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Lani · 01-05-2007, 10:10 PM

Dr. Dennis Slamon has commented at several conferences that he thinks that Faslodex (fulvestrant) is the most effective antihormonal drug for her2 breast cancer, based on its mechanism of action.

AIs still work in her2+ patient but less well than in her2- patients and WHEN GIVEN IN COMBINATION WITH HERCEPTIN (at least for the first year)

It is usually given when a patient with metastatic disease fails tamoxifen or an AI, but may be beginning to be given in the adjuvant setting--I think someone on this board commented that they are on it and I know of someone else receiving it adjuvantly, particularly in someone in whom there is an increased risk of DVT (as she already had one). It is an injectable medication, given monthly and works by a different mechanism of action than either tamoxifen (which sits on the ER blocking estrogen from getting theri) or AIs which block the production of estrogen via one of its 3 ways of being made in muscle, liver, breast, fat tissue, etc.

Perhaps she could get on a trial of Tykerb plus Herceptin vs Herceptin alone (neither option too shabby!) There are other new trials starting including Herceptin+Avastin adjuvantly...there are so many new options available.

As regards the inheritance, I have found two papers on familial her2+ breast cancer--here is the abstract of one:
Am J Clin Pathol. 2003 Dec;120(6):917-27. Links
Her-2/neu gene amplification in familial vs sporadic breast cancer. Impact on the behavior of the disease.

Espinosa AB,
Tabernero MD,
Garcia-Macias MC,
Primo D,
Bernal AG,
Cruz JJ,
Ramos M,
Font de Mora J,
Gomez Alonso A,
Orfao A.
Cancer Research Center, Department of Medicine, General Cytometry Service, University of Salamanca, Salamanca, Spain.
We compared the incidence of Her-2/neu amplification in patients with and without a family history of breast cancer and correlated gene status with clinicobiologic and prognostic features in sporadic and familial cases. Of 108 patients, 28.7% had gene amplification. Among 96 cases with family history information available, 28 had an affected first-degree relative. The gene was amplified more frequently in familial than in sporadic cases (13/28 [46%] vs 14/68 [21%]; P = .01). Among familial cases, amplification was associated with adverse clinicobiologic features (poorly differentiated tumors [P = .05], larger tumors [P = .05], more lymph nodes involved [P = .04], and DNA aneuploid [P = .02] and highly proliferative tumors [P = .005]), and the relapse (P = .02) and disease-related death (P = .05) rates were higher than in cases without amplification. Among sporadic cases, amplification was not associated with significantly different disease features, except for a higher incidence of DNA aneuploid tumors (P = .01), percentage of S-phase tumor cells (P = .006), and lower proportion of estrogen (P = .001) and progesterone (P = .002) receptors. Her-2/neu amplification was observed more frequently among patients with a family history of breast cancer, in whom it was associated with adverse clinicobiologic features and a worse clinical outcome.
PMID: 14671981 [PubMed - indexed for MEDLINE]
will try to post the abstract of the other

Please remember to add your case and that of your sister to my previous posting asking those with her2+breast cancer if there were others with breast cancer in their immediate families and if they knew if the others were her2 as well.

By the way, if you don't mind sharing, how do your tumor characteristics (%ER,%PR, LVI, SIZE, LYMPH NODE INVOLVEMENT, KI-67, ETC) AND THOSE OF YOUR SISTER COMPARE?

Best of luck!

01-05-2007, 10:10 PM	#2
Lani Senior Member Join Date: Mar 2006 Posts: 4,778	Kirsten--where are you located? Dr. Dennis Slamon has commented at several conferences that he thinks that Faslodex (fulvestrant) is the most effective antihormonal drug for her2 breast cancer, based on its mechanism of action. AIs still work in her2+ patient but less well than in her2- patients and WHEN GIVEN IN COMBINATION WITH HERCEPTIN (at least for the first year) It is usually given when a patient with metastatic disease fails tamoxifen or an AI, but may be beginning to be given in the adjuvant setting--I think someone on this board commented that they are on it and I know of someone else receiving it adjuvantly, particularly in someone in whom there is an increased risk of DVT (as she already had one). It is an injectable medication, given monthly and works by a different mechanism of action than either tamoxifen (which sits on the ER blocking estrogen from getting theri) or AIs which block the production of estrogen via one of its 3 ways of being made in muscle, liver, breast, fat tissue, etc. Perhaps she could get on a trial of Tykerb plus Herceptin vs Herceptin alone (neither option too shabby!) There are other new trials starting including Herceptin+Avastin adjuvantly...there are so many new options available. As regards the inheritance, I have found two papers on familial her2+ breast cancer--here is the abstract of one: Am J Clin Pathol. 2003 Dec;120(6):917-27. Links Her-2/neu gene amplification in familial vs sporadic breast cancer. Impact on the behavior of the disease. Espinosa AB, Tabernero MD, Garcia-Macias MC, Primo D, Bernal AG, Cruz JJ, Ramos M, Font de Mora J, Gomez Alonso A, Orfao A. Cancer Research Center, Department of Medicine, General Cytometry Service, University of Salamanca, Salamanca, Spain. We compared the incidence of Her-2/neu amplification in patients with and without a family history of breast cancer and correlated gene status with clinicobiologic and prognostic features in sporadic and familial cases. Of 108 patients, 28.7% had gene amplification. Among 96 cases with family history information available, 28 had an affected first-degree relative. The gene was amplified more frequently in familial than in sporadic cases (13/28 [46%] vs 14/68 [21%]; P = .01). Among familial cases, amplification was associated with adverse clinicobiologic features (poorly differentiated tumors [P = .05], larger tumors [P = .05], more lymph nodes involved [P = .04], and DNA aneuploid [P = .02] and highly proliferative tumors [P = .005]), and the relapse (P = .02) and disease-related death (P = .05) rates were higher than in cases without amplification. Among sporadic cases, amplification was not associated with significantly different disease features, except for a higher incidence of DNA aneuploid tumors (P = .01), percentage of S-phase tumor cells (P = .006), and lower proportion of estrogen (P = .001) and progesterone (P = .002) receptors. Her-2/neu amplification was observed more frequently among patients with a family history of breast cancer, in whom it was associated with adverse clinicobiologic features and a worse clinical outcome. PMID: 14671981 [PubMed - indexed for MEDLINE] will try to post the abstract of the other Please remember to add your case and that of your sister to my previous posting asking those with her2+breast cancer if there were others with breast cancer in their immediate families and if they knew if the others were her2 as well. By the way, if you don't mind sharing, how do your tumor characteristics (%ER,%PR, LVI, SIZE, LYMPH NODE INVOLVEMENT, KI-67, ETC) AND THOSE OF YOUR SISTER COMPARE? Best of luck!