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549 results on '"Kähäri, Veli-Matti"'

6. Immunomodulatory Synthetic Glycocluster Molecule Prevents Melanoma Growth in vivo

Author

Honkanen, Meija, primary, Narvi, Elli, additional, Ojala, Veera, additional, Jokilammi, Anne, additional, Rantakari, Pia, additional, Kronqvist, Pauliina, additional, Kähäri, Veli-Matti, additional, Veräjänkorva, Esko, additional, Kurppa, Kari J, additional, Rahkila, Jani, additional, Ekambaram, Ramesh, additional, Savolainen, Johannes, additional, Leino, Reko, additional, and Elenius, Klaus, additional

Published
2024
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7. Cancer‐associated fibroblast activation predicts progression, metastasis, and prognosis of cutaneous squamous cell carcinoma.

Author

Knuutila, Jaakko S., Riihilä, Pilvi, Nissinen, Liisa, Heiskanen, Lauri, Kallionpää, Roosa E., Pellinen, Teijo, and Kähäri, Veli‐Matti

Subjects
SQUAMOUS cell carcinoma, SKIN cancer, PROGNOSIS, PLATELET-derived growth factor, METASTASIS, FIBROBLASTS
Abstract

Cutaneous squamous cell carcinoma (cSCC) is the most common metastatic skin cancer and the metastatic disease is associated with poor prognosis. Cancer‐associated fibroblasts (CAFs) promote progression of cancer, but their role in cSCC is largely unknown. We examined the potential of CAF markers in the assessment of metastasis risk and prognosis of primary cSCC. We utilized multiplexed fluorescence immunohistochemistry for profiling CAF landscape in metastatic and non‐metastatic primary human cSCCs, in metastases, and in premalignant epidermal lesions. Quantitative high‐resolution image analysis was performed with two separate panels of antibodies for CAF markers and results were correlated with clinical and histopathological parameters including disease‐specific mortality. Increased stromal expression of fibroblast activation protein (FAP), α‐smooth muscle actin, and secreted protein acidic and rich in cysteine (SPARC) were associated with progression to invasive cSCC. Elevation of FAP and platelet‐derived growth factor receptor‐β (PDGFRβ) expression was associated with metastasis risk of primary cSCCs. High expression of PDGFRβ and periostin correlated with poor prognosis. Multimarker combination defined CAF subset, PDGFRα−/PDGFRβ+/FAP+, was associated with invasion and metastasis, and independently predicted poor disease‐specific survival. These results identify high PDGFRβ expression alone and multimarker combination PDGFRα−/PDGFRβ+/FAP+ by CAFs as potential biomarkers for risk of metastasis and poor prognosis. [ABSTRACT FROM AUTHOR]

Published
2024
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8. Consensus statement on the diagnosis and treatment of sclerosing diseases of the skin, Part 2: Scleromyxoedema and scleroedema.

Author

Knobler, Robert, Geroldinger‐Simić, Marija, Kreuter, Alexander, Hunzelmann, Nicolas, Moinzadeh, Pia, Rongioletti, Franco, Denton, Christopher, Mouthon, Luc, Cutolo, Maurizio, Smith, Vanessa, Gabrielli, Armando, Bagot, Martine, Olesen, Anne B., Foeldvari, Ivan, Jalili, Ahmad, Kähäri, Veli Matti, Kárpáti, Sarolta, Kofoed, Kristian, Olszewska, Malgorzata, and Panelius, Jaana

Subjects
SKIN diseases, THERAPEUTICS, DIAGNOSIS, DIFFERENTIAL diagnosis, MEDICAL personnel
Abstract

The term 'sclerosing diseases of the skin' comprises specific dermatological entities, which have fibrotic changes of the skin in common. These diseases mostly manifest in different clinical subtypes according to cutaneous and extracutaneous involvement and can sometimes be difficult to distinguish from each other. The present consensus provides an update to the 2017 European Dermatology Forum Guidelines, focusing on characteristic clinical and histopathological features, diagnostic scores and the serum autoantibodies most useful for differential diagnosis. In addition, updated strategies for the first‐ and advanced‐line therapy of sclerosing skin diseases are addressed in detail. Part 2 of this consensus provides clinicians with an overview of the diagnosis and treatment of scleromyxoedema and scleroedema (of Buschke). [ABSTRACT FROM AUTHOR]

Published
2024
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12. Long noncoding RNA plasmacytoma variant translocation 1 is overexpressed in cutaneous squamous cell carcinoma and exon 2 is critical for its oncogenicity

Author

Li, Chen, primary, Sun, Chengxi, additional, Mahapatra, Kunal Das, additional, Riihilä, Pilvi, additional, Knuutila, Jaakko, additional, Nissinen, Liisa, additional, Lapins, Jan, additional, Kähäri, Veli-Matti, additional, Homey, Bernhard, additional, Sonkoly, Enikö, additional, and Pivarcsi, Andor, additional

Published
2023
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13. Long noncoding RNA plasmacytoma variant translocation 1 is overexpressed in cutaneous squamous cell carcinoma and exon 2 is critical for its oncogenicity.

Author

Li, Chen, Sun, Chengxi, Mahapatra, Kunal Das, Riihilä, Pilvi, Knuutila, Jaakko, Nissinen, Liisa, Lapins, Jan, Kähäri, Veli-Matti, Homey, Bernhard, Sonkoly, Enikö, and Pivarcsi, Andor

Subjects
LINCRNA, CYCLIN-dependent kinases, REVERSE transcriptase polymerase chain reaction, SQUAMOUS cell carcinoma, SYNCRIP protein, NUCLEIC acids, CYCLIN-dependent kinase inhibitors, CYCLIN-dependent kinase inhibitor-2A, CELL cycle
Abstract

Background Cutaneous squamous cell carcinoma (cSCC) is one of the most common and fastest increasing forms of cancer worldwide with metastatic potential. Long noncoding RNAs (lncRNAs) are a group of RNA molecules with essential regulatory functions in both physiological and pathological processes. Objectives To investigate the function and mode of action of lncRNA plasmacytoma variant translocation 1 (PVT1) in cSCC. Methods Quantitative reverse transcriptase polymerase chain reaction and single-molecule in situ hybridization were used to quantify the expression level of PVT1 in normal skin, premalignant skin lesions, actinic keratosis (AK) and primary and metastatic cSCCs. The function of PVT1 in cSCC was investigated both in vivo (tumour xenografts) and in vitro (competitive cell growth assay, 5-ethynyl-2′-deoxyuridine incorporation assay, colony formation assay and tumour spheroid formation assay) upon CRISPR-Cas9-mediated knockout of the entire PVT1 locus, the knockout of exon 2 of PVT1 , and locked nucleic acid (LNA) gapmer-mediated PVT1 knockdown. RNA sequencing analysis was conducted to identify genes and processes regulated by PVT1. Results We identified PVT1 as a lncRNA upregulated in cSCC in situ and cSCC, associated with the malignant phenotype of cSCC. We showed that the expression of PVT1 in cSCC was regulated by MYC. Both CRISPR-Cas9 deletion of the entire PVT1 locus and LNA gapmer-mediated knockdown of PVT1 transcript impaired the malignant behaviour of cSCC cells, suggesting that PVT1 is an oncogenic transcript in cSCC. Furthermore, knockout of PVT1 exon 2 inhibited cSCC tumour growth both in vivo and in vitro , demonstrating that exon 2 is a critical element for the oncogenic role of PVT1. Mechanistically, we showed that PVT1 was localized in the cell nucleus and its deletion resulted in cellular senescence, increased cyclin-dependent kinase inhibitor 1 (p21/CDKN1A) expression and cell cycle arrest. Conclusions Our study revealed a previously unrecognized role for exon 2 of PVT1 in its oncogenic role and that PVT1 suppresses cellular senescence in cSCC. PVT1 may be a potential biomarker and therapeutic target in cSCC. [ABSTRACT FROM AUTHOR]

Published
2024
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16. Supplementary Table S1 from Senescence Sensitivity of Breast Cancer Cells Is Defined by Positive Feedback Loop between CIP2A and E2F1

Author

Laine, Anni, primary, Sihto, Harri, primary, Come, Christophe, primary, Rosenfeldt, Mathias T., primary, Zwolinska, Aleksandra, primary, Niemelä, Minna, primary, Khanna, Anchit, primary, Chan, Edward K., primary, Kähäri, Veli-Matti, primary, Kellokumpu-Lehtinen, Pirkko-Liisa, primary, Sansom, Owen J., primary, Evan, Gerard I., primary, Junttila, Melissa R., primary, Ryan, Kevin M., primary, Marine, Jean-Christophe, primary, Joensuu, Heikki, primary, and Westermarck, Jukka, primary

Published
2023
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17. Supplementary Methods from Senescence Sensitivity of Breast Cancer Cells Is Defined by Positive Feedback Loop between CIP2A and E2F1

Author

Laine, Anni, primary, Sihto, Harri, primary, Come, Christophe, primary, Rosenfeldt, Mathias T., primary, Zwolinska, Aleksandra, primary, Niemelä, Minna, primary, Khanna, Anchit, primary, Chan, Edward K., primary, Kähäri, Veli-Matti, primary, Kellokumpu-Lehtinen, Pirkko-Liisa, primary, Sansom, Owen J., primary, Evan, Gerard I., primary, Junttila, Melissa R., primary, Ryan, Kevin M., primary, Marine, Jean-Christophe, primary, Joensuu, Heikki, primary, and Westermarck, Jukka, primary

Published
2023
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18. Data from Senescence Sensitivity of Breast Cancer Cells Is Defined by Positive Feedback Loop between CIP2A and E2F1

Author

Laine, Anni, primary, Sihto, Harri, primary, Come, Christophe, primary, Rosenfeldt, Mathias T., primary, Zwolinska, Aleksandra, primary, Niemelä, Minna, primary, Khanna, Anchit, primary, Chan, Edward K., primary, Kähäri, Veli-Matti, primary, Kellokumpu-Lehtinen, Pirkko-Liisa, primary, Sansom, Owen J., primary, Evan, Gerard I., primary, Junttila, Melissa R., primary, Ryan, Kevin M., primary, Marine, Jean-Christophe, primary, Joensuu, Heikki, primary, and Westermarck, Jukka, primary

Published
2023
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19. Supplementary Figure 3 from Senescence Sensitivity of Breast Cancer Cells Is Defined by Positive Feedback Loop between CIP2A and E2F1

Author

Laine, Anni, primary, Sihto, Harri, primary, Come, Christophe, primary, Rosenfeldt, Mathias T., primary, Zwolinska, Aleksandra, primary, Niemelä, Minna, primary, Khanna, Anchit, primary, Chan, Edward K., primary, Kähäri, Veli-Matti, primary, Kellokumpu-Lehtinen, Pirkko-Liisa, primary, Sansom, Owen J., primary, Evan, Gerard I., primary, Junttila, Melissa R., primary, Ryan, Kevin M., primary, Marine, Jean-Christophe, primary, Joensuu, Heikki, primary, and Westermarck, Jukka, primary

Published
2023
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20. Supplementary Figure 4 from Senescence Sensitivity of Breast Cancer Cells Is Defined by Positive Feedback Loop between CIP2A and E2F1

Author

Laine, Anni, primary, Sihto, Harri, primary, Come, Christophe, primary, Rosenfeldt, Mathias T., primary, Zwolinska, Aleksandra, primary, Niemelä, Minna, primary, Khanna, Anchit, primary, Chan, Edward K., primary, Kähäri, Veli-Matti, primary, Kellokumpu-Lehtinen, Pirkko-Liisa, primary, Sansom, Owen J., primary, Evan, Gerard I., primary, Junttila, Melissa R., primary, Ryan, Kevin M., primary, Marine, Jean-Christophe, primary, Joensuu, Heikki, primary, and Westermarck, Jukka, primary

Published
2023
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21. Supplementary Figure 2 from Senescence Sensitivity of Breast Cancer Cells Is Defined by Positive Feedback Loop between CIP2A and E2F1

Author

Laine, Anni, primary, Sihto, Harri, primary, Come, Christophe, primary, Rosenfeldt, Mathias T., primary, Zwolinska, Aleksandra, primary, Niemelä, Minna, primary, Khanna, Anchit, primary, Chan, Edward K., primary, Kähäri, Veli-Matti, primary, Kellokumpu-Lehtinen, Pirkko-Liisa, primary, Sansom, Owen J., primary, Evan, Gerard I., primary, Junttila, Melissa R., primary, Ryan, Kevin M., primary, Marine, Jean-Christophe, primary, Joensuu, Heikki, primary, and Westermarck, Jukka, primary

Published
2023
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22. Supplementary Figure 1 from Senescence Sensitivity of Breast Cancer Cells Is Defined by Positive Feedback Loop between CIP2A and E2F1

Author

Laine, Anni, primary, Sihto, Harri, primary, Come, Christophe, primary, Rosenfeldt, Mathias T., primary, Zwolinska, Aleksandra, primary, Niemelä, Minna, primary, Khanna, Anchit, primary, Chan, Edward K., primary, Kähäri, Veli-Matti, primary, Kellokumpu-Lehtinen, Pirkko-Liisa, primary, Sansom, Owen J., primary, Evan, Gerard I., primary, Junttila, Melissa R., primary, Ryan, Kevin M., primary, Marine, Jean-Christophe, primary, Joensuu, Heikki, primary, and Westermarck, Jukka, primary

Published
2023
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23. Supplementary Figure 5 from Senescence Sensitivity of Breast Cancer Cells Is Defined by Positive Feedback Loop between CIP2A and E2F1

Author

Laine, Anni, primary, Sihto, Harri, primary, Come, Christophe, primary, Rosenfeldt, Mathias T., primary, Zwolinska, Aleksandra, primary, Niemelä, Minna, primary, Khanna, Anchit, primary, Chan, Edward K., primary, Kähäri, Veli-Matti, primary, Kellokumpu-Lehtinen, Pirkko-Liisa, primary, Sansom, Owen J., primary, Evan, Gerard I., primary, Junttila, Melissa R., primary, Ryan, Kevin M., primary, Marine, Jean-Christophe, primary, Joensuu, Heikki, primary, and Westermarck, Jukka, primary

Published
2023
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25. Long noncoding RNA plasmacytoma variant translocation 1 is overexpressed in cutaneous squamous cell carcinoma and exon 2 is critical for its oncogenicity

Author

Li, Chen, Sun, Chengxi, Mahapatra, Kunal Das, Riihilä, Pilvi, Knuutila, Jaakko, Nissinen, Liisa, Lapins, Jan, Kähäri, Veli-Matti, Homey, Bernhard, Sonkoly, Enikö, Pivarcsi, Andor, Li, Chen, Sun, Chengxi, Mahapatra, Kunal Das, Riihilä, Pilvi, Knuutila, Jaakko, Nissinen, Liisa, Lapins, Jan, Kähäri, Veli-Matti, Homey, Bernhard, Sonkoly, Enikö, and Pivarcsi, Andor

Abstract

Background Cutaneous squamous cell carcinoma (cSCC) is one of the most common and fastest increasing forms of cancer worldwide with metastatic potential. Long noncoding RNAs (lncRNAs) are a group of RNA molecules with essential regulatory functions in both physiological and pathological processes. Objectives To investigate the function and mode of action of lncRNA plasmacytoma variant translocation 1 (PVT1) in cSCC. Methods Quantitative reverse transcriptase polymerase chain reaction and single-molecule in situ hybridization were used to quantify the expression level of PVT1 in normal skin, premalignant skin lesions, actinic keratosis (AK) and primary and metastatic cSCCs. The function of PVT1 in cSCC was investigated both in vivo (tumour xenografts) and in vitro (competitive cell growth assay, 5-ethynyl-2′-deoxyuridine incorporation assay, colony formation assay and tumour spheroid formation assay) upon CRISPR-Cas9-mediated knockout of the entire PVT1 locus, the knockout of exon 2 of PVT1, and locked nucleic acid (LNA) gapmer-mediated PVT1 knockdown. RNA sequencing analysis was conducted to identify genes and processes regulated by PVT1. Results We identified PVT1 as a lncRNA upregulated in cSCC in situ and cSCC, associated with the malignant phenotype of cSCC. We showed that the expression of PVT1 in cSCC was regulated by MYC. Both CRISPR-Cas9 deletion of the entire PVT1 locus and LNA gapmer-mediated knockdown of PVT1 transcript impaired the malignant behaviour of cSCC cells, suggesting that PVT1 is an oncogenic transcript in cSCC. Furthermore, knockout of PVT1 exon 2 inhibited cSCC tumour growth both in vivo and in vitro, demonstrating that exon 2 is a critical element for the oncogenic role of PVT1. Mechanistically, we showed that PVT1 was localized in the cell nucleus and its deletion resulted in cellular senescence, increased cyclin-dependent kinase inhibitor 1 (p21/CDKN1A) expression and cell cycle arrest. Conclusions Our study revealed a previously unrecogni, Correction in: British Journal of Dermatology, ljae157DOI: 10.1093/bjd/ljae157

Published
2023
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26. Supplementary information from Discovery of a Novel CIP2A Variant (NOCIVA) with Clinical Relevance in Predicting TKI Resistance in Myeloid Leukemias

Author

Mäkelä, Eleonora, primary, Pavic, Karolina, primary, Varila, Taru, primary, Salmenniemi, Urpu, primary, Löyttyniemi, Eliisa, primary, Nagelli, Srikar G., primary, Ammunét, Tea, primary, Kähäri, Veli-Matti, primary, Clark, Richard E., primary, Elo, Laura L., primary, Bachanaboyina, Venkata Kumari, primary, Lucas, Claire M., primary, Itälä-Remes, Maija, primary, and Westermarck, Jukka, primary

Published
2023
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45. Retrospective, Registry-based, Cohort Investigation of Clinical Outcomes in Patients with Cutaneous Squamous Cell Carcinoma and Basal Cell Carcinoma in Finland

Author

Tuominen, Samuli, primary, Ukkola-Vuoti, Liisa, additional, Riihilä, Pilvi, additional, Knuutila, Jaakko S., additional, Kähäri, Veli-Matti, additional, Lassenius, Mariann, additional, Ranki, Tuuli, additional, Pousar, Katariina, additional, Vassilev, Lotta, additional, Vuoti, Sauli, additional, and Mattila, Kalle, additional

Published
2022
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50. Collagens XV and XVIII show different expression and localisation in cutaneous squamous cell carcinoma: type XV appears in tumor stroma, while XVIII becomes upregulated in tumor cells and lost from microvessels

Author

Karppinen, Sanna-Maria, Honkanen, Hanne-Kaisa, Heljasvaara, Ritva, Riihilä, Pilvi, Autio-Harmainen, Helena, Sormunen, Raija, Harjunen, Vanessa, Väisänen, Marja-Riitta, Väisänen, Timo, Hurskainen, Tiina, Tasanen, Kaisa, Kähäri, Veli-Matti, and Pihlajaniemi, Taina

Published
2016
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