been tested together and often later we learn of antagonistic effects. The antipsychotic drugs and herceptin reports recently are a prime example.

cheers
KK1[attachmentid=12]

[al from canada]

Here is one link suggesting the activation of HER2 during the healing process:
http://content.kluweronline.com/article/380717/fulltext.pdf
Here is a transcipt about the same issue:

Rapid Decline After Surgery
1 September 2003

print-friendly


Researchers in Italy investigated why some people go downhill rapidly after having surgery for cancer.


Program Transcript

Norman Swan: Welcome to the program.

Today on The Health Report, what Middle East terrorism is doing to the psyche of its citizens: some surprising findings. What obesity is doing or not doing to the psyche of Australians, and the impact of weight loss.

Plus a common belief that you might think is just anecdotal, with no evidence. It’s the story many of us have heard: the granny, the father, the spouse who was fine till the surgeons opened him up, or her up, then after the operation the cancer ran wild and she or he was dead in no time.

Well it turns out this is real, although not always or not often as dramatic, and it could be a missed cause of cancer relapse. The good news is there may now be an explanation and indeed a solution.

Research from Italy has been investigating this phenomenon in women with breast cancer. Dr Sylvie Menard is Director of the Molecular Targeting Unit at the National Cancer Institute in Milan.

Sylvie Menard: It’s important first of all to identify at time of surgery who are these kind of patients in order to be ready to do something in terms of what surgical therapy. Probably with this oncogene overexpression and amplification we have identified this kind of patient.

Norman Swan: Sylvie Menard’s laboratory in Milan has been studying what she referred to there as oncogenes: genes which produce substances involved in the growth and multiplication of cells. One of these is called the HER2 receptor, which is turned on by growth factors. And when the HER2 receptors are in high numbers in women with breast cancer, it tends to predict a poor outcome. It turns out that women who have an early worsening of their breast cancer after surgery, tend to be HER2 positive.

Sylvie Menard: HER2 is a receptor for growth factors, so it’s very likely to be stimulated by growth factors. So we have tried to identify the mechanism, why these patients have a probability of relapse, and this is why we addressed the issue. What happened at the time of surgery, which kind makes a difference?

Norman Swan: So what did you find that it was about surgery that seemed to cause the problem?

Sylvie Menard: The surgery you must have, wound healing, to repair the damage of the surgery through growth factors.

Norman Swan: So the very facts that you’ve created a wound, and the wound has got to repair itself, the stuff that the wound –

Sylvie Menard: Yes, and with reparation of the wound occur through factors that in some way stimulate the tumour.

Norman Swan: So in a tragic biological irony, the growth factors which are needed to promote wound healing seem to target this HER2 receptor on the tumour cells, promoting their growth as well.

Sylvie Menard again.

Sylvie Menard: The same receptor, and therefore the same kind of proliferation. There are many, many different factors that can stimulate this kind of receptor, and therefore you have stimulation of the wound, but stimulation also of the tumour.

Norman Swan: Now you might be able to imagine that if you got these factors at the site of the wound, it might induce a recurrence of a tumour at the site of the breast, but not necessarily further away.

Sylvie Menard: This factor can go to stimulate dormant tumour cells anywhere. So if you have tumour cells in the bone marrow, tumour cells in the liver.

Norman Swan: So these growth factors go from the wound into the blood stream and spread throughout the body?

Sylvie Menard: Yes.

Norman Swan: So there are two solutions to this: one is you don’t do the operation, and the other presumably is –

Sylvie Menard: This is an impossible situation because surgery is the most important therapy for tumour. The point is that we can plan some therapy in order to operate. Maybe the wound will take a little bit more time to be repaired, but the tumour will not be stimulated.

Norman Swan: And in fact there is an antibody available which blocks the HER2 receptor. It’s called trastuzumab and Dr Menard and her colleagues tried it in the lab and found it works in the test tube. Now they’re doing a trial of it in women undergoing surgery. But this observation that surgery can speed the downhill path of a person with cancer applies to other tumours as well.

Sylvie Menard: There have been a reports for example with colon cancer, which in some cases it has been well demonstrated that after surgery there’s been an early recurrence of disease with multiple metastases. There are many different factors and looking at them and the corresponding receptors on the tumour cell, we will be able to say which tumours will be stimulated by surgery and which not. For HER2 it’s very specific for breast carcinoma.

Norman Swan: So you’re not convinced it’s HER2 in the others, and you’ve got to find out which ones it is?

Sylvie Menard: Yes. So we have to investigate now what kind of factor and what kind of receptor on the tumour cells for all the tumours.

Norman Swan: And then you’ve got to find the blocker that works for them?

Sylvie Menard: Yes, from any kind of surgery, not necessarily an oncological surgery. This may happen even with any kind of surgery which requires repair of the surgical damage.

Norman Swan: So you could have a tumour and have appendicitis, have your appendix out, and the appendix operation could cause this, because the wound for the appendicectomy would produce these growth factors as well?

Sylvie Menard: Yes, this is something that we are looking at, looking at recurrence of the disease later and seeing if the patient has had surgery in between or not. This is not something that’s easy, because the record of the patients are not always very complete. But this may be a possibility that some recurrences occur because dormant cells have been “rescued” from dormancy just because of an operation, which was not a cancer operation, it was for some other problem.

Norman Swan: And what about injuries, like fractures and things like that? Could they also produce these growth factors?

Sylvie Menard: It depends if you have blood clotting. The growth factor is released during the activation of platelets. If you don’t have blood clotting you don’t have release of growth factors. So it’s something that is very specific when you have damage of the tissue and you have blood clotting at the level of the damage.

Norman Swan: And the challenge now is to take this out of the lab into the clinic, using real people to confirm the relevance of the findings.

Dr Sylvie Menard runs the Molecular Targeting Unit at the National Cancer Institute in Milan.

Reference:
Tagliabue E et al Role of HER2 in wound-induced breast carcinoma proliferation. The Lancet August 16, 2003;362:527-533


Guests on this program:
Dr Sylvie Menard
Director,
Molecular Targeting Unit
Department of Experimental Oncology,
Istituto Nazionale Tumori,
via Venezian 1,
20133 Milano, Italy

Presenter: Norman Swan
Producer: Brigitte Seega

[al from canada]

Here is another article on stimulating HER2 through wound healing.
http://breast-cancer-research.com/content/3/S1/A2

Al

[StephN]

Thanks, Al -
As usual, you come up with great articles!

My doctor was hesitant to do any kind of resection with my last two stubborn spots in my liver and we tried to rely on the chemo working - we discussed some of the points brought out in this interview.
He felt that my disease was just too agressive and preferred some sort of ablation, but the placement of one spot was not real good for that - it had been a large tumor (4 cm) wrapped around a hepatic vein.