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Old 05-05-2006, 10:25 PM   #1
Lani
Senior Member
 
Join Date: Mar 2006
Posts: 4,778
how many started out with DCIS with or without microinvasion

a few of you have posted that you started out with DCIS and then went on ...even to Stage IV

This has concerned many with DCIS, as the oncologists' mantra has seemed to be that it need only be treated with surgery and radiation.

Almost all DCIS does not recur distally or even spread to the lymph nodes according to the literature it seems, and about 60% of them are her2+ it seems. Yet some on this site are wondering how small a her2 tumor has to be such that they can just have surgery and radiation and "not have to worry about it"

Jean recently found out that her DCIS with microinvasion (.3mm) had a very high OncoDx score--OncoDX is not officially meant or validated for DCIS, only for Stage I node negative ER+ invasive ductal carcinoma.Nevertheless, Dr. Slamon felt, as small as it was, that her her2+ area of microinvasion warranted treatment with chemo and herceptin.

I post an abstract showing that someone is looking to find which markers on DCIS might portend a more aggressive behavior and ask all those who started out with a Diagnosis of DCIS to help share info so others starting with DCIS can get a handle on the situation.

I know very little about DCIS--I first started looking it up when asked by an oncologist to try to explain to a reluctant patient something about breast cancer and her2neu to help explain why she couldn't just pretend everything was ok and no treatment was needed when her DCIS with microinvasion suddenly became associated with a lymph node which appeared and grew tremendously over four weeks' time. She thought I explained things well, but actually the whole experience was a bust. (as I posted previously).
I had not looked up DCIS before then really and haven't made it my baileywick, but it seems like an area where there is still a tremendous amount of knowledge lacking.

Jean asked me why I thought there wasn't general knowledge or agreement on what is going on with DCIS with microinvasion especially with her2+ status. We agreed to try to start a roll call to see if the her2group could produce enough information to attract a researcher or Genentech. If a certain profile of DCIS with microinvasion and her2 postivity can be asociated with a substantial risk of distant recurrence, they might be able ton alter the natural history of the disease AND market their drug to more people.

Please list age at dx, pre or post menopausal status, size of dcis, whether microinvasion(s) and size of microinvasion, her2 status by IHC or FISH in the DCIS, ER and PR status, grade of DCIS, type of surgery you had, margins of surgery, whether you had radiation therapy, hormonal therapy, any other therapy. How long until recurred, where, subsequent treatment.

It seems we must try to push to move "science" along sometimes...

Thanks to all who join in!

Lani

Appl Immunohistochem Mol Morphol. 2005 Mar;13(1):14-8. Related Articles, Links

Correlation of HER2 gene amplification with expression of the apoptosis-suppressing genes bcl-2 and bcl-x-L in ductal carcinoma in situ of the breast.

Siziopikou KP, Khan S.

Department of Pathology, Rush University Medical Center, Chicago, IL 60612, USA. Kalliopi_P_Siziopikou@rush.edu

The protein product of the HER2 oncogene is overexpressed in an estimated 25 to 30% of breast carcinomas and is considered an indicator of poor clinical outcome. The bcl-2 and the bcl-x-L genes are the 2 main genes of the bcl-2 gene family that suppress tumor cell death/apoptosis. HER2 gene amplification is also described in a percentage of cases of ductal carcinoma in situ (DCIS) of the breast. However, the relationship of such overexpression with the apoptosis-suppressing genes is currently unknown. A total of 37 consecutive cases of DCIS were immunostained for HER2 overexpression (clone CB11, Ventana), and expression of bcl-2 and bcl-x-L. DCIS cases were graded using the criteria of Holland et al. HER2 overexpression was scored 0 to 3+; 0 and 1+ were considered negative staining and 2+ and 3+ were considered positive staining. HER2 gene amplification was also confirmed with fluorescent in situ hybridization (FISH). HER2 was positive in 22 of the 37 DCIS cases (60%) in accordance with previous reports. Immunohistochemical overexpression of HER2 was also highly correlated with HER2 amplification by FISH. HER2 overexpression (confirmed by FISH) was mostly seen in grade II (9 of 17) and grade III (9 of 12) DCIS lesions. Only 1 of the HER2-amplified cases was a grade I lesion. Furthermore, HER2 overexpression correlated with the presence of necrosis (P=0.003). Similarly, of the cases overexpressing HER2 at the highest level (3+), 90% were grade II or grade III lesions. A total of 73% of these cases also exhibited necrosis. Overexpression of HER2 3+ was also highly correlated with the presence of the apoptosis-suppressing gene bcl-x-L (coexpression in 87% of cases, P=0.01) but not with the prototype apoptosis-suppressing gene bcl-2 (coexpression in 50% of cases, P value not significant). First, in DCIS overexpression of HER2 the majority of grade II and grade III lesions is seen, and this correlates with the presence of necrosis. Second, HER2 overexpression is also highly correlated with the expression of the apoptosis-suppressing gene bcl-x-L, but not with the prototype apoptosis-suppressing gene bcl-2. These differences may prove useful in defining groups of DCIS lesions with enhanced tumor cell growth and propensity for progression to invasion.
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