More than 1 type Triple Neg & Her2+++

[Sheila]

My sister met with the oncologist today and she falls into a very rare and unusual category...even her breast oncologist said she would probably present her case at ASCO, because of the path reports. My sister was originally diagnosed with a 9mm Papillary breast cancer on the left side, triple negative, and due to the MRI results, and the possibility of dense Breast tissue and DCIS on the right, she opted for a bilateral mastectomy. She had a sentinel node biopsy on both sides...which were negative. The pathology report revealed a secondary IDC 5mm. On the left side, which was also triple negative. The right side, revealed a 4mm IDC and a small amount of DCIS...the IDC on the right is HER2+++, ER+ and PR-
She will undergo 6 rounds of Taxotere/Cytoxin, with Herceptin for 1 year. She is needless to say very thankful that she opted for bilateral and the second type of cancer was found, but very scared due to the rarity of this diagnosis. The oncologist wants the records of my Moms breast cancer, and has mine....very unusual since I was Neg for BRCA 1&2....
Please keep her in you prayers.

[Jackie07]

Thanks for the update, Sheila.

That is certainly an unusual case. Glad that she had chosen mastectomy and they were able to catch the tumor that's not shown on the scans. I wondered if many of the 'recurrences' after lumpectomy are really tumors that were missed in the initial scans.

Will continue to remember her in our prayers.

[Becky]

Wow - that is surprising but the same thing happened to my cousin who had 3 tumors in one breast (but also had a bilateral). Two tumors were the same - both moderately ER+Pr+ but the third tumor was ER+Pr-. Neither was Her2.

I also want to add that since I was diagnosed so was my cousin (above), my mother and my sister (dcis - high grade). All of us were BRCA tested and were negative.

Is it a fluke? I think not. Is it a gene that was not discovered yet. Maybe but maybe not but it could be something genetic or metabolic (which of course is genetic). For example, all of us had extremely low vitamin D readings at diagnosis. My cousin and mother were so low (0 - yea, zero) that they had an IV drip and then took the 50,000 iu pills. Two years ago, my oldest daughter had a physical and her doctor called her to tell her that her vitamin D level was only 8 and put her on a prescription and she takes 4000iu a day now and is well in the normal range. I take 4000iu a day (summer and winter) and just got my reading of 46 (normal is 32-100) so even taking alot, I am not at the upper end. Is this our problem metabolically? Maybe it is, maybe not.

All in all, disease results on how our genetics interplay with the environment. Even some BRCA+ women don't get breast or ovarian cancer. Stats for bc if BRCA 1 are 80% and BRCA 2 is 60%. So, who knows. Also, family members are raised together, experience the same environment while growing up (a critical time in development), have the same culture and likes/dislikes of the same foods. We will never know why. I am like you in a way in that I hope it is not a BRCA 3 or 4 or 5 as it will affect my kids. Right now, I am dosing them with vitamin D just because it is a problem but it may not be the problem.

My heart is with you and your sister. I always think about you Sheila.

[Lani]

I have previously posted the following and hope that everyone with a strong family history of her2+ breast cancer chimes in so that, if it is the case, we can interest some up and coming geneticist to take an interest and clarify the situation so oncologists have more data to reveal whether or not there may be a hereditary/familial subtype of her2+ breast cancer. It comes from a thread that I will try to provide a link for from June of 2010:


CELL
Volume 129, Issue 7, 29 June 2007, Pages 1275-1286
doi:10.1016/j.cell.2007.04.034
Article


FOXP3 Is an X-Linked Breast Cancer Suppressor Gene and an Important Repressor of the HER-2/ErbB2 Oncogene
Tao Zuo2, Lizhong Wang1, Carl Morrison3, Xing Chang1, Huiming Zhang1, Weiquan Li1, Yan Liu1, Yin Wang1, Xingluo Liu3, Michael W.Y. Chan2, Jin-Qing Liu3, Richard Love4, Chang-gong Liu2, Virginia Godfrey5, Rulong Shen3, Tim H.-M. Huang2, Tianyu Yang3, Bae Keun Park6, Cun-Yu Wang6, Pan Zheng1, , and Yang Liu1, ,
1Division of Immunotherapy, Section of General Surgery, Department of Surgery, Comprehensive Cancer Center, and Program of Molecular Mechanisms of Disease, University of Michigan, Ann Arbor, MI 48109, USA
2Program in Molecular, Cellular, and Developmental Biology and Department of Molecular Virology, Immunology, and Medical Genetics, Ohio State University Medical Center and Comprehensive Cancer Center, Columbus, OH 43210, USA
3Department of Pathology, Ohio State University Medical Center and Comprehensive Cancer Center, Columbus, OH 43210, USA
4Department of Internal Medicine, Ohio State University Medical Center and Comprehensive Cancer Center, Columbus, OH 43210, USA
5Department of Pathology, University of North Carolina, Chapel Hill, NC 27599, USA
6Laboratory of Molecular Signaling and Apoptosis, Department of Biologic and Materials Sciences, School of Dentistry, University of Michigan, Ann Arbor, MI 48109, USA Received 6 July 2006; revised 12 September 2006; accepted 10 April 2007. Published online: June 14, 2007. Available online 14 June 2007.

SUMMARY
The X-linked Foxp3 is a member of the forkhead/ winged helix transcription factor family. Germ- line mutations cause lethal autoimmune dis- eases in males. Serendipitously, we observed that female mice heterozygous for the ‘‘scurfin’’ mutation of the Foxp3 gene (Foxp3sf/+) devel- oped cancer at a high rate. The majority of the cancers were mammary carcinomas in which the wild-type Foxp3 allele was inactivated and HER-2/ErbB2 was overexpressed. Foxp3 bound and repressed the HER-2/ErbB2 promoter. Dele- tion, functionally significant somatic mutations, and downregulation of the FOXP3 gene were commonly found in human breast cancer sam- ples and correlated significantly with HER-2/ ErbB2 overexpression, regardless of the status of HER-2 amplification. Our data demonstrate that FOXP3 is an X-linked breast cancer sup- pressor gene and an important regulator of the HER-2/ErbB2 oncogene.

My comment at the time:

When a male inherits an X chromosome affected by this FOX-P3 mutation, they can die in utero or be born with severe immunodeficiency with a named syndrome, IPEX., so I doubt this is what caused your father's prostate cancer. Interestingly they contrast her2 overexpression and her2 amplification perhaps part of the problem as to why your sister's her2 status results were inconsistant. By the way, one of the ways ER+her2- tumors excape antihormonal treatment is by becoming her2+ which also might be what happened to your sister. There are so many possibilities.

http://her2support.org/vbulletin/sho...ITED+HER2+Lani

http://her2support.org/vbulletin/sho...R2+Lani&page=2

[WolverineFan]

Hey Shelia,

I had one tumor that was triple positive and a DCIS mass that was ER-,PR-. I was told the her2 status wasn't checked because it was DCIS. The odd thing with my case was that the mass of DCIS and the invasive tumor shared the same wall. I was 90% ER+ and 95% PR+ on the invasive tumor. My surgical oncologist said it was very rare and there was a review of my case with the hospital's oncology board. I've had great success with my treatments, so despite this rare case, it is my understanding that the prognosis can be very good. I will continue to keep you and your sister in my prayers.

Hayley

[NanaJoni]

I had two tumors in the same quadrant - less than an inch apart (one was deeper in the breast tissue). One was triple negative and the other ER-/PR-/HER2+++. My surgeon's comment was: "your treatment will be complicated by this". Actually turned out not to be so complicated - I was given the TCH regimen (treating both types) with Herceptin (to take care of the HER2 tumor). Since the only treatment for triple negative is chemo and I wasn't able to complete but 4 of 6 treatments, I did radiation for 6 weeks. I also did Herceptin every three weeks for almost a year but had to stop with only 3 treatments to go due to radiation pneumonitis. Now I wait - since triple negative is very agressive and usually recurs within the first 3 years after diagnosis, I've got two more years of high risk (and associated worry) before the risk lowers to compare with rates for the other types of bc (er+/pr+, etc). I am hoping we covered all the bases and were as agressive as possible but the triple negative is much more scary than the HER2+++. I've put it all away in a little mental lockbox with a big concrete vault around it so it doesn't occupy my thoughts all the time. Occasionally it squeezes out of from under that concrete lid and I have a little meltdown, but mostly I can keep it there (this mental imagery really helps me deal with the fear of recurrence). I'm BRCA negative, too, so just one of those weird things that happens on this journey.

[Jean]

Sheila,
Will certainly keep you and your sister in my prayers.
Hugs
Jean

[Rich66]

I bet the situation is not that rare..just rarely detected. I have always been concerned about the comprehensive diagnostic/pathologic integrity of inherently limited biopsies. Maybe it would be of comfort to your sister to hear that she is not necessarily rare..just more accurately diagnosed.