LCIS - genetic link?
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Hi-
My sister was just diagnosed with Atypical Lobular cells after having an excisional biopsy due to calcifications. In March 2006, I was diagnosed with Stage one bc (tubular), and they also found LCIS.
My question - Is it typical for us to both have LCIS? Should we have genetic testing? We are both in our 40's, though we don't have the "typical" characteristics that point to a genetic link.
Thanks!
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Well, I can only tell you my experience. I have LCIS and ALH. (LCIS on my initial core biopsy for calcifications, LCIS and 'features of ALH' on my excision, then I had genetic counseling. ALH was diagnosed on a re-read of the slides.)
First, I would question, from what you have wrote, if your sister has LCIS.
I am not sure, but I thought that they usually thought the progression went from normal cells become hyperplasia (many cells line the ducts or lobules), then these become atypical (irregular), then, when all of the lobule fills up with these atypical cells and you have LCIS. So, from what I understand, I thought LCIS was different from ALH, and most people thought that LCIS women (without anything worse) had a higher risk for bc than ALH (and not anything worse) women. This was borne out by the study by Port et al at Sloan Kettering, where most of the bc in a group of women with LCIS or atypia was in the LCIS group. 2 out of the 14 cancers detected were in AH women, though the groups were of unequal size.
1: Ann Surg Oncol. 2007 Mar;14(3):1051-7. Epub 2007 Jan 7. Links
Results of MRI screening for breast cancer in high-risk patients with LCIS and atypical hyperplasia.
Port ER, Park A, Borgen PI, Morris E, Montgomery LL.
Breast Service, Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA. porte@mskcc.org
BACKGROUND: Magnetic resonance imaging (MRI) can detect breast cancer in high-risk patients, but is associated with a significant false-positive rate resulting in unnecessary breast biopsies. More data are needed to define the role of MRI screening for specific high-risk groups. We describe our experience with MRI screening in patients with atypical hyperplasia (AH) and lobular carcinoma in situ (LCIS). METHODS: We retrospectively reviewed data from our high-risk screening program prospective database for the period from April 1999 (when screening MRI was first performed at our institution) to July 2005. Patients with AH or LCIS demonstrated on previous surgical biopsy were identified. All patients underwent yearly mammography and twice yearly clinical breast examination. Additional screening MRI was performed at the discretion of the physician and patient. RESULTS: We identified 378 patients; 126 had AH and 252 had LCIS. Of these, 182 (48%) underwent one or more screening MRIs (mean, 2.6 MRIs; range, 1-8) during this period, whereas 196 (52%) did not. Those who had MRIs were younger (P < 0.001) with stronger family histories of breast cancer (P = 0.02). In MRI-screened patients, 55 biopsies were recommended in 46/182 (25%) patients, with 46/55 (84%) biopsies based on MRI findings alone. Cancer was detected in 6/46 (13%) MRI-generated biopsies. None of the six cancers detected on MRI were seen on recent mammogram. All six cancers were detected in five patients (one with bilateral breast cancer) with LCIS; none were detected by MRI in the AH group. Thus, cancer was detected in 5/135 (4%) of patients with LCIS undergoing MRI. The yield of MRI screening overall was cancer detection in 6/46 (13%) biopsies, 5/182 (3%) MRI-screened patients and 5/478 (1%) total MRIs done. In two additional MRI-screened patients, cancer was detected by a palpable mass in one, and on prophylactic surgery in the other and missed by all recent imaging studies. For 196 non-MRI-screened patients, 21 (11%) underwent 22 biopsies during the same period. Eight of 22 (36%) biopsies yielded cancer in seven patients. All MRI-detected cancers were stage 0-I, whereas all non-MRI cancers were stage I-II. CONCLUSION: Patients with AH and LCIS selected to undergo MRI screening were younger with stronger family histories of breast cancer. MRI screening generated more biopsies for a large proportion of patients, and facilitated detection of cancer in only a small highly selected group of patients with LCIS.
PMID: 17206485 [PubMed - indexed for MEDLINE]
I went to genetic counseling at a board-certified place. For the purposes of genetic counseling, they were treating my LCIS as breast cancer, even though most oncologists consider LCIS to be a benign condition. There is controversy though, with almost all aspects of LCIS, from its name to its risk for bc to its treatment.
From what I have read, the incidence of LCIS (without anything worse) is unknown, because normally they can only diagnose it on biopsy, and not every woman has a breast biopsy. I think the average age that LCIS is diagnosed is in ones' 40s or 50s. I was diagnosed at age 51, and for my age group, one paper opined that the incidence was something like 1:10,000 women years. In the SEER study, there were about 4500 women in the US who were reported to the SEER registry who were diagnosed with LCIS (and nothing worse) from about 1988 to 2001. There were about six times this number who were diagnosed with DCIS (and nothing worse) in this same time period.
I have read figures that about up to about ????10% of breast cancers have concurrent LCIS. I don't know how solid that figure is, though.
I had genetic counseling, and all I had in my family was 2 second degree relatives with bc on different sides of the family, though one generation was male only. -
cayenneblue--I am a little confused too. From what you wrote, I'm not sure if your sister just has ALH, or if she has both ALH and LCIS? Or were you asking what was the probability of her having LCIS too since you were diagnosed with it? (the possibility of her having it certainly exists, as LCIS is the next step further along after ALH on the bc spectrum (with double the risk 7 to 10x, versus 3 to 5x with ALH); she automatically has an increased risk of bc (double) because you are a primary relative (sister) with an invasive bc. (I was diagnosed with LCIS 4 years ago, my mom had ILC, so I have a similar situation; I worry about my 2 older sisters). I don't have a lot of the "red flags" for the BRCA gene (several primary relatives with premenopausal bc, family history of ovarian ca or male bc, ashkenazi jewish heritage), so my oncologist feels I'm probably low risk, but now is suggesting I consider the genetic counseling/ testing anyway. I probably will within the next year. It might be something you and your sister would want to consider. There are other bc genes that haven't been identified yet.
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Hi-
Thanks for your responses. I haven't gotten the definitive word from my sister of what exactly she was diagnosed with since she hasn't met with the oncologist. All's I know is that she had "atypical lobular cells"...... their words. So, I suppose it is ALH, not LCIS.... I didn't know there was a progression.
I DID have LCIS found when they did my mastectomy, so I do wonder if LCIS has a genetic component.
I'll try to see if she has gotten her pathology report and can read it to me.
Thanks!
Theresa
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