Multi-focal vs mutli-centric BC

[al from Canada]

Hi Ladies,
This just came out today and has some interesting conclusions on multi focual vs Multi-centric BC

Regards,
Al
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Journal of Clinical Oncology, Vol 23, No 30 (October 20), 2005: pp. 7497-7502
© 2005 American Society of Clinical Oncology
DOI: 10.1200/JCO.2005.02.1147
Multifocal and Multicentric Breast Cancer: Does Each Focus Matter?

Nathan J. Coombs, John Boyages


From the New South Wales Breast Cancer Institute, University of Sydney, Westmead Hospital, Westmead, NSW 2145, Australia

Address reprint requests to: A/Professor John Boyages, New South Wales Breast Cancer Institute, Westmead Hospital, Westmead, Sydney, NSW 2145, Australia; e-mail: johnb@bci.org.au

PURPOSE: The identification of multiple tumors in the breast is associated with increased nodal involvement when compared with similar staged unifocal disease. This study compares two methods of tumor size assessment to predict tumor behavior in the relationship between size and axillary node involvement for patients with multifocal and multicentric breast cancer.

METHODS: The histologic reports of every patient with multifocal breast cancer treated in New South Wales between April 1995 and September 1995 were examined. Tumors were assessed using two size estimates: (1) largest tumor focus diameter and (2) the aggregate diameters of all tumor foci. The dimensions were compared with unifocal tumors and against node positivity.

RESULTS: Ninety-four (11.1%) of 848 women had multifocal breast cancer and of these 49 women (52.1%) had axillary node involvement compared with 37.5% with unifocal breast cancer (P =.007). The use of aggregate dimension reclassified significant numbers of multifocal tumors at a more advanced stage. Use of this method to stage cancers, rather than the largest tumor size, removed the excess node positivity when compared with unifocal, stage-matched breast carcinomas.

CONCLUSION: The tendency of breast tumors to metastasize is a reflection of the total tumor load. Failure to measure the additional tumor burden provided by multiple small foci may understage a woman's disease. This may deny patients the opportunity of adjuvant therapies if the contribution of the smaller foci to the incidence of node positivity and survival is ignored. Authors' disclosures of potential conflicts of interest are found at the end of this article

Hmmm...doesn't this just suggest that nodes should be assessed regardless?

[al from Canada]

Rich,
Exactly, because in multi-focal you can't add up the individual tumors to present accurate tumor staging.
Al

I had discussed this with my onc after my preliminary scans-mamo,ultrasound and MRI that showed 4 tumor sites. Her response at the time was that they only count the primary and one other. I have always felt that it would be inacurate due to the importance of the size of the tumor in stageing of a single tumor. I don't understand why the others do not count just because there were normal cells in between. The total tumor load seems to me to be more important. In my mind I always counted the total and adjusted for it.I would like to read more on this if anyone has more info.
Thank you

[al from Canada]

Dear Guest,

This is as recent as it gets, the periodical came out today. If I run across any more info I will post it.

Regards,
Al

[Alice]

Thanks Al

I'm now officially registered and not a guest anymore!
I love this site and its foremat.
You have all been very informative and encouraging.
Alice (guest)

[al from Canada]

Welcome Alice!

It will be a pleasure to have you post on our board... the information here never gets old!

Take care,
Al

I guess I mean that thi sowuld only change practice in a situation where a doctor wouldn't normally smaple nodes..but that seemed like bad medicine before the article...although exactly that approach was suggested for my mom, eventually convinced them to sample. BTW, she was multifocal.

[Alice]

Guest,
It sometimes is hard to get Dr's to change from thier standard of care such as node samples in your moms case. if you are concerned about anything though they should do what needs to be done to get the most accurate picture and therefore the most apropriate treatment.Sometimes it is difficult but dont ever be afraid to speak up and let them know when you have concerns or if you need more info than thier standard is providing.
I dont know what your moms diagnosis is but to let you know there are a lot of encouraging treatments out there.
I was diagnosed in april 05 with 4 tumors totaling 6.5cm not counting the auxillary and nodes under the arm that showed positive on MRI and pet scan.
Grade 3 stage 2? IDC er- pr- her2+++. I had 4 rounds AC 3 rounds carbo-taxol-herceptin before surgery. Had surgery on 10/7 waiting for the path report was the worst next to hearing the c word.anyway I didnt mean to drag this out so long as a note of encouragement my path report was clear of all cancer!!!!Now just waiting to see if any more chemo or radiation.
I hope your mom has as good results
Good luck, Alice

Re potential of tumour type to change.

RB




http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum

1: Mod Pathol. 2002 Feb;15(2):116-24. Related Articles, Links

Amplification of Her-2/neu gene in Her-2/neu-overexpressing and -nonexpressing breast carcinomas and their synchronous benign, premalignant, and metastatic lesions detected by FISH in archival material.

Xu R, Perle MA, Inghirami G, Chan W, Delgado Y, Feiner H.

New York University School of Medicine, Department of Pathology, New York, New York, USA.

Amplification of Her-2/neu in breast carcinoma is associated with poor prognosis, short disease-free interval, and short survival time in both node-negative and -positive patients. Little is known about the starting point of amplification of Her-2/neu and how it progresses from benign to malignant breast lesions. We attempted to address these questions by evaluating amplification of Her-2/neu in benign, premalignant, and malignant lesions using fluorescence in situ hybridization (FISH). Twenty-six patients with Her-2/neu-overexpressing invasive ductal carcinomas (as judged by strong immunoreactivity with Her-2/neu antibody) and coexisting lesions of ductal hyperplasia (DH), atypical ductal hyperplasia (ADH), ductal carcinoma in situ (DCIS) in the vicinity of the invasive tumor (as judged by review of the hematoxylin and eosin-stained sections), as well as metastatic carcinoma in axillary lymph nodes (mets) were selected for this study. In the primary carcinomas, a close relationship was present between overexpression as detected by immunohistochemistry (IHC) and amplification as demonstrated by FISH (85% concordance). Among these patients, amplification of Her-2/neu in ADH was demonstrated in 7 of 13 cases with ADH, and in DCIS, in 21 of 22 cases with DCIS. There was no amplification in DH or normal ductal epithelium. Significantly, in all 12 patients with synchronous positive axillary lymph nodes, there was concordant amplification of Her-2/neu in the primary and metastatic carcinoma. Amplification was consistent in multifocal metastases, despite morphological heterogeneity in some patients. Amplification ratios increased from ADH to DCIS to invasive carcinoma (P <.01, ADH versus DCIS; P <.05, DCIS versus invasive cancer), but there was no difference in amplification ratios between primary cancers and synchronous axillary metastases (P >.05). We also evaluated Her-2/neu amplification in 21 patients without Her-2/neu overexpression in their primary carcinomas (as judged by absent immunoreactivity with Her-2/neu antibody). Three showed amplification in both primary and metastatic lesions, with a low amplification ratio (approximately 2). One patient had amplification in the primary tumor but not in an axillary metastasis. Two patients exhibited slight amplification in the metastatic carcinoma (ratios 1.6 and 2), but not in their primary cancers. This FISH study indicates that amplification of Her-2/neu can emerge de novo in any stage of the disease process, from ADH to metastatic lesions, but most often appears first in ADH or DCIS. The degree of Her-2/neu amplification increases with progression to invasive carcinoma, there being no further increase in synchronous metastasis. Our data suggest that amplification of Her-2/neu appears to be mainly involved in initiation of breast oncogenesis and that its role in progression of breast cancers is uncertain.

PMID: 11850540 [PubMed - indexed for MEDLINE]

Ummm..my feeble attempt to paraphrase this is that her2 may do its most damage early on in diagnosis..up to being classified as invasive. (My guess is most BC is diagosed at the invasive stage.)
Close?

[al from Canada]

Dear Rich,
Sorry, but not so. We have no idea how many tumors change HER2 status as I don't think anyone does post mortem HER2 testing. We know that HER2 status as well as ER status can change with mets, that is a well documented fact. In fact, I stand corrected, if it was a well documented fact then oncologistrs would be doing core biopies of mets of any patient who reoccurred as a HER2 (-) and re-testing their HER2 status.

How many patients are missing the benefits of herceptin because the retesting protocals are not in place?

It's a scarey thought. what we know about cancer is that there are no rules, it can morph into a totally different disease, and when it does, convensional treatment (defined as treatments based on primary tumor targetting), cease to work.

Linda and I talked to our onc today and I said, "the current standard of treatment is unacceptable". After seeing that I had offended him (and there was no offence implied), I qualified it by saying that "a treatment plan is consided as acceptable when it cures a patient".

Back to your point Rich, I think the reason many treatment plans fail is because they are based upon the intial diagnosis (and targetting).

Respectfully,
Al

[Alice]

Thank you both for bringing this subject back up.I have not thought of this in a long time. I don't know if we will ever have the answers to questions about the human body and when we think we are getting close the body will change.
I used to try to get all the answers I could and now I wonder why?
Will it change my prognosis?
Will it change how I live?
Should it?
I would like to know what my chances are of a recurrance are but for now I am going to live my life for now and not for what might be!