Herceptin only?

That's a big, largely unanswered question. From what I have read, there is not much info since Herceptin is almost always given in conjunction with standard chemo for stage 1 to 3 in the US. Herceptin solo is sometimes used with stage VI and for early stage for older HER2 patients who can't tolerate or don't want chemo, more commonly in Europe.  I am HER2+, had a BMX in late January after a 4cm tumor found in one breast.  SNB was negative.  Chemo and Herceptin highly recommended, but I have done neither at this point. I had a PET which was negative (and yes, I know that it is no guarantee that there are not mets, just not ones visible at this point), and was considering solo Herceptin when a hospital acquired staph infection landed me back in the hospital for a week followed by another 2 weeks of IV antibiotics--I'd had one step reconstruction with implants and lost one of the implants to the infection. It is hard when you were feeling perfectly fine, and boom, the "treatment" makes you miserable. I am back at work and thankfully feel well now. I saw two oncologists prior to the infection and while both emphatically recommended the standard chemo treatment, both also offered solo Herceptin when I indicated that chemo was a non-starter for me.  I am in a different situation than you; I am older (56) and I am OK with possibly not doing anything further beyond monitoring; I accept the possible repercussions of that decision. Kid is raised, I have had satisfying work and relationships--I don't feel like putting myself and my loved ones through it. I have probably read a thousand blogs, articles, studies, patient comments etc. since getting diagnosed back in December. This site in particular has been very helpful in getting a window on what it is like to deal with breast cancer. The treatments are not for me; I loathe being a patient, medical environments and reliance on others, and in my particular situation, QOL is key.  The bottom line: chemo/Herceptin regimens improve your chances statistically. Most oncologists feel that there is a synergy with chemo/Herceptin and that the chemo increases the effectiveness of Herceptin. There is a price for whatever decision we make; the choice to undertake the treatment is a uniquely personal one. Herceptin is definitely more attractive than the standard chemo since it actually targets something and seems to do less overall damage than chemo, although there is a small heart risk. And even Herceptin does not work on everyone; from what I have read it will benefit 30 to 50% of patients--the stats vary.  One of the oncologists emailed me recently about considering Herceptin again.  At this point, so far past surgery, I am not sure of the benefit, but I am willing to listen.  Another writer on these boards, AlaskaAngel, is a proponent of  solo Herceptin for early stagers and may have more specific info for you, and SpecialK is so very knowledgeable. I get how confused you are and how heartsick some of the entries here can make you.  Some women have suffered terribly, and there is so little clarity on how or if we will benefit from these treatments. This is a chemo-positive website in general, and that makes sense since there is just not much else. I don't think we will ever graduate to drastically different treatment until there is a bit of a medical and patient revolution. The techniques being developed to analyze tumors are so much more sophisticated than the treatments.

I definitely would have tried Herceptin if it were not for my family heart issues...entire family passed in their 60s, and 50s from heart related issues...I am pushing 70...was not sure if my heart could handle it...I have read of women who had to stop Herceptin due to heart issues.....it is a personal choice...good luck to everyone facing this issue.

Heart issues run in my family, too. But, I was OK with Herceptin because my oncologist has been monitoring my heart very carefully. I am relatively young, though (46 at diagnosis, now 48).

Anyone itchy across the shoulders?? I just found out this is a common SE and treated with claritin! I've been going nuts thinking it was something else! Hope this helps someone!

Topaz, I recommend the Herceptine site online. It has so much info that you will find helpful.

AlaskaAngel - I have been following this thread, but have never posted. I guess the real reason is I never wanted to advocate for my choice to do herceptin only since it was not the standard of care. I will be finishing my year of treatments next month. It is not my intention to convince anyone to follow my treatment plan, but I have to admit that I was very encouraged by your friend who is NED since 2006. My reason for not doing chemo was because of a comorbidity. I was diagnosed with follicular lymphoma at the time I discovered my breast cancer, and am not being treated for it at this time. It was all so overwhelming, and all I could think of at the time was weakening my immune system with chemo, and unleashing the indolent lymphoma. I know that may not be rational, but that was my fear. Anyway, I convinced myself that herceptin alone was better than no adjuvant treatment, and my MO agreed. She has always made me feel like I made a good decision, even though it was not the recommendation of the tumor board (taxol plus herceptin, of course). It seemed to me that the herceptin could handle whatever stray cancer cells may be present after surgery. I don't know that; I just believe it.

P.S.

What I do think is relevant to mention (and that explains the "synergy" of chemo added to trastuzumab) is the benefit that occurs with treatments that bring about ovarian suppression/menopause. Chemo does this for most (since the majority of bc patients are over the age of 40).

The issue there is, since ovarian suppression can be done through other, far less toxic and expensive methods that don't tinker with the immune system, it doesn't make sense to use chemo to do it.

Ovarian suppression/menopause affects the rate of metabolism, slowing it down. That is what brings about weight gain. Weight gain then gradually contributes to recurrences by increasing the amount of body fat, since body fat is a source of more estrogen. However, when the metabolism is slower, there is more time for abnormal cells as well as normal cells to proceed through the normal process of dying instead of the process of cancer cells multiplying rapidly.

The points here are:

1) that we probably aren't going to be able to avoid the sexual slowdown involved with either chemo or ovarian ablation, but of the two, OA may be preferable as a natural process that allows the immune system to continue to function -- especially if one chooses to use a form of ovarian suppression that one can choose to stop at a point in time, rather than choosing permanent removal of the ovaries.

2) that younger patients, who have a higher recurrence rate, likely should make sure they do add some form of OA to the trastuzumab, and not just dump the chemo and rely on trastuzumab.

3) and weight management through diet and exercise also are likely to make a real difference in terms of recurrence.

A.A.

BarredOwl, I think you hit the nail on the head about the difference in treatment for triple positive and only Her2positive. The treatment options are completely different. Hormone therapy is a powerful tool for ER/PR positive but will do nothing for ER/PR negative. And the triple neg. have nothing to fall back on except chemo.

MamaBexar,

I note you are HR-negative, and am sorry for the dilemma you face. My only comment is to question whether we should continue down the road of maintaining that every drug has to be compared to the significantly poor success of chemotherapy, and never get the chance to see if new drugs like trastuzumab IF used alone demonstrate at least comparable results for some bc patients, if not superior results (due to a more intact immune system when trastuzumab is used without chemo?)

Here is a recent discussion that I think makes more sense and provides more hope than simply relying on chemotherapy + trastuzumab as if it were superior to OA + trastuzumab:

http://www.pharmaceutical-technology.com/features/featureheadline-bringing-cancers-engine-to-a-halt-4517218/

Hi MamaBexar:

Yes, my concern would be that any potential benefits of trastuzumab plus endocrine therapy (without chemotherapy) in hormone-responsive, HER2-positive disease may not be predictive of the potential benefit of trastuzumab alone (without chemotherapy or endocrine therapy) in ER- PR- HER2-positive disease.

I hope you are tolerating your treatment well.

BarredOwl

Hi WarriorCheryl:

I am sorry about your recent diagnosis. I note that radiation is a loco-regional treatment only and cannot reach any cells that may have already traveled via the lymph or blood to distant sites. So unfortunately, radiation therapy cannnot substitute for chemotherapy and/or trastuzumab (Herceptin).

From another thread you said no nodes are affected so far. Does that mean you are node-negative as determined by sentinel node biopsy?

Do you have a copy of your pathology report and the following information (1) tumor size; (2) estrogen-receptor (ER) status; and (3) progesterone-receptor (PR) status?

Also, do you know what chemotherapy drug or regimen was recommended?

With this information, others with similar diagnoses can share their experiences or maybe direct you to other helpful threads.

BarredOwl

airstrip trip - My dx was similar to yours and my oncologist team at MD Anderson insisted on the same treatment thatyours are recommending. I was to first have a lumpectomy and when I asked if I could skip the chemo if I chose to have both breast removed, they said no. I would still have the same treatment plan after surgery, either way.

BTW - be sure to join the Triple Positive thread

BatyaD:

Cells have receptors on them. These are docking ports for certain molecules, called "ligands" that set off a chain of events in the cell, which can ultimately cause the cell to divide, and thus proliferate, or inhibit cells from doing so, depending.

In ER positive breast cancer, the cells contain estrogen receptors, which, when activated by the binding of estrogen to the receptor site, cause cell proliferation. The goal of Tamoxifen or AIs is to limit the amount of estrogen in the body that is available to bind to estrogen receptors, thus reducing cell proliferation.

Another receptor which causes cell proliferation when activated is HER2, which stands for "human epidermal (growth factor) receptor 2". Many normal cells have these receptors in small numbers...something like 20, but HER2 positive breast cancer cells have millions of them.

HER2 does not actually have a known ligand itself. It appears to be activated by the activation of other receptors, HER1, HER3, and HER4. When these receptors are activated, in addition to doing whatever they do, they sometimes attach to the HER2 receptor and activate it.

Herceptin works by attacking and damaging or destroying the HER2 receptors while Perjeta prevents other receptors from attaching to it and activating it.

BatyaD:

Cell receptors, including HER2, are like little switches on the surface of the cell. When the ligands attach to them, they get switched on and something happens.

Most or all cells in our body have receptors of various types, and many different cells have HER2 receptors. Having these receptors alone does not make the cell cancerous. HER2 positive cancer cells have mutations in the cell DNA that cause them to have too many HER2 receptors, and having too many HER2 receptors contributes to uncontrolled cell proliferation.