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• W1991574504 abstract "Fertility preservation in younger cancer patients undergoing adjuvant chemotherapy is gaining importance. Oocyte cryopreservation requires stimulation with gonadotropins, resulting in strong estradiol (E2) increase. There has been concern that this may propagate breast cancer progression, particularly in hormone receptor-positive disease. However, ovarian stimulation is currently considered safe, as a recent study showed that it did not affect recurrence rates during a follow-up of 23 months [1.Azim A.A. Costantini-Ferrando M. Oktay K. Safety of fertility preservation by ovarian stimulation with letrozole and gonadotropins in patients with breast cancer: a prospective controlled study.J Clin Oncol. 2008; 26: 2630-2635Crossref PubMed Scopus (390) Google Scholar]. Here, we report on a case where ovarian stimulation was unintentionally carried out in metastatic disease, progressing rapidly during this procedure. A 35-year-old woman was diagnosed with ductal invasive breast cancer in May 2009 (pT2, pN0, L0, V0, R0 and G3; no expression of hormone receptors and Her-2). At the time of lumpectomy and sentinel node dissection on 26 May, all tested laboratory parameters were in the normal range. A bone scan was without pathological findings except an abnormal radionuclide uptake in the seventh rib. Computed tomography (CT) on 4 June showed several suspicious lesions, one in the seventh rib and three others in the thoracic spine (maximum 1.2 cm; Figure 1A) without evidence of visceral metastases. While staging investigations were still ongoing, the patient contacted a fertility practice for oocyte asservation before chemotherapy. Ovarian stimulation was started on 19 June, leading to an increase of E2 levels from 30 pg/ml (day 0) to 864 pg/ml on 7 July. Immediately after oocyte harvest on 8 July, the patient presented with massive bone pain in an orthopedic clinic. Plasma calcium concentrations were elevated (3.5 mmol/l, normal range 2.22–2.65 mmol/l), and creatinine values had risen from 0.64 mg/dl preoperatively to 1.02 mg/dl (0.55–1.02 mg/dl). A CT scan demonstrated disseminated osteolytic lesions in the spine, sternum, right acromion, pelvis and right femur (Figure 1B and C) as well as two liver metastases. A bone scan on 14 July showed inhomogeneous uptake especially in the spine and proximal femurs, indicative of diffuse metastases. The same day, the patient was referred to our department with hypercalcemia and beginning acute renal failure (creatinine 2.78 mg/dl, calcium 3.73 mmol/l). E2 levels were back to normal (32 pg/ml), while serum concentrations of relaxin, which were measured as described previously [2.Binder C. Simon A. Binder L. et al.Elevated concentrations of serum relaxin are associated with metastatic disease in breast cancer patients.Breast Cancer Res Treat. 2004; 87: 157-166Crossref PubMed Scopus (63) Google Scholar], were extremely high (1.52 ng/ml, normal range <0.3). Renal function improved rapidly and calcium levels returned to normal upon volume substitution, induction of diuresis, administration of bisphosphonates and chemotherapy with docetaxel and gemcitabine. Triple-negative breast cancers with basal-like features are aggressive tumors. However, rapid progression with development of disseminated metastases within only 8 weeks is unusual even for this unfavorable entity. In the presented case, the increase of creatinine and calcium values concurred with elevation of E2 levels during ovarian stimulation. Induction of hypercalcemia by estrogens is a well-described phenomenon. However, it seems less clear, how this treatment may have affected malignant progression, as the tumor was hormone receptor negative. There is increasing evidence that the tumor stroma is critical for cancer progression. Estrogens are known to induce angiogenesis [3.Einspanier A. Lieder K. Husen B. et al.Relaxin supports implantation and early pregnancy in the marmoset monkey.Ann N Y Acad Sci. 2009; 1160: 140-146Crossref PubMed Scopus (30) Google Scholar], important for tumor neovascularization. Estrogens also stimulate the insulin-like growth factor-I (IGF-I) pathway [4.Kleinberg D.A. Wood T.L. Furth P.A. Lee A.V. Growth hormone and insulin-like growth factor-I in the transition from normal mammary development to preneoplastic mammary lesions.Endocr Rev. 2009; 30: 51-74Crossref PubMed Scopus (122) Google Scholar]. IGF-I has been shown to promote breast cancer growth, and its receptor is overexpressed in basal-like cancers [5.Lerma E. Peiro G. Ramon T. Fernandez S. Immunohistochemical heterogeneity of breast carcinomas negative for estrogen receptors, progesterone receptors and Her2/neu (basal-like breast carcinomas).Mod Pathol. 2007; 20: 1200-1207Crossref PubMed Scopus (67) Google Scholar]. Estrogens up-regulate expression of a close relative of IGF-I, the peptide hormone relaxin [6.Larkin L.H. Ogilvie S. Wubbel L. Welch D.E. Effects of estradiol and progesterone on accumulation of relaxin- and carbohydrate-containing granules in endometrial gland cells of the guinea pig.Am J Anat. 1987; 179: 333-341Crossref PubMed Scopus (11) Google Scholar] that induces stromal remodeling as a prerequisite for malignant spread and has been shown to foster tumor cell invasion [7.Silvertown J.D. Summerlee A.S. Klonisch T. Relaxin-like peptides in cancer.Int J Cancer. 2003; 107: 513-519Crossref PubMed Scopus (66) Google Scholar]. Relaxin also triggers chemotaxis of leukocytes [8.Figueiredo K.A. Mui A.L. Nelson C.C. Cox M.E. Relaxin stimulates leukocyte adhesion and migration through a relaxin receptor LGR7-dependent mechanism.J Biol Chem. 2006; 281: 3030-3039Abstract Full Text Full Text PDF PubMed Scopus (26) Google Scholar], leading to enhanced tissue infiltration by monocytes/macrophages [3.Einspanier A. Lieder K. Husen B. et al.Relaxin supports implantation and early pregnancy in the marmoset monkey.Ann N Y Acad Sci. 2009; 1160: 140-146Crossref PubMed Scopus (30) Google Scholar], critical for tumor progression [9.Mantovani A. Allavena P. Sica A. Balkwill F. Cancer-related inflammation.Nature. 2009; 454: 436-444Crossref Scopus (8189) Google Scholar]. Significantly higher relaxin levels have been demonstrated in patients with breast cancer metastases than in those without, correlating with poor clinical outcome [2.Binder C. Simon A. Binder L. et al.Elevated concentrations of serum relaxin are associated with metastatic disease in breast cancer patients.Breast Cancer Res Treat. 2004; 87: 157-166Crossref PubMed Scopus (63) Google Scholar]. Relaxin concentrations in our patient were as high as the highest observed values in the mentioned study. Although we cannot rule out that the dramatic deterioration reflects the natural course of an extremely unfavorable breast cancer variant, the temporal coincidence is highly indicative of a causative role of ovarian stimulation. If so, it has to be postulated that the effect was mediated indirectly by the surrounding stromal compartment. This underlines that more clinical data are needed to assess whether fertility preserving methods with hormonal stimulation can be safely carried out in the adjuvant breast cancer setting. There is no conflict of interest for any of the authors." @default.
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• W1991574504 title "Rapid progression of hormone receptor-negative breast cancer concomitant with ovarian stimulation—a paradoxon?" @default.
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