title: Molecular phenotype is associated with survival in breast cancer patients with spinal bone metastases.
abstract: To aid in therapy selection for patients with spinal bone metastases (SBM), predictive models have been developed. These models consider SBM from breast cancer a positive predictive factor, but do not take phenotypes based on estrogen (ER), progesterone (PR) and human epidermal growth factor 2 (HER2) receptors into account. The aim of this study was to ascertain whether receptors are associated with survival, when the disease has progressed up to SBM. All patients who were treated for SBM from breast cancer between 2005 and 2012 were included in this international multi-center retrospective study (n = 111). Reports were reviewed for ER, PR and HER2 status and subsequently subdivided into one of four categories; luminal A, luminal B, HER2 and triple negative. Survival time was calculated as the difference between start of treatment for SBM and date of death. Analysis was performed using the Kaplan-Meier method and log-rank tests. Median follow-up was 3.7 years. Survival times in the luminal B and HER2 categories were not significantly different to the luminal A category and were joined into a single receptor positive category. Eighty-five patients (77 %) had a receptor positive phenotype and 25 (23 %) had a triple negative phenotype. Median survival time was 22.5 months (95 %CI 18.0-26.9) for the receptor positive category and 6.7 months (95 %CI 2.4-10.9) for the triple negative category (p < 0.001). Patients with SBM from breast cancer with a triple negative phenotype have a shorter survival time than patients with a receptor positive phenotype. Models estimating survival should be adjusted accordingly.
authors.affiliation: Department of Orthopedic Surgery, Leiden University Medical Center, Albinusdreef 2, P.O. Box 9600, 2300 RC, Leiden, The Netherlands, l.bollen@lumc.nl.
authors.forename: L
authors.initials: L
authors.lastname: Bollen
authors.forename: C
authors.initials: C
authors.lastname: Wibmer
authors.forename: M
authors.initials: M
authors.lastname: Wang
authors.forename: Y M
authors.initials: YM
authors.lastname: van der Linden
authors.forename: A
authors.initials: A
authors.lastname: Leithner
authors.forename: C E
authors.initials: CE
authors.lastname: Bünger
authors.forename: A B
authors.initials: AB
authors.lastname: Jensen
authors.forename: M
authors.initials: M
authors.lastname: Fiocco
authors.forename: G
authors.initials: G
authors.lastname: Bratschitsch
authors.forename: W
authors.initials: W
authors.lastname: Pondaag
authors.forename: J V M G
authors.initials: JV
authors.lastname: Bovée
authors.forename: P D S
authors.initials: PD
authors.lastname: Dijkstra
mesh_terms: D014408:Biomarkers, Tumor / Q000378:metabolism*; D018572:Disease-Free Survival; D005260:Female; D006801:Humans; D008875:Middle Aged; D010641:Phenotype; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000378:metabolism*; D011960:Receptors, Estrogen / Q000378:metabolism; D011980:Receptors, Progesterone / Q000378:metabolism; D012189:Retrospective Studies; D013125:Spinal Neoplasms / Q000401:mortality* / Q000556:secondary*; D064726:Triple Negative Breast Neoplasms / Q000378:metabolism* / Q000401:mortality* / Q000473:pathology
chemical_list: D014408:Biomarkers, Tumor; D018719:Erb-b2 Receptor Tyrosine Kinases; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; C508053:ERBB2 protein, human