HER2 Support Group Forums - View Single Post - Link to 2007 ASCO guidelines for tumor markers

Gerri · 11-28-2007, 10:02 AM

I copied the following from the article:

Literature update and discussion. Complex interactions exist between the HER2 and ER pathways. HER2 expression in human breast cancer cells is downregulated by estrogens.136 Conversely, overexpression of HER2 promotes estrogen-independent growth and is associated with resistance to tamoxifen in vitro and in animal models, possibly by promoting ligand-independent growth. These observations are consistent with the inverse association of estrogen and progesterone receptors with HER2 overexpression and also provide a rationale for the lower response of HER2-overexpressing tumors to endocrine therapy shown in several clinical studies.107,137-141 However, most of these studies were retrospective and nonrandomized. To date, randomized trials have not led to consensus on this association.142-145 The interaction of HER2 with endocrine therapy may vary depending on the type of hormonal agent in question. Ellis et al146 have shown that HER2- and/or EGFR-positive tumors were more likely to respond to neoadjuvant letrozole than tamoxifen in a randomized trial of 324 primary breast cancer patients. In contrast, an analysis (presented in abstract form only) of the Anastrozole versus Tamoxifen versus a Combination of the two (ATAC) trial, failed to show that HER2-overexpressing tumors benefit more from the aromatase inhibitor.147,148 In summary, there are insufficient data to support the use of HER2 in tissue (or serum, as discussed below) as a predictor of response to endocrine therapy, although the evidence does suggest that in patients with ER-positive tumors, the relative benefit from antiestrogens for those with HER2-positive cancers is likely to be lower than for those with HER2-negative cancers. It is not at all clear that the benefit of aromatase inhibitors in this group is any greater than in the HER2-negative, ER-positive group. 


To me this is confirmation that continuing with Tamoxifen until I naturally enter menopause is reasonable.

11-28-2007, 10:02 AM	#7
Gerri Senior Member Join Date: Oct 2006 Location: Southern California Posts: 900	Tamoxifen vs AI in HER2 I copied the following from the article: Literature update and discussion. Complex interactions exist between the HER2 and ER pathways.<SUP> </SUP>HER2 expression in human breast cancer cells is downregulated<SUP> </SUP>by estrogens.<SUP>136</SUP> Conversely, overexpression of HER2 promotes<SUP> </SUP>estrogen-independent growth and is associated with resistance<SUP> </SUP>to tamoxifen in vitro and in animal models, possibly by promoting<SUP> </SUP>ligand-independent growth. These observations are consistent<SUP> </SUP>with the inverse association of estrogen and progesterone receptors<SUP> </SUP>with HER2 overexpression and also provide a rationale for the<SUP> </SUP>lower response of HER2-overexpressing tumors to endocrine therapy<SUP> </SUP>shown in several clinical studies.<SUP>107,137-141</SUP> However, most<SUP> </SUP>of these studies were retrospective and nonrandomized. To date,<SUP> </SUP>randomized trials have not led to consensus on this association.<SUP>142-145</SUP><SUP> </SUP>The interaction of HER2 with endocrine therapy may vary depending<SUP> </SUP>on the type of hormonal agent in question. Ellis et al<SUP>146</SUP> have<SUP> </SUP>shown that HER2- and/or EGFR-positive tumors were more likely<SUP> </SUP>to respond to neoadjuvant letrozole than tamoxifen in a randomized<SUP> </SUP>trial of 324 primary breast cancer patients. In contrast, an<SUP> </SUP>analysis (presented in abstract form only) of the Anastrozole<SUP> </SUP>versus Tamoxifen versus a Combination of the two (ATAC) trial,<SUP> </SUP>failed to show that HER2-overexpressing tumors benefit more<SUP> </SUP>from the aromatase inhibitor.<SUP>147,148</SUP><SUP> </SUP>In summary, there are insufficient data to support the use of<SUP> </SUP>HER2 in tissue (or serum, as discussed below) as a predictor<SUP> </SUP>of response to endocrine therapy, although the evidence does<SUP> </SUP>suggest that in patients with ER-positive tumors, the relative<SUP> </SUP>benefit from antiestrogens for those with HER2-positive cancers<SUP> </SUP>is likely to be lower than for those with HER2-negative cancers.<SUP> </SUP>It is not at all clear that the benefit of aromatase inhibitors<SUP> </SUP>in this group is any greater than in the HER2-negative, ER-positive<SUP> </SUP>group.<SUP> </SUP> <SUP></SUP> <SUP></SUP> <SUP>To me this is confirmation that continuing with Tamoxifen until I naturally enter menopause is reasonable.</SUP> <SUP></SUP> __________________ Gerri Dx: 11/23/05, Lumpectomy 12/12/05 Tumor 2.2 cm, Stage II, Grade 3, Sentinel Node biopsy negative ER+ (30%) /PR+ (50%), HER2+++ AC X 4 dose dense, Taxol X 4 dose dense Herceptin started with 2nd Taxol, given weekly until chemo done then given every 3 weeks for one year ending on March 16, 2007 Radiation 30 treatments Tamoxifen - 2 yrs (pre-menopausal) May 2008 - Feb 2012 Femara Aug 2008 - Feb 2012 Zometa every 6 months March 2012 - Stop Femara, now Evista for bone strengthening ********** Enjoy the little things, for one day you may look back and realize they were the big things. - Robert Brault