M
Maria Sundvall
Researcher at University of Turku
Publications - 6
Citations - 1038
Maria Sundvall is an academic researcher from University of Turku. The author has contributed to research in topics: ErbB & ERBB4. The author has an hindex of 6, co-authored 6 publications receiving 987 citations. Previous affiliations of Maria Sundvall include University of Miami.
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Journal ArticleDOI
Signaling via ErbB2 and ErbB3 Associates with Resistance and Epidermal Growth Factor Receptor (EGFR) Amplification with Sensitivity to EGFR Inhibitor Gefitinib in Head and Neck Squamous Cell Carcinoma Cells
Kaisa Erjala,Maria Sundvall,Teemu T. Junttila,Na Zhang,Mika Savisalo,Pekka Mali,Jarmo Kulmala,Jaakko Pulkkinen,Reidar Grénman,Klaus Elenius +9 more
TL;DR: EGFR amplification may predict sensitivity to gefitinib in HNSCC, however, other EGFR/ErbB receptor family members than EGFR may contribute to resistance to g EFITinib.
Journal ArticleDOI
Cleavable ErbB4 isoform in estrogen receptor-regulated growth of breast cancer cells.
Teemu T. Junttila,Maria Sundvall,Mikael Lundin,Johan Lundin,Minna Tanner,Pirkko Härkönen,Heikki Joensuu,Jorma Isola,Klaus Elenius +8 more
TL;DR: The results suggest that the association of ErbB4 expression with clinical outcome is dependent on the subcellular localization of ErBB4 and that a proteinase-cleavable Erb B4 isoform promotes growth of ER-positive breast cancer and enhances ER-mediated gene transcription.
Journal Article
Cleavable ErbB4 isoform in estrogen receptor-regulated growth of breast cancer cells
Teemu T. Junttila,Maria Sundvall,Mikael Lundin,Johan Lundin,Minna Tanner,Pirkko Härkönen,Heikki Joensuu,Jorma Isola,Klaus Elenius +8 more
TL;DR: In this article, the authors assessed the clinical significance of the proteolytically cleavable ErbB4 isoforms in breast cancer patients and investigated their functions in vitro.
Journal ArticleDOI
A natural ErbB4 isoform that does not activate phosphoinositide 3-kinase mediates proliferation but not survival or chemotaxis.
Varpu Kainulainen,Maria Sundvall,Jorma A. Määttä,Eric Santiestevan,Michael Klagsbrun,Klaus Elenius +5 more
TL;DR: The results suggest a novel mechanism by which cellular responses such as chemotaxis and survival may be regulated by the expression of alternative receptor-tyrosine kinase isoforms that differ in their coupling to PI3-K signaling.
Journal ArticleDOI
Erbb4 and its isoforms: selective regulation of growth factor responses by naturally occurring receptor variants.
TL;DR: Four naturally occurring receptor variants provide a new level of diversity to the control of growth factor-stimulated cellular responses and may have distinct and specific roles in the regulation of various developmental and pathological processes.