Lena Claesson-Welsh

ORCID iD
orcid.org/0000-0003-4275-2000
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Lena Welsh

Sources:
Lena Claesson-Welsh (2015-02-08)

  • Country
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Sweden

Sources:
Lena Claesson-Welsh (2016-01-24)

  • Keywords
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Angiogenesis, signal transduction, VEGF, FGF, PDGF, cancer, permeability, development

Sources:
Lena Claesson-Welsh (2015-02-08)

Biography

Lena Claesson-Welsh is a Professor in Medical Biochemistry at Uppsala University, Sweden. Her undergraduate training was in medicine, at Uppsala University. The PhD training, also at Uppsala University, was supervised by Dr. Per A. Peterson, and concerned the structure and function of class II histocompatibility antigens. She went on to a postdoc position with Dr. Patricia Spear at the University of Chicago, focusing on herpes simplex virus glycoproteins. She returned to the Ludwig Institute for Cancer Research in Uppsala, to work with Dr. Carl-Henrik Heldin on the structure/function of growth factors/receptors on mesenchymal cells, such PDGF and FGF and their receptors. She cloned several growth factor receptors, and identified signal transduction pathways regulating different biological responses to PDGF and FGF. She spent several sabbatical periods with Dr. Judah Folkman, Harvard Medical School in Boston, working on angiogenesis inhibitors and development of therapies aimed to suppress tumor vascularization and growth. Lena Claesson-Welsh´s group at Uppsala University is now focusing on the mechanism of action of angiogenic growth factors, in particular vascular endothelial growth factors (VEGFs). Her group has mapped tyrosine phosphorylation site in the three VEGF receptors. The group is now following this up by replacing potential tyrosine phosphorylation site residues with phenylalanine residues in the VEGF receptors in mice. A particular interest is to identify the signal transduction pathway that regulates permeability downstream of VEGF. The group has moreover identified an endogenous regulator, histidine-rich glycoprotein (HRG), which regulates the phenotype of inflammatory cells by promoting a switch from M2 to M1 in macrophages. HRG suppresses primary tumor growth but more importantly, efficiently inhibits tumor spread.
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