Responding to same endocrine treatment again.

[Nguyen]

Does anyone here responding to the SAME endocrine treatment (such as Femara, Anastrozole, etc) after treatment stopped DUE to acquired resistance.

For some patients and chemotherapy, the tumour can reverse the acquired resistance to that chemotherapy after not being treated with that chemotherapy for a period time (a few years if I remember correctly).

I was wondering about this with respect to endocrine treatment, then found the abstract below.

- Nguyen
Stopping Treatment Can Reverse Acquired Resistance to Letrozole

Gauri J. Sabnis¹, Luciana F. Macedo¹, Olga Goloubeva², Adam Schayowitz¹ and Angela M.H. Brodie^1,2
1 Department of Pharmacology and Experimental Therapeutics, University of Maryland School of Medicine and ² University of Maryland Greenebaum Cancer Center, Baltimore, Maryland
Requests for reprints: Angela M.H. Brodie, Department of Pharmacology and Experimental Therapeutics, University of Maryland, School of Medicine, Health Science Facility I, Room 580G, 685 West Baltimore Street, Baltimore, MD 21201. Phone: 410-706-3137; Fax: 410-706-0032; E-mail: abrodie@umaryland.edu .

Key Words: aromatase inhibitors • estrogen • letrozole • ER • Her-2
Using the intratumoral aromatase xenograft model, we have observed that despite long-lasting growth inhibition, tumors eventually begin to grow during continued letrozole treatment. In cells isolated from these long-term letrozole-treated tumors (LTLT-Ca), estrogen receptor- (ER) levels were decreased, whereas signaling proteins in the mitogen-activated protein kinase cascade were up-regulated along with human epidermal growth factor receptor 2 (Her-2). In the current study, we evaluated the effect of discontinuing letrozole treatment on the growth of letrozole-resistant cells and tumors. The cells formed tumors equally well in the absence or presence of letrozole and had similar growth rates. After treatment was discontinued for 6 weeks, letrozole was administered again. Marked tumor regression was observed with this second course of letrozole treatment. Similarly, in MCF-7Ca xenografts, a 6-week break in letrozole treatment prolonged the responsiveness of the tumors to letrozole. To understand the mechanisms of this effect, LTLT-Ca cells were cultured in the absence of letrozole for 16 weeks. The resulting cell line (RLT-Ca) exhibited properties similar to MCF-7Ca cells. The cell growth was inhibited by letrozole and stimulated by estradiol. The expression of phosphorylated mitogen-activated protein kinase (MAPK) was reduced and ER and aromatase levels increased compared with LTLT-Ca cells and were similar to levels in MCF-7Ca cells. These results indicate that discontinuing treatment can reverse letrozole resistance. This could be a beneficial strategy to prolong responsiveness to aromatase inhibitors for patients with breast cancer. [Cancer Res 2008;68(12):4518–24]