Her3

[rinaina]

What is the difference between Her 3+ and the Her2+ I am familiar with?

[PatriceH]

Never heard of Her3...perhaps this is yet another advancement. I'll be curious to see what others post.

[radiant]

Rina -

I believe it means that the her2+ is amplified to be her2+++, versus her2++.

HTH,
Kim

[Jackie07]

Her1, Her2, Her3 are different types of epidermal growth factors.
http://www.spandidos-publications.com/ijo/33/1/195

Her2+, Her2++, Her2+++ reflects the number of copies of of Her2 breast cancer genes found on the tumor cells. More copies means the cancer is reproducing faster and more aggressive.

[Becky]

There is a HER family of growth factors. Her1 (aka EGFR - it is referred to this way in literature sometimes), Her 2, Her 3 and Her 4.

[Joan M]

Rina,

As mentioned, HER3 is one of the four-family growth factors. Out of all the growth factors, it links easily to HER2. The drug lapatinib (Tykerb) is an HER3 inhibitor.

EGFR overexpression is particularly dangerous in a certain type of lung cancer and is being studied being studied in breast cancer. HER4 does not seem to have a role in cancer development.

Joan

[fluffqueen01]

I have a question that I can't seem to find the answer for and forgot to ask my onc yesterday. I am highly her2 positive. However, I had a grade 1, stage 2 tumor, a bilateral mastectomy, no lymph, clean margins.

With that pathology for that particular tumor, does the her2 high positive status make a difference for the future versus being less her2 positive? Or just the fact that I am her2 positive, no matter what high or low ranking, make me susceptible to a scary future?

I hope this makes sense. I guess what I am really trying to ask is if the her2 ranking affects long term recurrence in other locations?

[Lien]

Dear Fluffqueen,
It seems to me that you have been treated very heavily for the kind of path report you had. Yours is even more favorable than mine and I'm 7,5 years out from diagnosis. I never had Chemo or Herceptin.

Here in Europe we tend to be less aggressive because we think quality of life is important too.

I think you shouldn't worry too much. Your prognosis is quite favorable. Has your doc discussed hormone tx with you? That's the only other weapon you might want to use. Allthough it seems that you've been doing a lot already to keep the beast from returning.

Like my doc said to me: I don't expect to see you back here, so go on, enjoy life.

Hugs

Jacqueline

[Joan M]

Fluffqueen,

That's the $64,000 question. That is, scientists don't really know. Some bc survivors are stages 0 and 1 and progress to stage 4.

Scientists are splitting DNA hairs more and more to determine which bc patients respond to which treatments, which hopefully will result in patients not getting chemos that aren't really going to help them.

I was originally stage 2 and progressed to stage 4. I had local treatment for my mets and no chemo, only Herceptin, since progressing in January 2007. And I've had a good quality of life because of that. But it's a crap shoot, and I never know when the next scan is going to show more cancer.

A HER2+ friend of mine who died from bc a few years ago felt deeply angry and hurt by her oncologist who told her, go home, you're cured, after her treatment for early stage bc. I live from scan to scan. If I don't have any cancer at the moment, I go on and enjoy life. Your concern is understandable.

Joan

[fluffqueen01]

Thanks, I guess I can't figure out if being highly positive is worse than being mildly positive, or if the fact that you are positive for her2 is equally bad regarding recurrence.

I will start a hormonal drug. Not sure which one as I am considering a oopherectomy also, so that would change. I was starting menopause when this happened and chemo has thrown me into it. The only reason I am having chemo is that it works better with the herceptin, at least that is what all three of the oncs I interviewed believe. Otherwise, chemo wouldn't have been in my picture.

I too have read about people who started with the same thing I had and then the next thing they have a recurrence and are stage IV. My onc is not a big doer of continuous scans and testing saying it often leads to seeing things that are really nothing.

I will be pushing for everything I can get!

[Laurel]

Fluffqueen (love the name),

I seem to recall in my estrogen deprived, chemo-brain, that being highly Her2 positive makes us typically more responsive to Herceptin. Now your question of whether it makes us more susceptible to recurrence, I cannot recall. Perhaps they do not yet know. There are several variables that affect our response to Herceptin such as whether we are Her3 overexpressors.

I think the take away of the above is to live your life. Cancer gets further in your rear view mirror as time passes. It's forever there, an ever present pall on our futures, but as time passes you will look up into your rear view mirror less and less. What will be will be. Live and enjoy.

[Jackie07]

Found this abstract about the different survival predicting factors. Lower grades tends to recur after very long period of time (wondered if it's because they weren't treated aggressively the first time around.) Keep in mind the time period covered in the study includes the many years before Herceptin was approved by FDA (in 2005).

Breast Cancer Res Treat. (http://her2support.org/vbulletin/#) 2011 May 20. [Epub ahead of print]
Biologic markers determine both the risk and the timing of recurrence in breast cancer.

Esserman LJ (http://her2support.org/pubmed?term=%22Esserman%20LJ%22%5BAuthor%5D), Moore DH (http://her2support.org/pubmed?term=%22Moore%20DH%22%5BAuthor%5D), Tsing PJ (http://her2support.org/pubmed?term=%22Tsing%20PJ%22%5BAuthor%5D), Chu PW (http://her2support.org/pubmed?term=%22Chu%20PW%22%5BAuthor%5D), Yau C (http://her2support.org/pubmed?term=%22Yau%20C%22%5BAuthor%5D), Ozanne E (http://her2support.org/pubmed?term=%22Ozanne%20E%22%5BAuthor%5D), Chung RE (http://her2support.org/pubmed?term=%22Chung%20RE%22%5BAuthor%5D), Tandon VJ (http://her2support.org/pubmed?term=%22Tandon%20VJ%22%5BAuthor%5D), Park JW (http://her2support.org/pubmed?term=%22Park%20JW%22%5BAuthor%5D), Baehner FL (http://her2support.org/pubmed?term=%22Baehner%20FL%22%5BAuthor%5D), Kreps S (http://her2support.org/pubmed?term=%22Kreps%20S%22%5BAuthor%5D), Tutt AN (http://her2support.org/pubmed?term=%22Tutt%20AN%22%5BAuthor%5D), Gillett CE (http://her2support.org/pubmed?term=%22Gillett%20CE%22%5BAuthor%5D), Benz CC (http://her2support.org/pubmed?term=%22Benz%20CC%22%5BAuthor%5D).
Source

Department of Surgery and Radiology, University of California, San Francisco, CA, USA, laura.esserman@ucsfmedctr.org.

Abstract

Breast cancer has a long natural history. Established and emerging biologic markers address overall risk but not necessarily timing of recurrence.

346 adjuvant naïve breast cancer cases from Guy's Hospital with 23 years minimum follow-up and archival blocks were recut and reassessed for hormone-receptors (HR), HER2-receptor and grade. Disease-specific survival (DSS) was analyzed by recursive partitioning.

To validate insights from this analysis, gene-signatures (proliferative and HR-negative) were evaluated for their ability to predict early versus late metastatic risk in 683 node-negative, adjuvant naïve breast cancers annotated with expression microarray data. Risk partitioning showed that adjuvant naïve node-negative outcome risk was primarily partitioned by tumor receptor status and grade but not tumor size.

HR-positive and HER2-negative (HRpos) risk was partitioned by tumor grade; low grade cases have very low early risk but a 20% fall-off in DSS 10 or more years after diagnosis. Higher grade HRpos cases have risk over >20 years. Triple-negative (Tneg) and HER2-positive (HER2pos) cases DSS events occurred primarily within the first 5 years.

Among node-positive cases, only low grade conferred late risk, suggesting that proliferative gene signatures that identify proliferation would be important for predicting early but not late recurrence.

Using pooled data from four publicly available data sets for node-negative tumors annotated with gene expression and outcome data, we evaluated four prognostic gene signatures: two proliferation-based and two immune function-based.

Tumor proliferative capacity predicted early but not late metastatic risk for HRpos cases. The immune function or HRneg specific signatures predicted only early metastatic risk in Tneg and HER2pos cases. Breast cancer prognostic signatures need to inform both risk and timing of metastatic events and may best be applied within subsets.

Current signatures predict for outcome risk within 5 years of diagnosis. Predictors of late risk for HR positive disease are needed.