- 2021. The constitutive extracellular protein release by acute myeloid leukemia cells—A proteomic study of patient heterogeneity and its modulation by mesenchymal stromal cells. Cancers. 25 sider.
- 2021. Proteomic comparison of bone marrow derived osteoblasts and mesenchymal stem cells. International Journal of Molecular Sciences.
- 2021. Proteomic Characterization of Spontaneous Stress-Induced In Vitro Apoptosis of Human Acute Myeloid Leukemia Cells; Focus on Patient Heterogeneity and Endoplasmic Reticulum Stress. Hemato. 607-627.
- 2020. The extracellular bone marrow microenvironment — a proteomic comparison of constitutive protein release by in vitro cultured osteoblasts and mesenchymal stem cells. Cancers.
- 2020. Stathmin expression associates with vascular and immune responses in aggressive breast cancer subgroups. Scientific Reports. 14 sider.
- 2019. PIK3CA amplification associates with aggressive phenotype but not markers of AKT-mTOR signaling in endometrial carcinoma. Clinical Cancer Research. 334-345.
- 2017. PIK3CA exon9 mutations associate with reduced survival, and are highly concordant between matching primary tumors and metastases in endometrial cancer. Scientific Reports. 1-12.
- 2017. Expression of Nestin associates with BRCA1 mutations, a basal-like phenotype and aggressive breast cancer. Scientific Reports. 1-12.
- 2015. Tumor necrosis is an important hallmark of aggressive endometrial cancer and associates with hypoxia, angiogenesis and inflammation responses. OncoTarget. 39676-39691.
- 2014. Stathmin Protein Level, a Potential Peredictive Marker for Taxane Treatment Response in Endometrial Cancer. PLOS ONE.
- 2014. Endometrial Carcinoma Recurrence Score (ECARS) validates to identify aggressive disease and associates with markers of epithelial-mesenchymal transition and PI3K alterations. Gynecologic Oncology. 599-606.
- 2013. Lack of estrogen receptor-alpha is associated with epithelial-mesenchymal transition and PI3K alterations in endometrial carcinoma. Clinical Cancer Research. 1094-1105.
- 2013. Integrated genomic analysis of the 8q24 amplification in endometrial cancers identifies ATAD2 as essential to MYC-dependent cancers. PLOS ONE. 9 sider.
- 2013. High phospho-stathmin(Serine38) expression identifies aggressive endometrial cancer and suggests an association with PI3K inhibition. Clinical Cancer Research. 2331-2341.
- 2013. ARID1A loss is prevalent in endometrial hyperplasia with atypia and low-grade endometrioid carcinomas. Modern Pathology. 428-434.
- 2012. Loss of GPER identifies new targets for therapy among a subgroup of ER alpha-positive endometrial cancer patients with poor outcome. British Journal of Cancer. 1682-1688.
- 2012. KRAS gene amplification and overexpression but not mutation associates with aggressive and metastatic endometrial cancer. British Journal of Cancer. 1997-2004.
- 2012. High-throughput mutation profiling of primary and metastatic endometrial cancers identifies KRAS, FGFR2 and PIK3CA to be frequently mutated. PLOS ONE.
- 2009. Epac-induced Alterations in the Proteome of Human SH-SY5Y Neuroblastoma Cells. Journal of Proteomics & Bioinformatics. 244-245.
- 2012. Stratification based on high tumour cell content in fresh frozen tissue promotes selection of aggressive endometrial carcinomas. Histopathology. 516-519.
- 2008. Quantitative proteomics of Epac signaling in differentiating human SH-SY5Y neuroblastoma cells.
- 2013. Mutations and gene amplifications in Endometrial Carcinomas. “Clinical characteristics and potential targets for therapyrelated to KRAS, MYC, ATAD2, PIK3CA and FGFR2 alterations.
- 2009. Epac-induced changes in the proteome of human SH-SY5Y neuroblastoma cells.