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5. Physical Training and Cancer-a Multicenter Clinical Trial (Phys-Can)

Author

The Swedish Research Council, Swedish Cancer Society, Nordic Cancer Union, Linkoeping University, Lund University, University of Agder, Copenhagen University Hospital, Denmark, Norwegian School of Sport Sciences, Amsterdam UMC, location VUmc, University of Amsterdam, University of Leeds, and Karin Nordin, Professor

Published
2023

9. Adjuvant Melatonin for Uveal Melanoma (AMUM)

Author

Karolinska Trial Alliance, Swedish Cancer Society, The Swedish Eye Foundation (Ögonfonden), The Swedish Society of Medicine, and Gustav Stalhammar, M.D. Ph.D.

Published
2023

30. Effectiveness of the Swedish National Tobacco Quitline (SNTQ)

Author

Karolinska Institutet, Region Stockholm, Västmanland County Council, Sweden, Swedish Heart Lung Foundation, Swedish Cancer Society, The Swedish Research Council, and Swedish Council for Working Life and Social Research

Published
2014

32. ARG1-expressing microglia show a distinct molecular signature and modulate postnatal development and function of the mouse brain

Author

Karolinska Institute, Swedish Research Council, Swedish Brain Foundation, Sigrid Juselius Foundation, Academy of Finland, Swedish Cultural Foundation, Swedish Cancer Society, Consejo Nacional de Ciencia y Tecnología (México), Fonds de la Recherche en Sante du Québec, Wenner-Gren Foundation, Ake Wiberg Foundation, Ministerio de Ciencia e Innovación (España), European Commission, Junta de Andalucía, Swedish Childhood Cancer Foundation, Canada Research Chairs, Stratoulias, Vassilis, Ruiz, Rocío, Kanatani, Shigeaki, Osman, Ahmed M., Keane, Lily, Armengol, José Ángel, Rodríguez-Moreno, Antonio, Murgoci, Adriana-Natalia, García-Domínguez, Irene, Alonso-Bellido, Isabel María, González Ibáñez, Fernando, Picard, Katherine, Vázquez Cabrera, Guillermo, Posada-Pérez, Mercedes, Vernoux, Nathalie, Tejera, Dario, Grabert, Kathleen, Cheray, Mathilde, González-Rodríguez, Patricia, Pérez-Villegas, Eva María, Martínez-Gallego, Irene, Lastra-Romero, Alejandro, Brodin, David, Ávila-Cariño, Javier, Cao, Yang, Airavaara, Mikko, Uhlén, Per, Heneka, Michael T., Tremblay, Marie-Ève, Blomgren, Klas, Venero, José L., Joseph, Bertrand, Karolinska Institute, Swedish Research Council, Swedish Brain Foundation, Sigrid Juselius Foundation, Academy of Finland, Swedish Cultural Foundation, Swedish Cancer Society, Consejo Nacional de Ciencia y Tecnología (México), Fonds de la Recherche en Sante du Québec, Wenner-Gren Foundation, Ake Wiberg Foundation, Ministerio de Ciencia e Innovación (España), European Commission, Junta de Andalucía, Swedish Childhood Cancer Foundation, Canada Research Chairs, Stratoulias, Vassilis, Ruiz, Rocío, Kanatani, Shigeaki, Osman, Ahmed M., Keane, Lily, Armengol, José Ángel, Rodríguez-Moreno, Antonio, Murgoci, Adriana-Natalia, García-Domínguez, Irene, Alonso-Bellido, Isabel María, González Ibáñez, Fernando, Picard, Katherine, Vázquez Cabrera, Guillermo, Posada-Pérez, Mercedes, Vernoux, Nathalie, Tejera, Dario, Grabert, Kathleen, Cheray, Mathilde, González-Rodríguez, Patricia, Pérez-Villegas, Eva María, Martínez-Gallego, Irene, Lastra-Romero, Alejandro, Brodin, David, Ávila-Cariño, Javier, Cao, Yang, Airavaara, Mikko, Uhlén, Per, Heneka, Michael T., Tremblay, Marie-Ève, Blomgren, Klas, Venero, José L., and Joseph, Bertrand

Abstract

Molecular diversity of microglia, the resident immune cells in the CNS, is reported. Whether microglial subsets characterized by the expression of specific proteins constitute subtypes with distinct functions has not been fully elucidated. Here we describe a microglial subtype expressing the enzyme arginase-1 (ARG1; that is, ARG1+ microglia) that is found predominantly in the basal forebrain and ventral striatum during early postnatal mouse development. ARG1+ microglia are enriched in phagocytic inclusions and exhibit a distinct molecular signature, including upregulation of genes such as Apoe, Clec7a, Igf1, Lgals3 and Mgl2, compared to ARG1- microglia. Microglial-specific knockdown of Arg1 results in deficient cholinergic innervation and impaired dendritic spine maturation in the hippocampus where cholinergic neurons project, which in turn results in impaired long-term potentiation and cognitive behavioral deficiencies in female mice. Our results expand on microglia diversity and provide insights into microglia subtype-specific functions.

Published
2023

33. Leveraging base-pair mammalian constraint to understand genetic variation and human disease

Author

Swedish Research Council, Knut and Alice Wallenberg Foundation, Swedish Cancer Society, Swedish Childhood Cancer Foundation, National Institute of Mental Health (US), Gladstone Institutes, National Institute on Drug Abuse (US), University College Dublin, National Human Genome Research Institute (US), National Institutes of Health (US), National Health and Medical Research Council (Australia), Juan, David [0000-0003-1912-9667], Marqués-Bonet, Tomàs [0000-0002-5597-3075], Muntané, Gerard [0000-0003-1541-8365], Navarro, Arcadi [0000-0003-2162-8246], Valenzuela, Alejandro [0000-0001-6120-6246], Sullivan, Patrick F., Meadows, Jennifer R. S., Gazal, Steven, Phan, BaDoi N., Li, Xue, Genereux, Diane P., Dong, Michael X., Bianchi, Matteo, Andrews, Gregory, Sakthikumar, Sharadha, Nordin, Jessika, Roy, Ananya, Christmas, Matthew J., Marinescu, Voichita D., Wang, Chao, Wallerman, Ola, Xue, James, Yao, Shuyang, Sun, Quan, Szatkiewicz, Jin, Wen, Jia, Huckins, Laura M., Lawler, Alyssa, Keough, Kathleen C., Zheng, Zhili, Zeng, Jian, Wray, Naomi R., Li, Yun, Johnson, Jessica, Chen, Jiawen, Zoonomia Consortium, Juan, David, Marqués-Bonet, Tomàs, Muntané, Gerard, Navarro, Arcadi, Serres-Armero, Aitor, Valenzuela, Alejandro, Paten, Benedict, Reilly, Steven K., Hughes, Graham M., Weng, Zhiping, Pollard, Katherine S., Pfenning, Andreas R., Forsberg-Nilsson, Karin, Karlsson, Elinor K., Lindblad-Toh, Kerstin, Swedish Research Council, Knut and Alice Wallenberg Foundation, Swedish Cancer Society, Swedish Childhood Cancer Foundation, National Institute of Mental Health (US), Gladstone Institutes, National Institute on Drug Abuse (US), University College Dublin, National Human Genome Research Institute (US), National Institutes of Health (US), National Health and Medical Research Council (Australia), Juan, David [0000-0003-1912-9667], Marqués-Bonet, Tomàs [0000-0002-5597-3075], Muntané, Gerard [0000-0003-1541-8365], Navarro, Arcadi [0000-0003-2162-8246], Valenzuela, Alejandro [0000-0001-6120-6246], Sullivan, Patrick F., Meadows, Jennifer R. S., Gazal, Steven, Phan, BaDoi N., Li, Xue, Genereux, Diane P., Dong, Michael X., Bianchi, Matteo, Andrews, Gregory, Sakthikumar, Sharadha, Nordin, Jessika, Roy, Ananya, Christmas, Matthew J., Marinescu, Voichita D., Wang, Chao, Wallerman, Ola, Xue, James, Yao, Shuyang, Sun, Quan, Szatkiewicz, Jin, Wen, Jia, Huckins, Laura M., Lawler, Alyssa, Keough, Kathleen C., Zheng, Zhili, Zeng, Jian, Wray, Naomi R., Li, Yun, Johnson, Jessica, Chen, Jiawen, Zoonomia Consortium, Juan, David, Marqués-Bonet, Tomàs, Muntané, Gerard, Navarro, Arcadi, Serres-Armero, Aitor, Valenzuela, Alejandro, Paten, Benedict, Reilly, Steven K., Hughes, Graham M., Weng, Zhiping, Pollard, Katherine S., Pfenning, Andreas R., Forsberg-Nilsson, Karin, Karlsson, Elinor K., and Lindblad-Toh, Kerstin

Abstract

[INTRODUCTION] Thousands of genetic variants have been associated with human diseases and traits through genome-wide association studies (GWASs). Translating these discoveries into improved therapeutics requires discerning which variants among hundreds of candidates are causally related to disease risk. To date, only a handful of causal variants have been confirmed. Here, we leverage 100 million years of mammalian evolution to address this major challenge., [RATIONALE] We compared genomes from hundreds of mammals and identified bases with unusually few variants (evolutionarily constrained). Constraint is a measure of functional importance that is agnostic to cell type or developmental stage. It can be applied to investigate any heritable disease or trait and is complementary to resources using cell type– and time point–specific functional assays like Encyclopedia of DNA Elements (ENCODE) and Genotype-Tissue Expression (GTEx)., [RESULTS] Using constraint calculated across placental mammals, 3.3% of bases in the human genome are significantly constrained, including 57.6% of coding bases. Most constrained bases (80.7%) are noncoding. Common variants (allele frequency ≥ 5%) and low-frequency variants (0.5% ≤ allele frequency < 5%) are depleted for constrained bases (1.85 versus 3.26% expected by chance, P < 2.2 × 10−308). Pathogenic ClinVar variants are more constrained than benign variants (P < 2.2 × 10−16). The most constrained common variants are more enriched for disease single-nucleotide polymorphism (SNP)–heritability in 63 independent GWASs. The enrichment of SNP-heritability in constrained regions is greater (7.8-fold) than previously reported in mammals and is even higher in primates (11.1-fold). It exceeds the enrichment of SNP-heritability in nonsynonymous coding variants (7.2-fold) and fine-mapped expression quantitative trait loci (eQTL)–SNPs (4.8-fold). The enrichment peaks near constrained bases, with a log-linear decrease of SNP-heritability enrichment as a function of the distance to a constrained base. Zoonomia constraint scores improve functionally informed fine-mapping. Variants at sites constrained in mammals and primates have greater posterior inclusion probabilities and higher per-SNP contributions. In addition, using both constraint and functional annotations improves polygenic risk score accuracy across a range of traits. Finally, incorporating constraint information into the analysis of noncoding somatic variants in medulloblastomas identifies new candidate driver genes., [CONCLUSION] Genome-wide measures of evolutionary constraint can help discern which variants are functionally important. This information may accelerate the translation of genomic discoveries into the biological, clinical, and therapeutic knowledge that is required to understand and treat human disease.

Published
2023

34. Different prognostic impact of recurrent gene mutations in chronic lymphocytic leukemia depending on IGHV gene somatic hypermutation status: a study by ERIC in HARMONY

Author

Associazione Italiana per la Ricerca sul Cancro, Ministero della Salute, Fundación la Caixa, American Association for Cancer Research, European Hematology Association, Lady Tata Memorial Trust, European Association for Cancer Research, Instituto de Salud Carlos III, Ministry of Innovation and Technology (Hungary), Università degli Studi di Ferrara, Associazione Italiana Contro le Leucemie - Linfomi e Mieloma, Danish Cancer Society Research Center, Cancer Research UK, Swedish Cancer Society, Swedish Research Council, Knut and Alice Wallenberg Foundation, Lions Cancerforskningsfond, Mansouri, Larry, Thorvaldsdottir, Birna, Sutton, Lesley-Ann, Karakatsoulis, Georgios, Meggendorfer, Manja, Parker, Helen, Nadeu, Ferran, Brieghel, Christian, Laidou, Stamatia, Moia, Riccardo, Rossi, Davide, Catherwood, Mark, Kotaskova, Jana, Delgado, Julio, Rodríguez-Vicente, Ana Eugenia, Benito, Rocío, Rigolin, Gian Matteo, Bonfiglio, Silvia, Scarfo, Lydia, Mattsson, Mattias, Davis, Zadie, Gogia, Ajay, Rani, Lata, Baliakas, Panagiotis, Foroughi-Asl, Hassan, Jylhä, Cecilia, Skaftason, Aron, Rapado, Inmaculada, Mirás, Fátima, Martínez-López, Joaquín, Serna, Javier de la, De Las Rivas, Javier, Thornton, Patrick, Larráyoz, María José, Calasanz, Mª Jose, Fésüs, Viktória, Mátrai, Zoltán, Bödör, Csaba, Smedby, Karin E, Espinet, Blanca, Puiggros, Anna, Gupta, Ritu, Bullinger, Lars, Bosch, Francesc, Tazón‐Vega, Bárbara, Baran-Marszak, Fanny, Oscier, David, Nguyen-Khac, Florence, Zenz, Thorsten, Terol, María José, Cuneo, Antonio, Hernández-Sánchez, María, Pospisilova, Sarka, Mills, Ken, Gaidano, Gianluca, Niemann, Carsten U, Campo, Elías, Strefford, Jonathan C, Ghia, Paolo, Stamatopoulos, Kostas, Rosenquist, Richard, Associazione Italiana per la Ricerca sul Cancro, Ministero della Salute, Fundación la Caixa, American Association for Cancer Research, European Hematology Association, Lady Tata Memorial Trust, European Association for Cancer Research, Instituto de Salud Carlos III, Ministry of Innovation and Technology (Hungary), Università degli Studi di Ferrara, Associazione Italiana Contro le Leucemie - Linfomi e Mieloma, Danish Cancer Society Research Center, Cancer Research UK, Swedish Cancer Society, Swedish Research Council, Knut and Alice Wallenberg Foundation, Lions Cancerforskningsfond, Mansouri, Larry, Thorvaldsdottir, Birna, Sutton, Lesley-Ann, Karakatsoulis, Georgios, Meggendorfer, Manja, Parker, Helen, Nadeu, Ferran, Brieghel, Christian, Laidou, Stamatia, Moia, Riccardo, Rossi, Davide, Catherwood, Mark, Kotaskova, Jana, Delgado, Julio, Rodríguez-Vicente, Ana Eugenia, Benito, Rocío, Rigolin, Gian Matteo, Bonfiglio, Silvia, Scarfo, Lydia, Mattsson, Mattias, Davis, Zadie, Gogia, Ajay, Rani, Lata, Baliakas, Panagiotis, Foroughi-Asl, Hassan, Jylhä, Cecilia, Skaftason, Aron, Rapado, Inmaculada, Mirás, Fátima, Martínez-López, Joaquín, Serna, Javier de la, De Las Rivas, Javier, Thornton, Patrick, Larráyoz, María José, Calasanz, Mª Jose, Fésüs, Viktória, Mátrai, Zoltán, Bödör, Csaba, Smedby, Karin E, Espinet, Blanca, Puiggros, Anna, Gupta, Ritu, Bullinger, Lars, Bosch, Francesc, Tazón‐Vega, Bárbara, Baran-Marszak, Fanny, Oscier, David, Nguyen-Khac, Florence, Zenz, Thorsten, Terol, María José, Cuneo, Antonio, Hernández-Sánchez, María, Pospisilova, Sarka, Mills, Ken, Gaidano, Gianluca, Niemann, Carsten U, Campo, Elías, Strefford, Jonathan C, Ghia, Paolo, Stamatopoulos, Kostas, and Rosenquist, Richard

Abstract

Recent evidence suggests that the prognostic impact of gene mutations in patients with chronic lymphocytic leukemia (CLL) may differ depending on the immunoglobulin heavy variable (IGHV) gene somatic hypermutation (SHM) status. In this study, we assessed the impact of nine recurrently mutated genes (BIRC3, EGR2, MYD88, NFKBIE, NOTCH1, POT1, SF3B1, TP53, and XPO1) in pre-treatment samples from 4580 patients with CLL, using time-to-first-treatment (TTFT) as the primary end-point in relation to IGHV gene SHM status. Mutations were detected in 1588 (34.7%) patients at frequencies ranging from 2.3–9.8% with mutations in NOTCH1 being the most frequent. In both univariate and multivariate analyses, mutations in all genes except MYD88 were associated with a significantly shorter TTFT. In multivariate analysis of Binet stage A patients, performed separately for IGHV-mutated (M-CLL) and unmutated CLL (U-CLL), a different spectrum of gene alterations independently predicted short TTFT within the two subgroups. While SF3B1 and XPO1 mutations were independent prognostic variables in both U-CLL and M-CLL, TP53, BIRC3 and EGR2 aberrations were significant predictors only in U-CLL, and NOTCH1 and NFKBIE only in M-CLL. Our findings underscore the need for a compartmentalized approach to identify high-risk patients, particularly among M-CLL patients, with potential implications for stratified management.

Published
2023

42. CtIP-dependent nascent RNA expression flanking DNA breaks guides the choice of DNA repair pathway

Author

Universidad de Sevilla. Departamento de Genética, Danish Cancer Society. Demmark, Lundbeck Foundation, Danish Council for Independent Research. Demmark, Novo Nordisk Foundation, Swedish Research Council, Swedish Cancer Foundation/Cancerfonden. Sweden, Danish National Research Foundation, Gómez Cabello, Daniel, Pappas, George, Aguilar Morante, Diana, Dinant, Christoffel, Bartek, Jiri, Universidad de Sevilla. Departamento de Genética, Danish Cancer Society. Demmark, Lundbeck Foundation, Danish Council for Independent Research. Demmark, Novo Nordisk Foundation, Swedish Research Council, Swedish Cancer Foundation/Cancerfonden. Sweden, Danish National Research Foundation, Gómez Cabello, Daniel, Pappas, George, Aguilar Morante, Diana, Dinant, Christoffel, and Bartek, Jiri

Abstract

The RNA world is changing our views about sensing and resolution of DNA damage. Here, we develop single-molecule DNA/RNA analysis approaches to visualize how nascent RNA facilitates the repair of DNA double-strand breaks (DSBs). RNA polymerase II (RNAPII) is crucial for DSB resolution in human cells. DSB-flanking, RNAPII-generated nascent RNA forms RNA:DNA hybrids, guiding the upstream DNA repair steps towards favouring the error-free Homologous Recombination (HR) pathway over Non-Homologous End Joining. Specific RNAPII inhibitor, THZ1, impairs recruitment of essential HR proteins to DSBs, implicating nascent RNA in DNA end resection, initiation and execution of HR repair. We further propose that resection factor CtIP interacts with and helps re-activate RNAPII when paused by the RNA:DNA hybrids, collectively promoting faithful repair of chromosome breaks to maintain genomic integrity.

Published
2022

43. NK cells and solid tumors therapeutic potential and persisting obstacles

Author

Universidad de Sevilla. Departamento de Bioquímica Médica y Biología Molecular e Inmunología, 2019 Laura Ziskin Prize in Translational Research, Cancer Research Foundations of Radiumhemmet, Dept. of Radiation Oncology at Weill Cornell Medicine (New York, US), donations from Promontory (New York, US), Functional Genomics Initiative (New York, US), Leukemia and Lymphoma Society (LLS), Luke Heller TECPR2 Foundation (Boston, US), Lytix Biopharma (Oslo, Norway), NIH/NCI, Noxopharm (Chatswood, Australia), Onxeo (Paris, France), Ricerchiamo (Brescia, Italy), romontory (New York, US), Sotio a.s. (Prague, Czech Republic), Stand Up to Cancer (SU2C), Swedish Cancer Society, Swedish Childhood Cancer Foundation, US DoD BCRP, Tong, Le, Jiménez Cortegana, Carlos, Tay, Apple H.M., Wickström, Stina, Galluzzi, Lorenzo, Lundqvist, Andreas, Universidad de Sevilla. Departamento de Bioquímica Médica y Biología Molecular e Inmunología, 2019 Laura Ziskin Prize in Translational Research, Cancer Research Foundations of Radiumhemmet, Dept. of Radiation Oncology at Weill Cornell Medicine (New York, US), donations from Promontory (New York, US), Functional Genomics Initiative (New York, US), Leukemia and Lymphoma Society (LLS), Luke Heller TECPR2 Foundation (Boston, US), Lytix Biopharma (Oslo, Norway), NIH/NCI, Noxopharm (Chatswood, Australia), Onxeo (Paris, France), Ricerchiamo (Brescia, Italy), romontory (New York, US), Sotio a.s. (Prague, Czech Republic), Stand Up to Cancer (SU2C), Swedish Cancer Society, Swedish Childhood Cancer Foundation, US DoD BCRP, Tong, Le, Jiménez Cortegana, Carlos, Tay, Apple H.M., Wickström, Stina, Galluzzi, Lorenzo, and Lundqvist, Andreas

Abstract

Natural killer (NK) cells, which are innate lymphocytes endowed with potent cytotoxic activity, have recently attracted attention as potential anticancer therapeutics. While NK cells mediate encouraging responses in patients with leukemia, the therapeutic effects of NK cell infusion in patients with solid tumors are limited. Preclinical and clinical data suggest that the efficacy of NK cell infusion against solid malignancies is hampered by several factors including inadequate tumor infiltration and persistence/activation in the tumor microenvironment (TME). A number of metabolic features of the TME including hypoxia as well as elevated levels of adenosine, reactive oxygen species, and prostaglandins negatively affect NK cell activity. Moreover, cancer-associated fibroblasts, tumor-associated macrophages, myeloid-derived suppressor cells, and regulatory T cells actively suppress NK cell-dependent anticancer immunity. Here, we review the metabolic and cellular barriers that inhibit NK cells in solid neoplasms as we discuss potential strategies to circumvent such obstacles towards superior therapeutic activity.

Published
2022

44. CtIP-dependent nascent RNA expression flanking DNA breaks guides the choice of DNA repair pathway

Author

Danish Cancer Society Research Center, Lundbeck Foundation, Danish Council for Independent Research, Novo Nordisk Foundation, Swedish Research Council, Swedish Cancer Society, European Commission, Asociación Española Contra el Cáncer, Gómez-Cabello, Daniel [0000-0002-2807-8438], Pappas, George [0000-0003-1762-4963], Aguilar Morante, Diana [0000-0001-9775-0841], Bartek, Jiri [0000-0003-2013-7525], Gómez-Cabello, Daniel, Pappas, George, Aguilar Morante, Diana, Dinant, Christoffel, Bartek, Jiri, Danish Cancer Society Research Center, Lundbeck Foundation, Danish Council for Independent Research, Novo Nordisk Foundation, Swedish Research Council, Swedish Cancer Society, European Commission, Asociación Española Contra el Cáncer, Gómez-Cabello, Daniel [0000-0002-2807-8438], Pappas, George [0000-0003-1762-4963], Aguilar Morante, Diana [0000-0001-9775-0841], Bartek, Jiri [0000-0003-2013-7525], Gómez-Cabello, Daniel, Pappas, George, Aguilar Morante, Diana, Dinant, Christoffel, and Bartek, Jiri

Abstract

The RNA world is changing our views about sensing and resolution of DNA damage. Here, we develop single-molecule DNA/RNA analysis approaches to visualize how nascent RNA facilitates the repair of DNA double-strand breaks (DSBs). RNA polymerase II (RNAPII) is crucial for DSB resolution in human cells. DSB-flanking, RNAPII-generated nascent RNA forms RNA:DNA hybrids, guiding the upstream DNA repair steps towards favouring the error-free Homologous Recombination (HR) pathway over Non-Homologous End Joining. Specific RNAPII inhibitor, THZ1, impairs recruitment of essential HR proteins to DSBs, implicating nascent RNA in DNA end resection, initiation and execution of HR repair. We further propose that resection factor CtIP interacts with and helps re-activate RNAPII when paused by the RNA:DNA hybrids, collectively promoting faithful repair of chromosome breaks to maintain genomic integrity.

Published
2022

45. The multiple faces of mnt and its role as a myc modulator

Author

Swedish Cancer Society, Swedish Childhood Cancer Foundation, Swedish Research Council, Karolinska Institute, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Liaño-Pons, Judith, Arsenian-Henriksson, Marie, León, Javier, Swedish Cancer Society, Swedish Childhood Cancer Foundation, Swedish Research Council, Karolinska Institute, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Liaño-Pons, Judith, Arsenian-Henriksson, Marie, and León, Javier

Abstract

MNT is a crucial modulator of MYC, controls several cellular functions, and is activated in most human cancers. It is the largest, most divergent, and most ubiquitously expressed protein of the MXD family. MNT was first described as a MYC antagonist and tumor suppressor. Indeed, 10% of human tumors present deletions of one MNT allele. However, some reports show that MNT functions in cooperation with MYC by maintaining cell proliferation, promoting tumor cell survival, and supporting MYC-driven tumorigenesis in cellular and animal models. Although MAX was originally considered MNT’s obligate partner, our recent findings demonstrate that MNT also works independently. MNT forms homodimers and interacts with proteins both outside and inside of the proximal MYC network. These complexes are involved in a wide array of cellular processes, from transcriptional repression via SIN3 to the modulation of metabolism through MLX as well as immunity and apoptosis via REL. In this review, we discuss the present knowledge of MNT with a special focus on its interactome, which sheds light on the complex and essential role of MNT in cell biology.

Published
2021

46. ADAR-mediated RNA editing of DNA:RNA hybrids is required for DNA double strand break repair

Author

Agencia Estatal de Investigación (España), Ministerio de Ciencia, Innovación y Universidades (España), Ministerio de Economía y Competitividad (España), European Research Council, Associazione Italiana per la Ricerca sul Cancro, Swedish Research Council, Swedish Cancer Society, European Commission, Stockholm University, EMBO, Junta de Andalucía, Jimeno, Sonia, Prados-Carvajal, Rosario, Fernández-Ávila, María Jesús, Silva, Sonia, Silvestris, Domenico Alessandro, Endara-Coll, Martin, Rodríguez-Real, Guillermo, Domingo-Prim, Judit, Mejías-Navarro, Fernando, Romero-Franco, Amador, Jimeno-González, Silvia, Barroso, Sonia, Cesarini, Valeriana, Aguilera, Andrés, Gallo, Ángela, Visa, Neus, Huertas Sánchez, Pablo, Agencia Estatal de Investigación (España), Ministerio de Ciencia, Innovación y Universidades (España), Ministerio de Economía y Competitividad (España), European Research Council, Associazione Italiana per la Ricerca sul Cancro, Swedish Research Council, Swedish Cancer Society, European Commission, Stockholm University, EMBO, Junta de Andalucía, Jimeno, Sonia, Prados-Carvajal, Rosario, Fernández-Ávila, María Jesús, Silva, Sonia, Silvestris, Domenico Alessandro, Endara-Coll, Martin, Rodríguez-Real, Guillermo, Domingo-Prim, Judit, Mejías-Navarro, Fernando, Romero-Franco, Amador, Jimeno-González, Silvia, Barroso, Sonia, Cesarini, Valeriana, Aguilera, Andrés, Gallo, Ángela, Visa, Neus, and Huertas Sánchez, Pablo

Abstract

The maintenance of genomic stability requires the coordination of multiple cellular tasks upon the appearance of DNA lesions. RNA editing, the post-transcriptional sequence alteration of RNA, has a profound effect on cell homeostasis, but its implication in the response to DNA damage was not previously explored. Here we show that, in response to DNA breaks, an overall change of the Adenosine-to-Inosine RNA editing is observed, a phenomenon we call the RNA Editing DAmage Response (REDAR). REDAR relies on the checkpoint kinase ATR and the recombination factor CtIP. Moreover, depletion of the RNA editing enzyme ADAR2 renders cells hypersensitive to genotoxic agents, increases genomic instability and hampers homologous recombination by impairing DNA resection. Such a role of ADAR2 in DNA repair goes beyond the recoding of specific transcripts, but depends on ADAR2 editing DNA:RNA hybrids to ease their dissolution.

Published
2021

47. Microglial subtypes: diversity within the microglial community

Author

Ministerio de Ciencia, Innovación y Universidades (España), European Commission, Canada Research Chairs, Swedish Research Council, Swedish Childhood Cancer Foundation, Swedish Cancer Society, Swedish Brain Foundation, Karolinska Institutet Foundation, Agencia Estatal de Investigación (España), Stratoulias, Vassilis, Venero, José L., Tremblay, Marie‐Ève, Joseph, Bertrand, Ministerio de Ciencia, Innovación y Universidades (España), European Commission, Canada Research Chairs, Swedish Research Council, Swedish Childhood Cancer Foundation, Swedish Cancer Society, Swedish Brain Foundation, Karolinska Institutet Foundation, Agencia Estatal de Investigación (España), Stratoulias, Vassilis, Venero, José L., Tremblay, Marie‐Ève, and Joseph, Bertrand

Abstract

Microglia are brain‐resident macrophages forming the first active immune barrier in the central nervous system. They fulfill multiple functions across development and adulthood and under disease conditions. Current understanding revolves around microglia acquiring distinct phenotypes upon exposure to extrinsic cues in their environment. However, emerging evidence suggests that microglia display differences in their functions that are not exclusively driven by their milieu, rather by the unique properties these cells possess. This microglial intrinsic heterogeneity has been largely overlooked, favoring the prevailing view that microglia are a single‐cell type endowed with spectacular plasticity, allowing them to acquire multiple phenotypes and thereby fulfill their numerous functions in health and disease. Here, we review the evidence that microglia might form a community of cells in which each member (or “subtype”) displays intrinsic properties and performs unique functions. Distinctive features and functional implications of several microglial subtypes are considered, across contexts of health and disease. Finally, we suggest that microglial subtype categorization shall be based on function and we propose ways for studying them. Hence, we advocate that plasticity (reaction states) and diversity (subtypes) should both be considered when studying the multitasking microglia.

Published
2019

48. EXOSC10 is required for RPA assembly and controlled DNA end resection at DNA double-strand breaks

Author

Swedish Research Council, Swedish Cancer Society, Ministerio de Economía y Competitividad (España), Stockholm University, EMBO, Domingo-Prim, Judit, Endara-Coll, Martin, Bonath, Franziska, Jimeno, Sonia, Prados-Carvajal, Rosario, Friedländer, Marc R., Huertas Sánchez, Pablo, Visa, Neus, Swedish Research Council, Swedish Cancer Society, Ministerio de Economía y Competitividad (España), Stockholm University, EMBO, Domingo-Prim, Judit, Endara-Coll, Martin, Bonath, Franziska, Jimeno, Sonia, Prados-Carvajal, Rosario, Friedländer, Marc R., Huertas Sánchez, Pablo, and Visa, Neus

Abstract

The exosome is a ribonucleolytic complex that plays important roles in RNA metabolism. Here we show that the exosome is necessary for the repair of DNA double-strand breaks (DSBs) in human cells and that RNA clearance is an essential step in homologous recombination. Transcription of DSB-flanking sequences results in the production of damage-induced long non-coding RNAs (dilncRNAs) that engage in DNA-RNA hybrid formation. Depletion of EXOSC10, an exosome catalytic subunit, leads to increased dilncRNA and DNA-RNA hybrid levels. Moreover, the targeting of the ssDNA-binding protein RPA to sites of DNA damage is impaired whereas DNA end resection is hyper-stimulated in EXOSC10-depleted cells. The DNA end resection deregulation is abolished by transcription inhibitors, and RNase H1 overexpression restores the RPA recruitment defect caused by EXOSC10 depletion, which suggests that RNA clearance of newly synthesized dilncRNAs is required for RPA recruitment, controlled DNA end resection and assembly of the homologous recombination machinery.

Published
2019

49. Mutational spectrum in a worldwide study of 29,700 families with BRCA1 or BRCA2 mutations

Author

Fundações de Amparo à Pesquisa (Brasil), Research Foundation - Flanders, University of Helsinki, Sigrid Juselius Foundation, Dutch Cancer Society, Netherlands Organization for Scientific Research, Asociación Española Contra el Cáncer, Generalitat de Catalunya, Ministero della Salute, Istituto Oncologico Veneto, University of Tasmania, Australian Cancer Research Foundation, Ministry of Health and Welfare (South Korea), Charles University (Czech Republic), National Research Foundation Singapore, Russian Foundation for Basic Research, Istituto Toscano Tumori, Israel Cancer Association USA, Swedish Cancer Society, Foundation for Women's Cancer, University of Pittsburgh, Cancer Australia, American Cancer Society, The Ohio State University, National Institutes of Health (US), Cancer Research UK, European Commission, Canadian Institutes of Health Research, Department of Trade and Industry (UK), Susan G. Komen Foundation, Breast Cancer Research Foundation, Genome Canada, National Cancer Institute (US), Research Council of Lithuania, Cancer Association of South Africa, Consejo Nacional de Investigaciones Científicas y Técnicas (Argentina), Instituto de Salud Carlos III, Ministerio de Economía y Competitividad (España), Ministerio de Sanidad y Política Social (España), Associazione Italiana per la Ricerca sul Cancro, Fondazione Italiana per la Ricerca sul Cancro, Ministero dell'Istruzione, dell'Università e della Ricerca, Institut Pasteur, Fondazione Cenci Bolognetti, Greek Government, Pontificia Universidad Javeriana, Royal Marsden NHS Foundation Trust, Kansas State University, Fundación Mutua Madrileña, Ligue Nationale contre le Cancer (France), Georgetown University, Rebbeck, Timothy R., Friebel, Tara M., Friedman, Eitan, Hamann, Ute, Huo, Dezheng, Kwong, Ava, Olah, Edith, Olopade, Olufunmilayo I., Solano, Angela R., Teo, Soo-Hwamg, Thomassen, Mads, Mebirouk, Noura, Meijers-Heijboer, Hanne, Meindl, Alfons, Mensenkamp, Arjen R., Kruse, Torben A., Benitez, Javier, Mickys, Ugnius, Greene, Mark H., Miller, Austin, thomas, Abigail, Cook, Jackie, Montagna, Marco, Moysich, Kirsten B., Mulligan, Anna Marie, Musinsky, Jacob, Neuhausen, Susan L., Nevanlinna, Heli, Ngeow, Joanne, Berger, Andreas, Nguyen, Huu Phuc, Palmero, Edenir Inêz, Davidson, Rosemarie, Bonadona, Valérie, Schmutzler, Rita Katharina, Niederacher, Dieter, Nielsen, Henriette Roed, Nielsen, Finn Cilius, Nussbaum, Robert L., Offit, Kenneth, Öfverholm, Anna, Ong, Kai-ren, Berger, Raanan, Hoya, Miguel de la, Osorio, Ana, Konstantopoulou, Irene, Papi, Laura, Papp, Janos, Senter, Leigha, Kyung Park, Sue, Pasini, Barbara, Pedersen, Inge Sokilde, Peixoto, Ana, Peruga, Nina, Leeneer, Kim de, Peterlongo, Paolo, Blanco, Amie M., Thull, Darcy L., Pohl, Esther, Pradhan, Nisha, Prajzendanc, Karolina, Prieur, Fabienne, Shah, Payal D., Pujol, Pascal, Torres, Diana, Pauw, Antoine de, Radice, Paolo, Sharma, Priyanka, Side, Lucy E., Tischkowitz, Marc, Blazer, Kathleen R., Simard, Jacques, Singer, Christian F., Skytte, Anne-Bine, Slavin, Thomas P., Snape, Katie, Rashid, Muhammad Usman, Gronwald, Jacek, McGuffog, Lesley, Sobol, Hagay, Southey, Melissa, Tognazzo, Silvia, Steele, Linda, Blok, Marinus J., Steinemann, Doris, Toland, Amanda Ewart, Topka, Sabine, Delnatte, Capucine, Trainer, Alison H., Tung, Nadine, Hahnen, Eric, Asperen, Christi J. van, Hout, Annemieke H. van der, Korach, Jacob, Hogervorst, Frans B. L., Leslie, Goska, Kolk, Lizet E. van der, Luijt, Rob B. van der, Weitzel, Jeffrey N., Heetvelde, Mattias van, Varesco, Liliana, Varon-Mateeva, Raymonda, Vega, Ana, Villarreal-Garza, Cynthia, Hauke, Jan, Laitman, Yael, Wachenfeldt, Anna von, Ramus, Susan J., Walker, Lisa, Díez, Orland, Wang-Gohrke, Shan, Aalfs, Cora M., Wappenschmidt, Barbara, Weber, Bernhard H. F., Yannoukakos, Drakoulis, Yoon, Sook-Yee, Zanzottera, Cristina, Lasa, Adrian, Zidan, Jamal, HEBON, Lee, Min Hyuk, Bonanni, Bernardo, Zorn, Kristin K., Selkirk, Christina G. Hutten, Hulick, Peter J., Chenevix-Trench, Georgia, Abugattas, Julio, Spurdle, Amanda B., Antoniou, Antonis C., Lasset, Christine, Nathanson, Katherine L., Sukiennicki, Grzegorz, Adlard, Julian, Agata, Simona, Bradbury, Angela R., Henderson, Alex, Aittomäki, Kristiina, Andrews, Lesley, Andrulis, Irene L., Arason, Adalgeir, Arnold, Norbert, Couch, Fergus J., Ding, Yuan Chun, Arun, Branu K., Asseryanis, Ella, Auerbach, Leo, Azzollini, Jacopo, Brewer, Carole, Balmaña, Judith, Hentschel, Julia, Barile, Monica, Buecher, Bruno, Buys, Saundra S., Ditsch, Nina, Lázaro, Conxi, Caldés, Trinidad, Caliebe, Almuth, Caligo, Maria A., Campbell, Ian, Caputo, Sandrine M., Rantala, Johanna, Honisch, Ellen, Chiquette, Jocelyne, Chung, Wendy K., Domchek, Susan M., Claes, Kathleen B., Lee, Annette T., Collée, J. Margriet, Evans, D. Gareth, Dorfling, Cecilia M., Velázquez Pérez, Carolina, Dworniczak, Bernd, Eason, Jacqueline, Rhiem, Kerstin, Easton, Douglas F., Eeles, Ros, Sutter, Christian, Schmidt, Ane Y., Imyanitov, Evgeny N., Ehrencrona, Hans, Ejlertsen, Bent, EMBRACE, Engel, Christoph, Engert, Stefanie, Faivre, Laurence, Feliubadaló, Lidia, Robson, Mark, szabo, Csilla I., Tan, Yen Y., Fert Ferrer, Sandra, Barkardottir, Rosa B., Foretova, Lenka, Fowler, Jeffrey, Isaacs, Claudine, Frost, Debra, Galvão, Henrique C. R., Ganz, Patricia A., Garber, Judy, Gauthier-Villars, Marion, Teixeira, Manuel R., Gehrig, Andrea, Rodriguez, Gustavo C., Lester, Jenny, GEMO Study Collaborators, Gerdes, Anne-Marie, Gesta, Paul, Giannini, Giuseppe, Izat, Louise, Giraud, Sophie, Glendon, Gord, Terry, Mary Beth, Godwin, Andrew K., Izquierdo, Angel, Jakubowska, Anna, Lesueur, Fabienne, Rogers, Mark T., James, Paul, Janavicius, Ramunas, Jensen, Uffe Birk, John, Esther M., Vijai, Joseph, Gutierrez-Barrera, Angelica, Chan, T. L., Kaczmarek, Katarzyna, Karlan, Beth Y., Kast, Karin, Liljegren, Annelie, KConFab Investigators, Rudaitis, Vilius, Kim, Sung-Won, Lindor, Noralane M., Longy, Michel, Teulé, Alex, Loud, Jennifer T., Lu, Karen H., Goldgar, David E., Lubinski, Jan, Machackova, Eva, Barrowdale, Daniel, Rensburg, Elizabeth J. van, Manoukian, Siranoush, Mari, Véronique, Martínez-Bouzaz, Cristina, Parsons, Michael T., Matrai, Zoltan, Fundações de Amparo à Pesquisa (Brasil), Research Foundation - Flanders, University of Helsinki, Sigrid Juselius Foundation, Dutch Cancer Society, Netherlands Organization for Scientific Research, Asociación Española Contra el Cáncer, Generalitat de Catalunya, Ministero della Salute, Istituto Oncologico Veneto, University of Tasmania, Australian Cancer Research Foundation, Ministry of Health and Welfare (South Korea), Charles University (Czech Republic), National Research Foundation Singapore, Russian Foundation for Basic Research, Istituto Toscano Tumori, Israel Cancer Association USA, Swedish Cancer Society, Foundation for Women's Cancer, University of Pittsburgh, Cancer Australia, American Cancer Society, The Ohio State University, National Institutes of Health (US), Cancer Research UK, European Commission, Canadian Institutes of Health Research, Department of Trade and Industry (UK), Susan G. Komen Foundation, Breast Cancer Research Foundation, Genome Canada, National Cancer Institute (US), Research Council of Lithuania, Cancer Association of South Africa, Consejo Nacional de Investigaciones Científicas y Técnicas (Argentina), Instituto de Salud Carlos III, Ministerio de Economía y Competitividad (España), Ministerio de Sanidad y Política Social (España), Associazione Italiana per la Ricerca sul Cancro, Fondazione Italiana per la Ricerca sul Cancro, Ministero dell'Istruzione, dell'Università e della Ricerca, Institut Pasteur, Fondazione Cenci Bolognetti, Greek Government, Pontificia Universidad Javeriana, Royal Marsden NHS Foundation Trust, Kansas State University, Fundación Mutua Madrileña, Ligue Nationale contre le Cancer (France), Georgetown University, Rebbeck, Timothy R., Friebel, Tara M., Friedman, Eitan, Hamann, Ute, Huo, Dezheng, Kwong, Ava, Olah, Edith, Olopade, Olufunmilayo I., Solano, Angela R., Teo, Soo-Hwamg, Thomassen, Mads, Mebirouk, Noura, Meijers-Heijboer, Hanne, Meindl, Alfons, Mensenkamp, Arjen R., Kruse, Torben A., Benitez, Javier, Mickys, Ugnius, Greene, Mark H., Miller, Austin, thomas, Abigail, Cook, Jackie, Montagna, Marco, Moysich, Kirsten B., Mulligan, Anna Marie, Musinsky, Jacob, Neuhausen, Susan L., Nevanlinna, Heli, Ngeow, Joanne, Berger, Andreas, Nguyen, Huu Phuc, Palmero, Edenir Inêz, Davidson, Rosemarie, Bonadona, Valérie, Schmutzler, Rita Katharina, Niederacher, Dieter, Nielsen, Henriette Roed, Nielsen, Finn Cilius, Nussbaum, Robert L., Offit, Kenneth, Öfverholm, Anna, Ong, Kai-ren, Berger, Raanan, Hoya, Miguel de la, Osorio, Ana, Konstantopoulou, Irene, Papi, Laura, Papp, Janos, Senter, Leigha, Kyung Park, Sue, Pasini, Barbara, Pedersen, Inge Sokilde, Peixoto, Ana, Peruga, Nina, Leeneer, Kim de, Peterlongo, Paolo, Blanco, Amie M., Thull, Darcy L., Pohl, Esther, Pradhan, Nisha, Prajzendanc, Karolina, Prieur, Fabienne, Shah, Payal D., Pujol, Pascal, Torres, Diana, Pauw, Antoine de, Radice, Paolo, Sharma, Priyanka, Side, Lucy E., Tischkowitz, Marc, Blazer, Kathleen R., Simard, Jacques, Singer, Christian F., Skytte, Anne-Bine, Slavin, Thomas P., Snape, Katie, Rashid, Muhammad Usman, Gronwald, Jacek, McGuffog, Lesley, Sobol, Hagay, Southey, Melissa, Tognazzo, Silvia, Steele, Linda, Blok, Marinus J., Steinemann, Doris, Toland, Amanda Ewart, Topka, Sabine, Delnatte, Capucine, Trainer, Alison H., Tung, Nadine, Hahnen, Eric, Asperen, Christi J. van, Hout, Annemieke H. van der, Korach, Jacob, Hogervorst, Frans B. L., Leslie, Goska, Kolk, Lizet E. van der, Luijt, Rob B. van der, Weitzel, Jeffrey N., Heetvelde, Mattias van, Varesco, Liliana, Varon-Mateeva, Raymonda, Vega, Ana, Villarreal-Garza, Cynthia, Hauke, Jan, Laitman, Yael, Wachenfeldt, Anna von, Ramus, Susan J., Walker, Lisa, Díez, Orland, Wang-Gohrke, Shan, Aalfs, Cora M., Wappenschmidt, Barbara, Weber, Bernhard H. F., Yannoukakos, Drakoulis, Yoon, Sook-Yee, Zanzottera, Cristina, Lasa, Adrian, Zidan, Jamal, HEBON, Lee, Min Hyuk, Bonanni, Bernardo, Zorn, Kristin K., Selkirk, Christina G. Hutten, Hulick, Peter J., Chenevix-Trench, Georgia, Abugattas, Julio, Spurdle, Amanda B., Antoniou, Antonis C., Lasset, Christine, Nathanson, Katherine L., Sukiennicki, Grzegorz, Adlard, Julian, Agata, Simona, Bradbury, Angela R., Henderson, Alex, Aittomäki, Kristiina, Andrews, Lesley, Andrulis, Irene L., Arason, Adalgeir, Arnold, Norbert, Couch, Fergus J., Ding, Yuan Chun, Arun, Branu K., Asseryanis, Ella, Auerbach, Leo, Azzollini, Jacopo, Brewer, Carole, Balmaña, Judith, Hentschel, Julia, Barile, Monica, Buecher, Bruno, Buys, Saundra S., Ditsch, Nina, Lázaro, Conxi, Caldés, Trinidad, Caliebe, Almuth, Caligo, Maria A., Campbell, Ian, Caputo, Sandrine M., Rantala, Johanna, Honisch, Ellen, Chiquette, Jocelyne, Chung, Wendy K., Domchek, Susan M., Claes, Kathleen B., Lee, Annette T., Collée, J. Margriet, Evans, D. Gareth, Dorfling, Cecilia M., Velázquez Pérez, Carolina, Dworniczak, Bernd, Eason, Jacqueline, Rhiem, Kerstin, Easton, Douglas F., Eeles, Ros, Sutter, Christian, Schmidt, Ane Y., Imyanitov, Evgeny N., Ehrencrona, Hans, Ejlertsen, Bent, EMBRACE, Engel, Christoph, Engert, Stefanie, Faivre, Laurence, Feliubadaló, Lidia, Robson, Mark, szabo, Csilla I., Tan, Yen Y., Fert Ferrer, Sandra, Barkardottir, Rosa B., Foretova, Lenka, Fowler, Jeffrey, Isaacs, Claudine, Frost, Debra, Galvão, Henrique C. R., Ganz, Patricia A., Garber, Judy, Gauthier-Villars, Marion, Teixeira, Manuel R., Gehrig, Andrea, Rodriguez, Gustavo C., Lester, Jenny, GEMO Study Collaborators, Gerdes, Anne-Marie, Gesta, Paul, Giannini, Giuseppe, Izat, Louise, Giraud, Sophie, Glendon, Gord, Terry, Mary Beth, Godwin, Andrew K., Izquierdo, Angel, Jakubowska, Anna, Lesueur, Fabienne, Rogers, Mark T., James, Paul, Janavicius, Ramunas, Jensen, Uffe Birk, John, Esther M., Vijai, Joseph, Gutierrez-Barrera, Angelica, Chan, T. L., Kaczmarek, Katarzyna, Karlan, Beth Y., Kast, Karin, Liljegren, Annelie, KConFab Investigators, Rudaitis, Vilius, Kim, Sung-Won, Lindor, Noralane M., Longy, Michel, Teulé, Alex, Loud, Jennifer T., Lu, Karen H., Goldgar, David E., Lubinski, Jan, Machackova, Eva, Barrowdale, Daniel, Rensburg, Elizabeth J. van, Manoukian, Siranoush, Mari, Véronique, Martínez-Bouzaz, Cristina, Parsons, Michael T., and Matrai, Zoltan

Abstract

The prevalence and spectrum of germline mutations in BRCA1 and BRCA2 have been reported in single populations, with the majority of reports focused on White in Europe and North America. The Consortium of Investigators of Modifiers of BRCA1/2 (CIMBA) has assembled data on 18,435 families with BRCA1 mutations and 11,351 families with BRCA2 mutations ascertained from 69 centers in 49 countries on six continents. This study comprehensively describes the characteristics of the 1,650 unique BRCA1 and 1,731 unique BRCA2 deleterious (disease-associated) mutations identified in the CIMBA database. We observed substantial variation in mutation type and frequency by geographical region and race/ethnicity. In addition to known founder mutations, mutations of relatively high frequency were identified in specific racial/ethnic or geographic groups that may reflect founder mutations and which could be used in targeted (panel) first pass genotyping for specific populations. Knowledge of the population-specific mutational spectrum in BRCA1 and BRCA2 could inform efficient strategies for genetic testing and may justify a more broad-based oncogenetic testing in some populations.

Published
2018

50. Interactions between Chemotherapy, Endocrine Therapy and Radiation

Author

Bengt Glimelius, Bo Nordenskjöld, Elisabeth Kjellén, Björn Zackrisson, and The Swedish Cancer Society Investigatio

Subjects
Oncology, medicine.medical_specialty, Chemotherapy, business.industry, medicine.medical_treatment, Endocrine therapy, Cancer, Hematology, General Medicine, medicine.disease, Expert group, Surgery, Radiation therapy, Internal medicine, Medicine, Combined Modality Therapy, Radiology, Nuclear Medicine and imaging, Hormone replacement therapy, business
Abstract

In an investigation by the Swedish Cancer Society, an expert group described the present status, critical issues and future aspects and potentials for each of nine major areas of radiation therapy research. This report deals with interactions between chemotherapy, endocrine therapy, other anti-tumour drugs and radiation.

Published
2017

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