Göran Andersson
Professor Emeritus
E-postadress: goran.andersson@ki.se
Telefon: +46852483860
Besöksadress: Nobels väg 7, 17165 Solna
Postadress: H5 Laboratoriemedicin, H5 Patologi, 141 52 Huddinge
Artiklar
- Article: JBMR PLUS. 2025;9(7):ziaf073Rathod B; Samvelyan HJ; Desai S; Bock L; Gustafsson N; Wu J; Ohlsson C; Magnusson P; Andersson G; Windahl SH
- Article: AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY. 2025;328(4):L497-L511Willems SH; Qian S; Lang P; Overtoom BE; Alimostafazadeh S; Fuentes-Mateos R; Vasse GF; van der Veen TA; Vlasma J; de Jager MH; Guryev V; Fejer G; Andersson G; Melgert BN
- Article: BONE. 2024;188:117223Rathod B; Desai S; Samvelyan HJ; Bock L; Wu J; Ohlsson C; Palmquist A; Alm JJ; Newton PT; Andersson G; Windahl SH
- Article: IMMUNOLOGY. 2024;171(4):583-594Bergwik J; Bhongir RKV; Padra M; Adler A; Olm F; Lang P; Lindstedt S; Andersson G; Egesten A; Tanner L
- Article: BONE REPORTS. 2023;19:101697Desai S; Lang P; Nareoja T; Windahl SH; Andersson G
- Article: FRONTIERS IN IMMUNOLOGY. 2022;13:1079775Tanner L; Bergwik J; Bhongir RKV; Puthia M; Lang P; Ali MN; Welinder C; Onnerfjord P; Erjefalt JS; Palmberg L; Andersson G; Egesten A
- Article: FEBS LETTERS. 2021;595(20):2616-2627Lang P; Patlaka C; Andersson G
- Article: EATING AND WEIGHT DISORDERS-STUDIES ON ANOREXIA BULIMIA AND OBESITY. 2020;25(5):1387-1397Patlaka C; Tubic B; Lang P; Paulie S; Swolin-Eide D; Magnusson P; Andersson G
- Article: BMC MOLECULAR AND CELL BIOLOGY. 2020;21(1):15Reithmeier A; Norgard M; Ek-Rylander B; Nareoja T; Andersson G
- Article: CALCIFIED TISSUE INTERNATIONAL. 2020;106(2):194-207Mira-Pascual L; Patlaka C; Desai S; Paulie S; Nareoja T; Lang P; Andersson G
- Article: SCIENTIFIC REPORTS. 2020;10(1):1451Eremo AG; Lagergren K; Othman L; Montgomery S; Andersson G; Tina E
- Article: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES. 2020;21(2):E538-538Mira-Pascual L; Tran AN; Andersson G; Nareoja T; Lang P
- Article: JOURNAL OF CELLULAR PHYSIOLOGY. 2019;234(9):16503-16516Amirhosseini M; Bernhardsson M; Lang P; Andersson G; Flygare J; Fahlgren A
- Article: JOURNAL OF CELLULAR AND MOLECULAR MEDICINE. 2019;23(2):1152-1163Kats A; Gerasimcik N; Nareoja T; Nederberg J; Grenlov S; Lagnohed E; Desai S; Andersson G; Yucel-Lindberg T
- Article: BONE REPORTS. 2018;9:27-36Lind T; Lugano R; Gustafson A-M; Norgård M; van Haeringen A; Dimberg A; Melhus H; Robertson SP; Andersson G
- Article: HELIYON. 2018;4(9):e00780Kylmaoja E; Nakamura M; Turunen S; Patlaka C; Andersson G; Lehenkari P; Tuukkanen J
- Article: BONE. 2018;112:10-18Bergstrom I; Isaksson H; Koskela A; Tuukkanen J; Ohlsson C; Andersson G; Windahl SH
- Article: CHEMICAL BIOLOGY & DRUG DESIGN. 2018;92(1):1255-1271Reithmeier A; Lundback T; Haraldsson M; Frank M; Ek-Rylander B; Nyholm P-G; Gustavsson A-L; Andersson G
- Article: BONE REPORTS. 2017;7:17-25Amirhosseini M; Andersson G; Aspenberg P; Fahlgren A
- Article: BIOMARKERS. 2017;22(8):764-774Patlaka C; Pascual LM; Paulie S; Henriksson A-F; Arner P; Lang P; Andersson G
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Alla övriga publikationer
- Corrigendum: OSTEOPOROSIS INTERNATIONAL. 2018;29(9):2161Bergstrom I; Kerns JG; Tornqvist AE; Perdikouri C; Mathavan N; Koskela A; Henriksson HB; Tuukkanen J; Andersson G; Isaksson H; Goodship AE; Windahl SH
- Corrigendum: BONE. 2012;50(5):1205Lind T; Lind PM; Jacobson A; Hu L; Sundqvist A; Risteli J; Yebra-Rodriguez A; Larsson S; Rodriguez-Navarro A; Andersson G; Melhus H
- Meeting abstract: BONE. 2009;44:S155Robertson-Remen KM; Nilsson ME; Gustafsson JA; Andersson G
- Published conference paper: JOURNAL OF BONE AND MINERAL RESEARCH. 2003;18(10):1912-1915Andersson G; Ek-Rylander B; Hollberg K; Ljusberg-Sjölander J; Lång P; Norgård M; Wang YL; Zhang SJ
- Review: TRENDS IN ENDOCRINOLOGY AND METABOLISM. 2002;13(5):195-200Windahl SH; Andersson G; Gustafsson J
- Review: PHYSIOLOGICAL REVIEWS. 2001;81(4):1535-1565Nilsson S; Mäkelä S; Treuter E; Tujague M; Thomsen J; Andersson G; Enmark E; Pettersson K; Warner M; Gustafsson J
- Published conference paper: JOURNAL OF INFECTIOUS DISEASES. 2000;182(6):1756-1760Halasz R; Sällberg M; Lundholm S; Andersson G; Lager B; Glaumann H; Weiland O
- Published conference paper: CONNECTIVE TISSUE RESEARCH. 1996;35(1-4):163-171Andersson G; Johansson EK
- Published conference paper: ANNALS OF THE NEW YORK ACADEMY OF SCIENCES. 1995;760:315-318HULTENBY K; REINHOLT FP; HEINEGARD D; ANDERSSON G; MARKS SC
- Published conference paper: ANNALS OF THE NEW YORK ACADEMY OF SCIENCES. 1995;760:213-222HEINEGARD D; ANDERSSON G; REINHOLT FP
Forskningsbidrag
- Swedish Cancer Society1 januari 2020The most important cause of ill health and mortality from cancer is the ability of cancer cells to spread from the site of origin to nearby or distant organs through so-called metastasis. In order to influence the spread of cancer cells, it is therefore of central importance to understand the mechanisms that give the cancer cells the ability to move and also the ability to break through tissue barriers such as basement membranes, extracellular matrix and vascular endothelium to end up in the lymph and blood circulation. TRAP is an enzyme produced by cancer cells that promotes their ability to spread and metastasize. The project focuses on studies of cancer of the breast and pancreas, which in both cases give rise to metastases in nearby and more distant organs and thus give rise to severe complications. The project investigates the molecular mechanisms by which the enzyme TRAP stimulates cancer cells to develop a behavior that leads to metastasis and whether the detection and quantification of this enzyme protein can be used to predict the aggressive properties of cancer cells. In various model systems, it will be investigated whether blocking the activity of the TRAP enzyme with new specific enzyme inhibitors can reduce the metastasis ability of cancer cells. The project aims to understand the mechanisms for how TRAP can drive cancer cells to spread and metastasize and develop low molecular weight inhibitory molecules to block the activity of the TRAP enzyme in order to slow down the spread of cancer cells. Since the level of the TRAP protein has been shown to increase in relation to the degree of aggressiveness of the cancer, it is hoped that TRAP can also be used as a tissue marker both in pathological diagnosis of cancer tissue and as a circulating marker in the blood to give an idea of the tumor's spread.
- Tartrate-resistant acid phosphatase (TRAP / AcP5) - potential diagnostic marker and treatment target for cancerSwedish Cancer Society1 januari 2019The most important cause of ill health and mortality from cancer is the ability of cancer cells to spread from the site of origin to nearby or distant organs through so-called metastasis. In order to influence the spread of cancer cells, it is therefore of central importance to understand the mechanisms that give the cancer cells the ability to move and also the ability to break through tissue barriers such as basement membranes, extracellular matrix and vascular endothelium to end up in the lymph and blood circulation. TRAP is an enzyme produced by cancer cells that promotes their ability to spread and metastasize. The project focuses on studies of cancer of the breast and pancreas, which in both cases give rise to metastases in nearby and more distant organs and thus give rise to severe complications. The project investigates the molecular mechanisms by which the enzyme TRAP stimulates cancer cells to develop a behavior that leads to metastasis and whether the detection and quantification of this enzyme protein can be used to predict the aggressive properties of cancer cells. In various model systems, it will be investigated whether blocking the activity of the TRAP enzyme with new specific enzyme inhibitors can reduce the metastasis ability of cancer cells. The project aims to understand the mechanisms for how TRAP can drive cancer cells to spread and metastasize and develop low molecular weight inhibitory molecules to block the activity of the TRAP enzyme in order to slow down the spread of cancer cells. Since the level of the TRAP protein has been shown to increase in relation to the degree of aggressiveness of the cancer, it is hoped that TRAP can also be used as a tissue marker both in pathological diagnosis of cancer tissue and as a circulating marker in the blood to give an idea of the tumor's spread.
- Tartrate resistant acid phosphatase / ACP5 - a regulator of growth and metastasis of cancer cellsSwedish Cancer Society1 januari 2018The main reason for cancer mortality is the ability of the cancer cells to spread or metastasize to adjacent organs by direct overgrowth or to distant organs by spreading through the lymphatic system or blood circulation. It is therefore important to identify the mechanisms that give cancer cells the property to move and move In addition, it is capable of breaking through tissue barriers such as basal bone, extracellular matrix and vascular endothelium. The research group has shown that the enzyme protein tartrate-resistant acid phosphatase (TRAP) from cancer cells gives these cells an increased ability to grow in numbers, to migrate faster on certain connective tissue proteins and to break through a barrier consisting of basement membrane proteins. The research project is now about moving on based on these observations and in detail identify which molecular signal mechanisms are controlled by TRAP. Furthermore, the TRAP protein's regulation of the metabolic cell metabolism will be studied in detail. In one study, chemical inhibitors of the TRAP protein have been identified, which are to be tested in cell, tissue and animal models. The project aims to understand how TRAP can drive cancer cells to metastasize and to develop methods to block the effects of this protein on cancer cells. The purpose is to test the hypothesis that TRAP and its intracellular mechanisms of action may be potentially interesting targets for treatment in order to prevent or slow the spread. of cancer from its primary origin.
- Tartrate resistant acid phosphatase / ACP5 - a regulator of growth and metastasis of cancer cellsSwedish Cancer Society1 januari 2017The main reason for cancer mortality is the ability of the cancer cells to spread or metastasize to adjacent organs by direct overgrowth or to distant organs by spreading through the lymphatic system or blood circulation. It is therefore important to identify the mechanisms that give cancer cells the property to move and move In addition, it is capable of breaking through tissue barriers such as basal bone, extracellular matrix and vascular endothelium. The research group has shown that the enzyme protein tartrate-resistant acid phosphatase (TRAP) from cancer cells gives these cells an increased ability to grow in numbers, to migrate faster on certain connective tissue proteins and to break through a barrier consisting of basement membrane proteins. The research project is now about moving on based on these observations and in detail identify which molecular signal mechanisms are controlled by TRAP. Furthermore, the TRAP protein's regulation of the metabolic cell metabolism will be studied in detail. In one study, chemical inhibitors of the TRAP protein have been identified, which are to be tested in cell, tissue and animal models. The project aims to understand how TRAP can drive cancer cells to metastasize and to develop methods to block the effects of this protein on cancer cells. The purpose is to test the hypothesis that TRAP and its intracellular mechanisms of action may be potentially interesting targets for treatment in order to prevent or slow the spread. of cancer from its primary origin.
- Tartrate-resistant acid phosphatase / ACP5 - a regulator of growth and metastasis of cancer cellsSwedish Cancer Society1 januari 2016The main reason for cancer mortality is the ability of the cancer cells to spread or metastasize to adjacent organs by direct overgrowth or to distant organs by spreading through the lymphatic system or blood circulation. It is therefore important to identify the mechanisms that give cancer cells the property of moving and, in addition, the ability to break through tissue barriers such as basal men, extracellular matrix and vascular endothelium. The research team has shown that the enzyme protein tartrate-resistant acid phosphatase (TRAP) from cancer cells gives these cells an increased ability to grow in numbers, to migrate faster on certain connective tissue proteins, and to break through a barrier consisting of basal membrane proteins. The research project is now about moving on based on these observations and identifying in detail which molecular signal mechanisms are controlled by TRAP. Furthermore, the TRAP protein's regulation of the metabolic cell metabolism will be studied in detail. In one study, a chemical inhibitor of the TRAP protein has been identified, which is to be tested in tissue systems and animal models. The project aims to understand how TRAP can drive cancer cells to metastasize and to develop methods to block the effects of this protein on cancer cells. The purpose is to test the hypothesis that TRAP and its intracellular mechanisms of action may be potentially interesting targets for treatment in order to prevent or slow the spread of cancer from its primary origin.
- Tartrate-resistant acid phosphatase / ACP5 - a regulator of growth and metastasis of cancer cellsSwedish Cancer Society1 januari 2015The main reason for cancer mortality is the ability of the cancer cells to spread or metastasize to adjacent organs by direct overgrowth or to distant organs by spreading through the lymphatic system or blood circulation. It is therefore important to identify the mechanisms that give cancer cells the property of moving and, in addition, the ability to break through tissue barriers such as basal men, extracellular matrix and vascular endothelium. The research team has shown that the enzyme protein tartrate-resistant acid phosphatase (TRAP) from cancer cells gives these cells an increased ability to grow in numbers, to migrate faster on certain connective tissue proteins, and to break through a barrier consisting of basal membrane proteins. The research project is now about moving on based on these observations and identifying in detail which molecular signal mechanisms are controlled by TRAP. Furthermore, the TRAP protein's regulation of the metabolic cell metabolism will be studied in detail. In one study, a chemical inhibitor of the TRAP protein has been identified, which is to be tested in tissue systems and animal models. The project aims to understand how TRAP can drive cancer cells to metastasize and to develop methods to block the effects of this protein on cancer cells. The purpose is to test the hypothesis that TRAP and its intracellular mechanisms of action may be potentially interesting targets for treatment in order to prevent or slow the spread of cancer from its primary origin.
- Swedish Research Council1 januari 2015 - 31 december 2018
- Swedish Research Council1 januari 2012 - 31 december 2014
- Swedish Research Council1 januari 2009 - 31 december 2011
Anställningar
- Professor Emeritus, Laboratoriemedicin, Karolinska Institutet, 2026-2029
- Professor, Laboratoriemedicin, Karolinska Institutet, 1999-2023
- Professor, Biträdande, Laboratoriemedicin, Karolinska Institutet, 1998-1998