Molecular mechanisms of tumor-stroma interaction - Pasonen-Seppänen lab

Refine your search

Research group

01.01.2021 -

Institute of Biomedicine, School of Medicine, Faculty of Health Sciences

Information People Publications

Leaders

Sanna Pasonen-Seppänen

Senior University Lecturer

Institute of Biomedicine, School of Medicine, Faculty of Health Sciences

Pasonen-Seppänen lab

The focus of our research is on tumor microenvironment (TME). Our overall goal is to elucidate how stromal cells, like fibroblasts and immune cells, and extracellular matrix molecules like hyaluronan affect melanoma progression and ICI-therapy (immune check point inhibitor) response. We are interested in tumor immunology, the role of macrophages and FoxP3+ regulatory T-cells in the formation of immunosuppressive TME in melanoma. The role of immune cells in tumor dissemination is well established yet the mechanisms that recruit the immune cells and regulate their function in the TME are poorly understood at the moment and are the targets of our research. In addition, we are seeking for new prognostic and predictive biomarkers for melanoma.

News

Inflammatory cells in tumour microenvironment promote the transformation of prostate cancer cells into treatment-resistant cells

Inflammatory cells in tumour microenvironment promote the transformation of prostate cancer cells into treatment-resistant cells
The 16th FCI Symposium 26.-27.9.2024 - Future of Clinical Decision Making

The 16th FCI Symposium 26.-27.9.2024 - Future of Clinical Decision Making
Cancer and Extracellular vesicles summer school 1.-2.6.2022

Cancer and Extracellular vesicles summer school 1.-2.6.2022

Cooperation

Kirsi Ketola

UEF
Carol de la Motte

Lerner Research Institute, Cleveland Clinic, Cleveland, USA
Kirsi Rilla

UEF
Multidisciplinary Cancer Research (CANCER) -Research community

UEF, Faculty of Health Sciences
Aino Rönkä

Kuopio University Hospital
Einari Niskanen

UEF
Ahmed Al-Samadi

University of Helsinki
Anthony Day

University of Manchester

Keywords

biomarker cancer ekstracellular matrix extracellular vesicle hyaluronan immunotherapy macrophage melanoma pro-tumor inflammation tumor microenvironment tumor-stroma interaction

Leaders

Sanna Pasonen-Seppänen

Senior University Lecturer

Institute of Biomedicine, School of Medicine, Faculty of Health Sciences

Senior Researchers

Sanna Oikari

University Teacher

Institute of Biomedicine, School of Medicine, Faculty of Health Sciences

Doctoral Researchers

Technicians

Taina Vihavainen

Senior Laboratory Technician

Institute of Biomedicine, School of Medicine, Faculty of Health Sciences

Supporting Staff

Taisto Kuosmanen

Project Controller

Financial Services, University Services

Other group members

Satu Salmi Satu.Salmi@uef.fi
Otto Jokelainen Otto.Jokelainen@kuh.fi
Amanda Dafoe adafoe@student.uef.fi
Veera Nurmela vnurmela@student.uef.fi

Publications

38 items

Refine your search

Molecular mechanisms of tumor-stroma interaction - Pasonen-Seppänen lab

Leaders

Sanna Pasonen-Seppänen

News

Inflammatory cells in tumour microenvironment promote the transformation of prostate cancer cells into treatment-​resistant cells

The 16th FCI Symposium 26.-27.9.2024 - Future of Clinical Decision Making

Cancer and Extracellular vesicles summer school 1.-2.6.2022

Cooperation

Keywords

Leaders

Sanna Pasonen-Seppänen

Senior Researchers

Sanna Oikari

Doctoral Researchers

Kirsi Kainulainen

Kaisa Mäki-Mantila

Technicians

Taina Vihavainen

Supporting Staff

Taisto Kuosmanen

Other group members

Differential expression analysis identifies a prognostically significant extracellular matrix–enriched gene signature in hyaluronan-positive clear cell renal cell carcinoma

Expression of Programmed Death Ligand 1 and Indoleamine 2,3‐Dioxygenase in Oral Lichen Planus and Oral Lichenoid Lesions

Oncogenic KEAP1 mutations activate TRAF2-NFκB signaling to prevent apoptosis in lung cancer cells

Secreted factors from M1 macrophages drive prostate cancer stem cell plasticity by upregulating NANOG, SOX2, and CD44 through NFκB-signaling

A practical prognostic peripheral blood-based risk model for the evaluation of the likelihood of a response and survival of metastatic cancer patients treated with immune checkpoint inhibitors

Irradiation Alters the Expression of MUC1, CD44 and Hyaluronan in Oral Mucosal Epithelium

M1 Macrophages Induce Protumor Inflammation in Melanoma Cells through TNFR–NF-κB Signaling

The Association of CD8+ Cytotoxic T Cells and Granzyme B+ Lymphocytes with Immunosuppressive Factors, Tumor Stage and Prognosis in Cutaneous Melanoma

The Impact of Hyaluronan on Tumor Progression in Cutaneous Melanoma

The calcium-activated chloride channel-associated protein rCLCA2 is expressed throughout rat epidermis, facilitates apoptosis and is downmodulated by UVB

The role of FoxP3+ regulatory T cells and IDO+ immune and tumor cells in malignant melanoma - an immunohistochemical study

Cellular hyaluronan is associated with a poor prognosis in renal cell carcinoma

High-Resolution Confocal Fluorescence Imaging of Serine Hydrolase Activity in Cryosections - Application to Glioma Brain Unveils Activity Hotspots Originating from Tumor-Associated Neutrophils

Activated hyaluronan metabolism in the tumor matrix - Causes and consequences

Alterations in the expression of EMT-related proteins claudin-1, -4 and -7, E-cadherin, TWIST1 and ZEB1 in oral lichen planus

HAS3-induced extracellular vesicles from melanoma cells stimulate IHH mediated c-Myc upregulation via the hedgehog signaling pathway in target cells

Melanocyte hyaluronan coat fragmentation enhances the UVB-induced TLR-4 receptor signaling and expression of proinflammatory mediators IL-6, IL-8, CXCL-1 and CXCL-10 via NF-κB activation

Nrf2 and SQSTM1/p62 jointly contribute to mesenchymal transition and invasion in glioblastoma

Elevated expression of hyaluronan synthase 2 associates with decreased survival in diffusely infiltrating astrocytomas

Extracellular ATP activates hyaluronan synthase 2 (HAS2) in epidermal keratinocytes via P2Y2, Ca2+-signaling, and MAPK pathways

Hyaluronan metabolism enhanced during epidermal differentiation is suppressed by vitamin C

The number and localization of CD68+ and CD163+ macrophages in different stages of cutaneous melanoma

Design, Synthesis, and Biological Evaluation of 2,4-Dihydropyrano[2,3-c]pyrazole Derivatives as Autotaxin Inhibitors

Human Keratinocytes Respond to Extracellular UTP by Induction of Hyaluronan Synthase 2 Expression and Increased Hyaluronan Synthesis

Decreased expression of hyaluronan synthase 1 and 2 associates with poor prognosis in cutaneous melanoma

Decreased hyaluronidase 1 expression is associated with early disease recurrence in human endometrial cancer

Hyaluronan synthase 1: a mysterious enzyme with unexpected functions

Hyaluronan synthase 3 (HAS3) overexpression downregulates MV3 melanoma cell proliferation, migration and adhesion

Low numbers of tryptase+ and chymase+ mast cells associated with reduced survival and advanced tumor stage in melanoma

The organic osmolyte betaine induces keratin 2 expression in rat epidermal keratinocytes - a genome-wide study in UVB irradiated organotypic 3D cultures

Altered expression of hyaluronan, HAS1-2, and HYAL1-2 in oral lichen planus

Synthesis, in vitro and in vivo evaluation of 1,3,5-triazines as cannabinoid CB2 receptor agonists

rClca2 is associated with epidermal differentiation and is strongly downregulated by ultraviolet radiation

Hyaluronan production enhances shedding of plasma membrane-derived microvesicles

Inverse expression of hyaluronidase 2 and hyaluronan synthases 1-3 is associated with reduced hyaluronan content in malignant cutaneous melanoma

Low Dose Ultraviolet B Irradiation Increases Hyaluronan Synthesis in Epidermal Keratinocytes via Sequential Induction of Hyaluronan Synthases Has1-3 Mediated by p38 and Ca2+/Calmodulin-dependent Protein Kinase II (CaMKII) Signaling

Mannose reduces hyaluronan and leukocytes in wound granulation tissue and inhibits migration and hyaluronan-dependent monocyte binding

Melanoma cell-derived factors stimulate hyaluronan in dermal fibroblasts by upregulating HAS2 through PDGFR-PI3K_AKT and p38 -signaling

Inflammatory cells in tumour microenvironment promote the transformation of prostate cancer cells into treatment-resistant cells