Polymorphisms within Autophagy-Related Genes as Susceptibility Biomarkers for Multiple Myeloma: A Meta-Analysis of Three Large Cohorts and Functional Characterization
Functional data used in this project have been meticulously catalogued and archived in the BBMRI-NL data infrastructure (https://hfgp.bbmri.nl/, accessed on 12 February 2020) using the MOLGENIS open-source platform for scientific data. Multiple myeloma (MM) arises following malignant proliferation o...
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| Published in | International Journal of Molecular Sciences Vol. 24; no. 10; pp. 8500 - 20 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Switzerland
MDPI AG
09.05.2023
Multidisciplinary Digital Publishing Institute MDPI |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1422-0067 1661-6596 1422-0067 1661-6596 |
| DOI | 10.3390/ijms24108500 |
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| Abstract | Functional data used in this project have been meticulously catalogued and archived in the BBMRI-NL data infrastructure (https://hfgp.bbmri.nl/, accessed on 12 February 2020) using the MOLGENIS open-source platform for scientific data.
Multiple myeloma (MM) arises following malignant proliferation of plasma cells in the bone marrow, that secrete high amounts of specific monoclonal immunoglobulins or light chains, resulting in the massive production of unfolded or misfolded proteins. Autophagy can have a dual role in tumorigenesis, by eliminating these abnormal proteins to avoid cancer development, but also ensuring MM cell survival and promoting resistance to treatments. To date no studies have determined the impact of genetic variation in autophagy-related genes on MM risk. We performed meta-analysis of germline genetic data on 234 autophagy-related genes from three independent study populations including 13,387 subjects of European ancestry (6863 MM patients and 6524 controls) and examined correlations of statistically significant single nucleotide polymorphisms (SNPs; p < 1 × 10−9) with immune responses in whole blood, peripheral blood mononuclear cells (PBMCs), and monocyte-derived macrophages (MDM) from a large population of healthy donors from the Human Functional Genomic Project (HFGP). We identified SNPs in six loci, CD46, IKBKE, PARK2, ULK4, ATG5, and CDKN2A associated with MM risk (p = 4.47 × 10−4−5.79 × 10−14). Mechanistically, we found that the ULK4rs6599175 SNP correlated with circulating concentrations of vitamin D3 (p = 4.0 × 10−4), whereas the IKBKErs17433804 SNP correlated with the number of transitional CD24+CD38+ B cells (p = 4.8 × 10−4) and circulating serum concentrations of Monocyte hemoattractant Protein (MCP)-2 (p = 3.6 × 10−4). We also found that the CD46rs1142469 SNP corre lated with numbers of CD19+ B cells, CD19+CD3− B cells, CD5+ IgD− cells, IgM− cells, IgD−IgM− cells, and CD4−CD8− PBMCs (p = 4.9 × 10−4−8.6 × 10−4 ) and circulating concentrations of interleukin (IL)-20 (p = 0.00082). Finally, we observed that the CDKN2Ars2811710 SNP correlated with levels of CD4+EMCD45RO+CD27− cells (p = 9.3 × 10−4 ). These results suggest that genetic variants within these six loci influence MM risk through the modulation of specific subsets of immune cells, as well as vitamin D3−, MCP-2−, and IL20-dependent pathways.
This work was supported by the European Union’s Horizon 2020 research and innovation program, N° 856620 and by grants from the Instituto de Salud Carlos III and FEDER (Madrid, Spain; PI17/02256 and PI20/01845), Consejería de Transformación Económica, Industria, Conocimiento y Universidades and FEDER (PY20/01282), from the CRIS foundation against cancer, from the Cancer Network of Excellence (RD12/10 Red de Cáncer), from the Dietmar Hopp Foundation and the German Ministry of Education and Science (BMBF: CLIOMMICS [01ZX1309]), and from National Cancer Institute of the National Institutes of Health under award numbers: R01CA186646, U01CA249955 (EEB).
This work was also funded d by Portuguese National funds, through the Foundation for Science and Technology (FCT)—project UIDB/50026/2020 and UIDP/50026/2020 and by the project NORTE-01-0145-FEDER-000055, supported by Norte Portugal Regional Operational Programme (NORTE 2020), under the PORTUGAL 2020 Partnership Agreement, through the European Regional Development Fund (ERDF). |
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| AbstractList | Multiple myeloma (MM) arises following malignant proliferation of plasma cells in the bone marrow, that secrete high amounts of specific monoclonal immunoglobulins or light chains, resulting in the massive production of unfolded or misfolded proteins. Autophagy can have a dual role in tumorigenesis, by eliminating these abnormal proteins to avoid cancer development, but also ensuring MM cell survival and promoting resistance to treatments. To date no studies have determined the impact of genetic variation in autophagy-related genes on MM risk. We performed meta-analysis of germline genetic data on 234 autophagy-related genes from three independent study populations including 13,387 subjects of European ancestry (6863 MM patients and 6524 controls) and examined correlations of statistically significant single nucleotide polymorphisms (SNPs;
< 1 × 10
) with immune responses in whole blood, peripheral blood mononuclear cells (PBMCs), and monocyte-derived macrophages (MDM) from a large population of healthy donors from the Human Functional Genomic Project (HFGP). We identified SNPs in six loci,
,
,
,
,
, and
associated with MM risk (
= 4.47 × 10
-5.79 × 10
). Mechanistically, we found that the
SNP correlated with circulating concentrations of vitamin D3 (
= 4.0 × 10
), whereas the
SNP correlated with the number of transitional CD24
CD38
B cells (
= 4.8 × 10
) and circulating serum concentrations of Monocyte Chemoattractant Protein (MCP)-2 (
= 3.6 × 10
). We also found that the
SNP correlated with numbers of CD19
B cells, CD19
CD3
B cells, CD5
IgD
cells, IgM
cells, IgD
IgM
cells, and CD4
CD8
PBMCs (
= 4.9 × 10
-8.6 × 10
) and circulating concentrations of interleukin (IL)-20 (
= 0.00082). Finally, we observed that the
SNP correlated with levels of CD4
EMCD45RO
CD27
cells (
= 9.3 × 10
). These results suggest that genetic variants within these six loci influence MM risk through the modulation of specific subsets of immune cells, as well as vitamin D3
, MCP-2
, and IL20-dependent pathways. We investigated the influence of autophagy-related variants in modulating Multiple Myeloma (MM) risk through a meta-analysis of germline genetic data on 234 autophagy-related genes from three independent study populations including 13,387 subjects of European ancestry (6863 MM patients and 6524 controls) and examined the functional mechanisms behind the observed associations. We identified SNPs within the six CD46, IKBKE, PARK2, ULK4, ATG5, and CDKN2A loci associated with MM risk and observed that their effect on disease risk was mediated by specific subsets of immune cells, as well as vitamin D3-, MCP-2-, and IL20-dependent mechanisms. Multiple myeloma (MM) arises following malignant proliferation of plasma cells in the bone marrow, that secrete high amounts of specific monoclonal immunoglobulins or light chains, resulting in the massive production of unfolded or misfolded proteins. Autophagy can have a dual role in tumorigenesis, by eliminating these abnormal proteins to avoid cancer development, but also ensuring MM cell survival and promoting resistance to treatments. To date no studies have determined the impact of genetic variation in autophagy-related genes on MM risk. We performed meta-analysis of germline genetic data on 234 autophagy-related genes from three independent study populations including 13,387 subjects of European ancestry (6863 MM patients and 6524 controls) and examined correlations of statistically significant single nucleotide polymorphisms (SNPs; p < 1 × 10[sup.−9]) with immune responses in whole blood, peripheral blood mononuclear cells (PBMCs), and monocyte-derived macrophages (MDM) from a large population of healthy donors from the Human Functional Genomic Project (HFGP). We identified SNPs in six loci, CD46, IKBKE, PARK2, ULK4, ATG5, and CDKN2A associated with MM risk (p = 4.47 × 10[sup.−4]−5.79 × 10[sup.−14]). Mechanistically, we found that the ULK4[sub.rs6599175] SNP correlated with circulating concentrations of vitamin D3 (p = 4.0 × 10[sup.−4]), whereas the IKBKE[sub.rs17433804] SNP correlated with the number of transitional CD24[sup.+]CD38[sup.+] B cells (p = 4.8 × 10[sup.−4]) and circulating serum concentrations of Monocyte Chemoattractant Protein (MCP)-2 (p = 3.6 × 10[sup.−4]). We also found that the CD46[sub.rs1142469] SNP correlated with numbers of CD19[sup.+] B cells, CD19[sup.+]CD3[sup.−] B cells, CD5[sup.+]IgD[sup.−] cells, IgM[sup.−] cells, IgD[sup.−]IgM[sup.−] cells, and CD4[sup.−]CD8[sup.−] PBMCs (p = 4.9 × 10[sup.−4]−8.6 × 10[sup.−4]) and circulating concentrations of interleukin (IL)-20 (p = 0.00082). Finally, we observed that the CDKN2A[sub.rs2811710] SNP correlated with levels of CD4[sup.+]EMCD45RO[sup.+]CD27[sup.−] cells (p = 9.3 × 10[sup.−4]). These results suggest that genetic variants within these six loci influence MM risk through the modulation of specific subsets of immune cells, as well as vitamin D3[sup.−], MCP-2[sup.−], and IL20-dependent pathways. Multiple myeloma (MM) arises following malignant proliferation of plasma cells in the bone marrow, that secrete high amounts of specific monoclonal immunoglobulins or light chains, resulting in the massive production of unfolded or misfolded proteins. Autophagy can have a dual role in tumorigenesis, by eliminating these abnormal proteins to avoid cancer development, but also ensuring MM cell survival and promoting resistance to treatments. To date no studies have determined the impact of genetic variation in autophagy-related genes on MM risk. We performed meta-analysis of germline genetic data on 234 autophagy-related genes from three independent study populations including 13,387 subjects of European ancestry (6863 MM patients and 6524 controls) and examined correlations of statistically significant single nucleotide polymorphisms (SNPs; p < 1 × 10−9) with immune responses in whole blood, peripheral blood mononuclear cells (PBMCs), and monocyte-derived macrophages (MDM) from a large population of healthy donors from the Human Functional Genomic Project (HFGP). We identified SNPs in six loci, CD46, IKBKE, PARK2, ULK4, ATG5, and CDKN2A associated with MM risk (p = 4.47 × 10−4−5.79 × 10−14). Mechanistically, we found that the ULK4rs6599175 SNP correlated with circulating concentrations of vitamin D3 (p = 4.0 × 10−4), whereas the IKBKErs17433804 SNP correlated with the number of transitional CD24+CD38+ B cells (p = 4.8 × 10−4) and circulating serum concentrations of Monocyte Chemoattractant Protein (MCP)-2 (p = 3.6 × 10−4). We also found that the CD46rs1142469 SNP correlated with numbers of CD19+ B cells, CD19+CD3− B cells, CD5+IgD− cells, IgM− cells, IgD−IgM− cells, and CD4−CD8− PBMCs (p = 4.9 × 10−4−8.6 × 10−4) and circulating concentrations of interleukin (IL)-20 (p = 0.00082). Finally, we observed that the CDKN2Ars2811710 SNP correlated with levels of CD4+EMCD45RO+CD27− cells (p = 9.3 × 10−4). These results suggest that genetic variants within these six loci influence MM risk through the modulation of specific subsets of immune cells, as well as vitamin D3−, MCP-2−, and IL20-dependent pathways. Multiple myeloma (MM) arises following malignant proliferation of plasma cells in the bone marrow, that secrete high amounts of specific monoclonal immunoglobulins or light chains, resulting in the massive production of unfolded or misfolded proteins. Autophagy can have a dual role in tumorigenesis, by eliminating these abnormal proteins to avoid cancer development, but also ensuring MM cell survival and promoting resistance to treatments. To date no studies have determined the impact of genetic variation in autophagy-related genes on MM risk. We performed meta-analysis of germline genetic data on 234 autophagy-related genes from three independent study populations including 13,387 subjects of European ancestry (6863 MM patients and 6524 controls) and examined correlations of statistically significant single nucleotide polymorphisms (SNPs; p < 1 × 10-9) with immune responses in whole blood, peripheral blood mononuclear cells (PBMCs), and monocyte-derived macrophages (MDM) from a large population of healthy donors from the Human Functional Genomic Project (HFGP). We identified SNPs in six loci, CD46, IKBKE, PARK2, ULK4, ATG5, and CDKN2A associated with MM risk (p = 4.47 × 10-4-5.79 × 10-14). Mechanistically, we found that the ULK4rs6599175 SNP correlated with circulating concentrations of vitamin D3 (p = 4.0 × 10-4), whereas the IKBKErs17433804 SNP correlated with the number of transitional CD24+CD38+ B cells (p = 4.8 × 10-4) and circulating serum concentrations of Monocyte Chemoattractant Protein (MCP)-2 (p = 3.6 × 10-4). We also found that the CD46rs1142469 SNP correlated with numbers of CD19+ B cells, CD19+CD3- B cells, CD5+IgD- cells, IgM- cells, IgD-IgM- cells, and CD4-CD8- PBMCs (p = 4.9 × 10-4-8.6 × 10-4) and circulating concentrations of interleukin (IL)-20 (p = 0.00082). Finally, we observed that the CDKN2Ars2811710 SNP correlated with levels of CD4+EMCD45RO+CD27- cells (p = 9.3 × 10-4). These results suggest that genetic variants within these six loci influence MM risk through the modulation of specific subsets of immune cells, as well as vitamin D3-, MCP-2-, and IL20-dependent pathways.Multiple myeloma (MM) arises following malignant proliferation of plasma cells in the bone marrow, that secrete high amounts of specific monoclonal immunoglobulins or light chains, resulting in the massive production of unfolded or misfolded proteins. Autophagy can have a dual role in tumorigenesis, by eliminating these abnormal proteins to avoid cancer development, but also ensuring MM cell survival and promoting resistance to treatments. To date no studies have determined the impact of genetic variation in autophagy-related genes on MM risk. We performed meta-analysis of germline genetic data on 234 autophagy-related genes from three independent study populations including 13,387 subjects of European ancestry (6863 MM patients and 6524 controls) and examined correlations of statistically significant single nucleotide polymorphisms (SNPs; p < 1 × 10-9) with immune responses in whole blood, peripheral blood mononuclear cells (PBMCs), and monocyte-derived macrophages (MDM) from a large population of healthy donors from the Human Functional Genomic Project (HFGP). We identified SNPs in six loci, CD46, IKBKE, PARK2, ULK4, ATG5, and CDKN2A associated with MM risk (p = 4.47 × 10-4-5.79 × 10-14). Mechanistically, we found that the ULK4rs6599175 SNP correlated with circulating concentrations of vitamin D3 (p = 4.0 × 10-4), whereas the IKBKErs17433804 SNP correlated with the number of transitional CD24+CD38+ B cells (p = 4.8 × 10-4) and circulating serum concentrations of Monocyte Chemoattractant Protein (MCP)-2 (p = 3.6 × 10-4). We also found that the CD46rs1142469 SNP correlated with numbers of CD19+ B cells, CD19+CD3- B cells, CD5+IgD- cells, IgM- cells, IgD-IgM- cells, and CD4-CD8- PBMCs (p = 4.9 × 10-4-8.6 × 10-4) and circulating concentrations of interleukin (IL)-20 (p = 0.00082). Finally, we observed that the CDKN2Ars2811710 SNP correlated with levels of CD4+EMCD45RO+CD27- cells (p = 9.3 × 10-4). These results suggest that genetic variants within these six loci influence MM risk through the modulation of specific subsets of immune cells, as well as vitamin D3-, MCP-2-, and IL20-dependent pathways. Simple SummaryWe investigated the influence of autophagy-related variants in modulating Multiple Myeloma (MM) risk through a meta-analysis of germline genetic data on 234 autophagy-related genes from three independent study populations including 13,387 subjects of European ancestry (6863 MM patients and 6524 controls) and examined the functional mechanisms behind the observed associations. We identified SNPs within the six CD46, IKBKE, PARK2, ULK4, ATG5, and CDKN2A loci associated with MM risk and observed that their effect on disease risk was mediated by specific subsets of immune cells, as well as vitamin D3-, MCP-2-, and IL20-dependent mechanisms.AbstractMultiple myeloma (MM) arises following malignant proliferation of plasma cells in the bone marrow, that secrete high amounts of specific monoclonal immunoglobulins or light chains, resulting in the massive production of unfolded or misfolded proteins. Autophagy can have a dual role in tumorigenesis, by eliminating these abnormal proteins to avoid cancer development, but also ensuring MM cell survival and promoting resistance to treatments. To date no studies have determined the impact of genetic variation in autophagy-related genes on MM risk. We performed meta-analysis of germline genetic data on 234 autophagy-related genes from three independent study populations including 13,387 subjects of European ancestry (6863 MM patients and 6524 controls) and examined correlations of statistically significant single nucleotide polymorphisms (SNPs; p < 1 × 10−9) with immune responses in whole blood, peripheral blood mononuclear cells (PBMCs), and monocyte-derived macrophages (MDM) from a large population of healthy donors from the Human Functional Genomic Project (HFGP). We identified SNPs in six loci, CD46, IKBKE, PARK2, ULK4, ATG5, and CDKN2A associated with MM risk (p = 4.47 × 10−4−5.79 × 10−14). Mechanistically, we found that the ULK4rs6599175 SNP correlated with circulating concentrations of vitamin D3 (p = 4.0 × 10−4), whereas the IKBKErs17433804 SNP correlated with the number of transitional CD24+CD38+ B cells (p = 4.8 × 10−4) and circulating serum concentrations of Monocyte Chemoattractant Protein (MCP)-2 (p = 3.6 × 10−4). We also found that the CD46rs1142469 SNP correlated with numbers of CD19+ B cells, CD19+CD3− B cells, CD5+IgD− cells, IgM− cells, IgD−IgM− cells, and CD4−CD8− PBMCs (p = 4.9 × 10−4−8.6 × 10−4) and circulating concentrations of interleukin (IL)-20 (p = 0.00082). Finally, we observed that the CDKN2Ars2811710 SNP correlated with levels of CD4+EMCD45RO+CD27− cells (p = 9.3 × 10−4). These results suggest that genetic variants within these six loci influence MM risk through the modulation of specific subsets of immune cells, as well as vitamin D3−, MCP-2−, and IL20-dependent pathways. Functional data used in this project have been meticulously catalogued and archived in the BBMRI-NL data infrastructure (https://hfgp.bbmri.nl/, accessed on 12 February 2020) using the MOLGENIS open-source platform for scientific data. Multiple myeloma (MM) arises following malignant proliferation of plasma cells in the bone marrow, that secrete high amounts of specific monoclonal immunoglobulins or light chains, resulting in the massive production of unfolded or misfolded proteins. Autophagy can have a dual role in tumorigenesis, by eliminating these abnormal proteins to avoid cancer development, but also ensuring MM cell survival and promoting resistance to treatments. To date no studies have determined the impact of genetic variation in autophagy-related genes on MM risk. We performed meta-analysis of germline genetic data on 234 autophagy-related genes from three independent study populations including 13,387 subjects of European ancestry (6863 MM patients and 6524 controls) and examined correlations of statistically significant single nucleotide polymorphisms (SNPs; p < 1 × 10−9) with immune responses in whole blood, peripheral blood mononuclear cells (PBMCs), and monocyte-derived macrophages (MDM) from a large population of healthy donors from the Human Functional Genomic Project (HFGP). We identified SNPs in six loci, CD46, IKBKE, PARK2, ULK4, ATG5, and CDKN2A associated with MM risk (p = 4.47 × 10−4−5.79 × 10−14). Mechanistically, we found that the ULK4rs6599175 SNP correlated with circulating concentrations of vitamin D3 (p = 4.0 × 10−4), whereas the IKBKErs17433804 SNP correlated with the number of transitional CD24+CD38+ B cells (p = 4.8 × 10−4) and circulating serum concentrations of Monocyte hemoattractant Protein (MCP)-2 (p = 3.6 × 10−4). We also found that the CD46rs1142469 SNP corre lated with numbers of CD19+ B cells, CD19+CD3− B cells, CD5+ IgD− cells, IgM− cells, IgD−IgM− cells, and CD4−CD8− PBMCs (p = 4.9 × 10−4−8.6 × 10−4 ) and circulating concentrations of interleukin (IL)-20 (p = 0.00082). Finally, we observed that the CDKN2Ars2811710 SNP correlated with levels of CD4+EMCD45RO+CD27− cells (p = 9.3 × 10−4 ). These results suggest that genetic variants within these six loci influence MM risk through the modulation of specific subsets of immune cells, as well as vitamin D3−, MCP-2−, and IL20-dependent pathways. This work was supported by the European Union’s Horizon 2020 research and innovation program, N° 856620 and by grants from the Instituto de Salud Carlos III and FEDER (Madrid, Spain; PI17/02256 and PI20/01845), Consejería de Transformación Económica, Industria, Conocimiento y Universidades and FEDER (PY20/01282), from the CRIS foundation against cancer, from the Cancer Network of Excellence (RD12/10 Red de Cáncer), from the Dietmar Hopp Foundation and the German Ministry of Education and Science (BMBF: CLIOMMICS [01ZX1309]), and from National Cancer Institute of the National Institutes of Health under award numbers: R01CA186646, U01CA249955 (EEB). This work was also funded d by Portuguese National funds, through the Foundation for Science and Technology (FCT)—project UIDB/50026/2020 and UIDP/50026/2020 and by the project NORTE-01-0145-FEDER-000055, supported by Norte Portugal Regional Operational Programme (NORTE 2020), under the PORTUGAL 2020 Partnership Agreement, through the European Regional Development Fund (ERDF). We investigated the influence of autophagy-related variants in modulating Multiple Myeloma (MM) risk through a meta-analysis of germline genetic data on 234 autophagy-related genes from three independent study populations including 13,387 subjects of European ancestry (6863 MM patients and 6524 controls) and examined the functional mechanisms behind the observed associations. We identified SNPs within the six CD46, IKBKE, PARK2, ULK4, ATG5, and CDKN2A loci associated with MM risk and observed that their effect on disease risk was mediated by specific subsets of immune cells, as well as vitamin D3-, MCP-2-, and IL20-dependent mechanisms. |
| Audience | Academic |
| Author | Marek Dudzinski Charles Dumontet Daniele Campa Małgorzata Razny Mitchell J. Machiela Miroslaw Markiewicz Elizabeth E. Brown Rui Manuel Reis Nicola J. Camp Niels Weinhold Grzegorz Mazur Paula Ludovico Angelica Macauda Angelika Stein Malwina Rybicka-Ramos Manuel Jurado Vibeke Andersen Ulla Vogel John J. Spinelli Elzbieta Iskierka-Jażdżewska Jan Maciej Zaucha Sara Galimberti Waldemar Tomczak Stefano Landi Abhishek Kumar Stephen J. Chanock Katalin Kadar Parveen Bhatti Shaji K. Kumar Asta Försti Francisco García Verdejo Ramón García-Sanz Joaquín Martínez-López Matteo Pelosini José Manuel Sanchez-Maldonado Arnon Nagler Kari Hemminki Agnieszka Druzd-Sitek Celine M. Vachon Judit Varkonyi Esther Clavero María Eugenia Sarasquete Michelle A. T. Hildebrandt Krzysztof Jamroziak Andrés Jerez Enrico Orciuolo Sonja I. Berndt Mihai G. Netea Federico Canzian Aaron D. Norman Jonathan N. Hofmann Miguel Inacio da Silva Filho Rob Ter Horst Marzena Wątek Pedro Sánchez Rovira Juan Sainz Niels Abildgaard Artur Jurczyszyn Juan José Rodríguez Sevilla Aleksandra Butrym Ma |
| AuthorAffiliation | 40 Division of Molecular Genetic Epidemiology, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 580, D-69120 Heidelberg, Germany; m.dasilvafilho@dkfz-heidelberg.de 52 Department of Hematology and Transplantology, Medical University of Gdansk, 80-210 Gdansk, Poland; jzaucha@gumed.edu.pl 46 Cancer Control Research, BC Cancer, Vancouver, BC V5Z 4E6, Canada; pbhatti@bccrc.ca 50 Centre for Individualised Infection Medicine (CiiM) & TWINCORE, Joint Ventures between the Helmholtz-Centre for Infection Research (HZI) and the Hannover Medical School (MHH), 30625 Hannover, Germany 11 Department of Lymphoma–Myeloma, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; mhildebr@mdanderson.org 27 Alfred Sokolowski Specialist Hospital in Walbrzych Oncology Support Centre for Clinical Trials, 58-309 Walbrzych, Poland 71 Hopp Children’s Cancer Center (KiTZ), 69120 Heidelberg, Germany 13 Department of Internal Medicine V, University of Heidelberg, 691 |
| AuthorAffiliation_xml | – name: 68 Department of Pathology, Heersink School of Medicine, The University of Alabama at Birmingham, Birmingham, AL 35294, USA; elizabethbrown@uabmc.edu – name: 72 Department of Biochemistry and Molecular Biology I, University of Granada, 18071 Granada, Spain – name: 23 Department of Biology, University of Pisa, 56126 Pisa, Italy; stefano.landi@unipi.it (S.L.); daniele.campa@unipi.it (D.C.) – name: 25 School of Population and Public Health, University of British Columbia, Vancouver, BC V6T 1Z4, Canada – name: 29 Manipal Academy of Higher Education (MAHE), Manipal 576104, India – name: 12 Myeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA; niels.weinhold@med.uni-heidelberg.de – name: 30 Hospital 12 de Octubre, Complutense University, CNIO, CIBERONC, 28041 Madrid, Spain; jmarti01@ucm.es – name: 51 Genetic Epidemiology and Risk Assessment Program, Mayo Clinic Comprehensive Cancer Center, Division of Biomedical Statistics and Informatics, Department of Health Sciences Research, Mayo Clinic, Rochester, MN 55902, USA – name: 14 Haematology Unit, Department of Clinical and Experimental Medicine, University of Pisa/AOUP, 56126 Pisa, Italy; ga.buda@libero.it (G.B.); sara.galimberti@med.unipi.it (S.G.); e.orciuolo@ao-pisa.toscana.it (E.O.) – name: 66 Department of Medicine, University of California San Francisco Helen Diller Family Comprehensive Cancer Center, San Francisco, CA 94143, USA; elad.ziv@ucsf.edu – name: 1 Hematology Department, Virgen de las Nieves University Hospital, 18012 Granada, Spain; eclaverosa@hotmail.com (E.C.); manuel.jurado.sspa@juntadeandalucia.es (M.J.) – name: 16 Department of Hematooncology and Bone Marrow Transplantation, Medical University of Lublin, 20-059 Lublin, Poland; waldemar.tomczak@umlub.pl – name: 27 Alfred Sokolowski Specialist Hospital in Walbrzych Oncology Support Centre for Clinical Trials, 58-309 Walbrzych, Poland – name: 41 St Johns Hospital, 62769 Budapest, Hungary; kadarkataeszter@gmail.com – name: 60 Division of Hematology, Department of Internal Medicine, Mayo Clinic, Rochester, MN 55902, USA; rajkumar.vincent@mayo.edu (V.R.); kumar.shaji@mayo.edu (S.K.K.) – name: 7 Life and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, 4710-057 Braga, Portugal; mbmarques@med.uminho.pt (B.S.-M.); pludovico@med.uminho.pt (P.L.) – name: 8 Plasma Cell Dyscrasias Center, Department of Hematology, Jagiellonian University Medical College, 31-066 Kraków, Poland; mmjurczy@cyf-kr.edu.pl – name: 11 Department of Lymphoma–Myeloma, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; mhildebr@mdanderson.org – name: 44 U.O. Dipartimento di Ematologia, Azienda USL Toscana Nord Ovest, 57124 Livorno, Italy; matteo.pelosini@ao-pisa.toscana.it – name: 20 Holycross Medical Oncology Center, 25-735 Kielce, Poland; marzena.watek@wp.pl – name: 53 Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, 4710-057 Braga, Portugal and ICVS/3B’s-PT Government Associate Laboratory, 4710-057 Braga/Guimarães, Portugal; rreis@med.uminho.pt – name: 17 National Research Centre for the Working Environment, DK-2100 Copenhagen, Denmark; ubv@nfa.dk – name: 4 Genomic Epidemiology Group, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany; angelicamacauda@gmail.com (A.M.); a.stein@dkfz.de (A.S.); f.canzian@dkfz.de (F.C.) – name: 71 Hopp Children’s Cancer Center (KiTZ), 69120 Heidelberg, Germany – name: 59 Faculty of Medicine and Biomedical Center in Pilsen, Charles University in Prague, 30605 Pilsen, Czech Republic – name: 69 Department for Immunology & Metabolism, Life and Medical Sciences Institute (LIMES), University of Bonn, 53115 Bonn, Germany – name: 39 Department of Medical Oncology, Complejo Hospitalario de Jaén, 23007 Jaén, Spain; francisco.garcia.verdejo.sspa@juntadeandalucia.es (F.G.V.); oncopsr@yahoo.es (P.S.R.) – name: 70 Division of Pediatric Neurooncology, German Cancer Research Center (DKFZ), German Cancer Consortium (DKTK), 69120 Heidelberg, Germany; a.foersti@kitz-heidelberg.de – name: 37 Department of Hematology, University Hospital No. 2, 85-168 Bydgoszcz, Poland; marcin.kruszewski5@wp.pl – name: 35 Precision Medicine, School of Clinical Sciences at Monash Health, Monash University, Clayton, VIC 3168, Australia – name: 52 Department of Hematology and Transplantology, Medical University of Gdansk, 80-210 Gdansk, Poland; jzaucha@gumed.edu.pl – name: 50 Centre for Individualised Infection Medicine (CiiM) & TWINCORE, Joint Ventures between the Helmholtz-Centre for Infection Research (HZI) and the Hannover Medical School (MHH), 30625 Hannover, Germany – name: 64 Semmelweis University, 1083 Budapest, Hungary; varkonyi.judit@med.semmelweis-univ.hu – name: 3 Instituto de Investigación Biosanataria IBs, Granada, 18014 Granada, Spain – name: 26 Department of Cancer Prevention and Therapy, Wroclaw Medical University, 50-367 Wroclaw, Poland; aleksandra.butrym@gmail.com – name: 36 Department of Hematology, Specialist Hospital No. 1 in Bytom, Academy of Silesia, Faculty of Medicine, 40-055 Katowice, Poland; malwina.rybicka@gmail.com – name: 43 Division of Hematology/Oncology, Department of Medicine, School of Medicine, Department of Pathology, School of Medicine, Susan and Henry Samueli College of Health Sciences, Chao Family Comprehensive Cancer Center, University of California at Irvine, Irvine, CA 92697, USA; wcozen@hs.uci.edu – name: 46 Cancer Control Research, BC Cancer, Vancouver, BC V5Z 4E6, Canada; pbhatti@bccrc.ca – name: 5 Department of Internal Medicine and Radboud Center for Infectious Diseases, Radboud University Medical Center, 6525 GA Nijmegen, The Netherlands; rob.terhorst@radboudumc.nl (R.T.H.); yang.li@helmholtz-hzi.de (Y.L.); mihai.netea@radboudumc.nl (M.G.N.) – name: 42 Department of Hematology, Rydygier Hospital, 31-826 Cracow, Poland; m.razny@wp.pl – name: 22 Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA; hofmannjn@mail.nih.gov (J.N.H.); berndts@mail.nih.gov (S.I.B.); chanocks@mail.nih.gov (S.J.C.); machielamj@mail.nih.gov (M.J.M.) – name: 13 Department of Internal Medicine V, University of Heidelberg, 69120 Heidelberg, Germany – name: 24 Division of Population Oncology, BC Cancer, Vancouver, BC V5Z 4E6, Canada; jspinelli@bccrc.ca – name: 63 UMR INSERM 1052/CNRS 5286, University of Lyon, Hospices Civils de Lyon, 69008 Lyon, France; charles.dumontet@chu-lyon.fr – name: 61 Department of Internal Diseases, Occupational Medicine, Hypertension and Clinical Oncology, Wroclaw Medical University, 50-368 Wroclaw, Poland; grzegorzmaz@yahoo.com – name: 34 Centre for Epidemiology and Biostatistics, School of Population and Global Health, The University of Melbourne, Melbourne, VIC 3010, Australia – name: 67 Department of Hematology, Rigshospitalet, Copenhagen University, DK-2100 Copenhagen, Denmark; annette.juul.vangsted@regionh.dk – name: 49 Department of Lymphoproliferative Diseases, Maria Skłodowska Curie National Research Institute of Oncology, 02-781 Warsaw, Poland; adruzd@coi.waw.pl – name: 56 Molecular Diagnostics and Clinical Research Unit, Institute of Regional Health Research, University Hospital of Southern Denmark, DK-6200 Aabenraa, Denmark; vibeke.andersen1@rsyd.dk – name: 19 Department of Hematology, University Hospital, 30-688 Kraków, Poland; dariafm@poczta.fm – name: 45 Department of Medicine, University of Granada, 18012 Granada, Spain – name: 57 Department of Hematology, Transplantology and Internal Medicine, Medical University of Warsaw, 02-097 Warsaw, Poland; krzysztof.jamroziak@wp.pl – name: 28 Institute of Bioinformatics, International Technology Park, Bangalore 560066, India; abhishek@ibioinformatics.org – name: 38 Department of Hematology, Odense University Hospital, DK-5000 Odense, Denmark; niels.abildgaard@rsyd.dk – name: 62 Hematology Division, Chaim Sheba Medical Center, Tel Hashomer 52621, Israel; a.nagler@sheba.health.gov.il – name: 33 Cancer Epidemiology Division, Cancer Council Victoria, Melbourne, VIC 3004, Australia; graham.giles@cancervic.org.au – name: 54 Molecular Oncology Research Center, Barretos Cancer Hospital, Barretos 14784-400, Brazil – name: 15 Diagnostic Laboratory Unit in Hematology, University Hospital of Salamanca, IBSAL, CIBERONC, Centro de Investigación del Cáncer-IBMCC (USAL-CSIC), 37007 Salamanca, Spain; rgarcia@usal.es (R.G.-S.); a9136@usal.es (M.E.S.) – name: 58 Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 280, 69120 Heidelberg, Germany; k.hemminki@dkfz-heidelberg.de – name: 47 Program in Epidemiology, Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA – name: 32 Department of Hematology, Medical University of Lodz, 90-419 Lodz, Poland; elzbieta.iskierka-jazdzewska@umed.lodz.pl – name: 55 Department of Hematology, Hospital del Mar, 08003 Barcelona, Spain; jrodsevilla@gmail.com – name: 21 Institute of Hematology and Transfusion Medicine, 00-791 Warsaw, Poland – name: 48 Department of Hematology, Institute of Medical Sciences, College of Medical Sciences, University of Rzeszow, 35-310 Rzeszow, Poland; marekdudzi@gmail.com (M.D.); mir.markiewicz@wp.pl (M.M.) – name: 6 CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, 1090 Vienna, Austria – name: 9 Department of Biostatistics and Epidemiology, Arnold School of Public Health, University of South Carolina, Greenville, SC 29208, USA; claygila@mailbox.sc.edu – name: 31 Department of Hematology, Military Institute of Medicine, 04-141 Warsaw, Poland; suboczka@poczta.onet.pl – name: 40 Division of Molecular Genetic Epidemiology, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 580, D-69120 Heidelberg, Germany; m.dasilvafilho@dkfz-heidelberg.de – name: 65 Division of Hematology, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT 84112, USA; nicki.camp@hci.utah.edu – name: 18 Department of Hematology, Experimental Hematology Unit, Vall d’Hebron Institute of Oncology (VHIO), University Hospital Vall d’Hebron, 08035 Barcelona, Spain; anjecayu@gmail.com – name: 10 Division of Epidemiology, Department of Health Sciences Research, Mayo Clinic, Rochester, MN 55902, USA; aarondeannorman@gmail.com (A.D.N.); vachon.celine@mayo.edu (C.M.V.) – name: 2 Genomic Oncology Area, GENYO, Centre for Genomics and Oncological Research, Pfizer/University of Granada/Andalusian Regional Government, PTS, 18016 Granada, Spain; josemanuel.sanchez@genyo.es |
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| Cites_doi | 10.1016/j.ceb.2009.11.003 10.1038/ncb1482 10.1046/j.1365-2141.2003.04355.x 10.1126/science.1262110 10.1016/j.tibs.2008.01.002 10.1093/jn/136.3.561 10.18632/oncotarget.10665 10.4049/jimmunol.1002404 10.1038/ng.2756 10.1038/ng.384 10.1016/j.biopha.2019.109434 10.4049/jimmunol.1102108 10.1016/S1470-2045(14)70442-5 10.1016/j.cell.2016.10.017 10.1038/nature07208 10.1155/2016/7870590 10.4049/jimmunol.1202493 10.1038/nrm2529 10.1126/science.1096645 10.1016/j.exphem.2014.06.005 10.1016/j.jbo.2019.100253 10.15252/embj.2021108863 10.3390/cancers13102326 10.1007/s00280-013-2156-3 10.1182/blood.V95.5.1869.005k09_1869_1871 10.1016/j.leukres.2017.06.002 10.1038/s41598-020-61331-5 10.1016/j.celrep.2016.10.053 10.1161/CIRCGENETICS.110.948935 10.1158/0008-5472.CAN-04-3684 10.1182/bloodadvances.2020001435 10.1093/bioinformatics/btq340 10.1158/1535-7163.MCT-08-1177 10.1182/blood-2005-03-1158 10.1038/sj.bjc.6600833 10.1016/j.tranon.2018.08.014 10.21037/atm-22-70 10.1146/annurev-immunol-020711-074948 10.1016/j.coi.2011.10.006 10.1038/ng.2981 10.1080/10428190310001625836 10.1038/nature12531 10.1038/s41375-018-0036-x 10.1046/j.1365-2141.1998.00609.x 10.1186/s12885-017-3715-5 10.18632/oncotarget.6365 10.4049/jimmunol.1002223 10.21037/tau-20-498 10.1038/ng.993 10.1371/journal.pgen.1000529 10.1212/WNL.0b013e3181f4d832 10.1007/s12032-015-0488-z 10.1038/leu.2014.110 10.3390/jcm11102913 10.1056/NEJMra1011442 10.1073/pnas.0610299104 10.1073/pnas.1334037100 10.1016/j.febslet.2010.02.060 10.3389/fimmu.2019.02759 10.4049/jimmunol.170.6.3125 10.1038/s41419-022-04629-8 10.1210/en.2008-1395 10.4065/78.1.21 10.1038/s41467-018-04989-w 10.4161/auto.5.5.8494 10.1016/j.immuni.2013.03.003 10.1038/leu.2012.159 10.1182/blood-2005-08-3531 10.1182/blood-2006-04-016055 10.1038/ncb1192 10.1371/journal.pone.0010693 10.1038/ncomms12050 10.1038/bcj.2012.47 10.1038/bjc.2016.20 10.3390/jcm9020552 10.1073/pnas.0501190102 10.4161/auto.29264 10.18632/oncotarget.2590 10.1038/ni921 10.1016/j.immuni.2013.07.017 10.18632/oncotarget.27190 |
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| Contributor | NIH - National Cancer Institute (NCI) (Estados Unidos) Fundacao para a Ciencia e a Tecnologia (FCT) Dietmar Hopp Foundation Unión Europea. Comisión Europea. Horizonte Europa Institut Català de la Salut [Clavero E] Hematology Department, Virgen de las Nieves University Hospital, Granada, Spain. [Sanchez-Maldonado JM] Genomic Oncology Area, GENYO, Centre for Genomics and Oncological Research, Pfizer/University of Granada/Andalusian Regional Government, PTS, Granada, Spain. Instituto de Investigación Biosanataria IBs, Granada, Granada, Spain. [Macauda A] Genomic Epidemiology Group, German Cancer Research Center (DKFZ), Heidelberg, Germany. [Ter Horst R] Department of Internal Medicine and Radboud Center for Infectious Diseases, Radboud University Medical Center, GA Nijmegen, The Netherlands. CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria. [Sampaio-Marques B] Life and Health Sciences Research Institute (ICVS), School of Medicine, University of M |
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| Copyright | COPYRIGHT 2023 MDPI AG 2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. Distributed under a Creative Commons Attribution 4.0 International License 2023 by the authors. 2023 |
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| Keywords | genetic variants multiple myeloma autophagy genetic susceptibility |
| Language | English |
| License | https://creativecommons.org/licenses/by/4.0 Distributed under a Creative Commons Attribution 4.0 International License: http://creativecommons.org/licenses/by/4.0 Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Article-2 ObjectType-Feature-1 content type line 23 These authors contributed equally to this work. |
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| References | Went (ref_38) 2018; 9 ref_50 Hildebrandt (ref_69) 2020; 4 Li (ref_83) 2016; 167 Fitzgerald (ref_45) 2003; 4 Tucci (ref_29) 2014; 42 ref_56 Rajkumar (ref_78) 2014; 15 Yu (ref_14) 2004; 304 Dykstra (ref_25) 2015; 6 Desantis (ref_26) 2018; 11 Ullah (ref_49) 2019; 17 Joosten (ref_84) 2016; 17 Canhao (ref_82) 2020; 10 Nedjic (ref_23) 2008; 455 Kuballa (ref_17) 2012; 30 Obeng (ref_6) 2006; 107 Escalante (ref_27) 2013; 71 Gschwandtner (ref_51) 2019; 10 Kay (ref_74) 1998; 100 Landowski (ref_8) 2005; 65 Kyle (ref_2) 2003; 78 Valkovic (ref_52) 2016; 2016 Aguilera (ref_67) 2008; 28 Catley (ref_10) 2006; 108 Broderick (ref_63) 2011; 44 Ma (ref_20) 2013; 38 Alexandrakis (ref_42) 2015; 32 Jin (ref_58) 2019; 119 Kay (ref_62) 2010; 75 Yousefi (ref_70) 2006; 8 Westra (ref_43) 2013; 45 Dilworth (ref_72) 2000; 95 Hudlebusch (ref_44) 2004; 45 Willer (ref_80) 2010; 26 Hoang (ref_5) 2009; 8 Tanaka (ref_61) 2010; 584 Chau (ref_46) 2008; 33 Lupianez (ref_76) 2016; 7 Heuck (ref_71) 2013; 190 Liang (ref_31) 2010; 22 Huang (ref_32) 2022; 13 Rohan (ref_68) 2009; 150 Consortium (ref_40) 2015; 348 Mitchell (ref_39) 2016; 7 ref_79 Martino (ref_81) 2012; 40 ref_34 ref_77 Mitsiades (ref_9) 2006; 107 Shimizu (ref_12) 2004; 6 ref_75 Yun (ref_24) 2017; 59 ref_73 Viziteu (ref_59) 2016; 114 Folkersen (ref_65) 2010; 3 Leich (ref_47) 2013; 3 Sukhdeo (ref_54) 2007; 104 Vogl (ref_28) 2014; 10 Kastritis (ref_3) 2014; 28 Jovanovic (ref_57) 2018; 32 Dengjel (ref_21) 2005; 102 Gilad (ref_48) 2019; 10 Bradwell (ref_4) 2013; 27 Gyory (ref_55) 2003; 170 Gong (ref_60) 2014; 46 Schwarten (ref_15) 2009; 5 Wang (ref_36) 2022; 10 Palumbo (ref_1) 2011; 364 Cross (ref_66) 2006; 136 Lee (ref_7) 2003; 100 Arsov (ref_11) 2011; 186 Cheng (ref_35) 2020; 9 Ma (ref_16) 2013; 39 Levy (ref_64) 2009; 41 Zhu (ref_37) 2019; 18 Broek (ref_53) 2003; 88 Klionsky (ref_30) 2021; 40 Kroemer (ref_13) 2008; 9 Deretic (ref_19) 2012; 189 Deretic (ref_18) 2012; 24 Jaganathan (ref_33) 2014; 5 Jia (ref_22) 2011; 186 Lappalainen (ref_41) 2013; 501 |
| References_xml | – volume: 22 start-page: 226 year: 2010 ident: ref_31 article-title: Autophagy genes as tumor suppressors publication-title: Curr. Opin. Cell Biol. doi: 10.1016/j.ceb.2009.11.003 – volume: 40 start-page: 625 year: 2012 ident: ref_81 article-title: Genetics and molecular epidemiology of multiple myeloma: The rationale for the IMMEnSE consortium (review) publication-title: Int. J. Oncol. – volume: 8 start-page: 1124 year: 2006 ident: ref_70 article-title: Calpain-mediated cleavage of Atg5 switches autophagy to apoptosis publication-title: Nat. Cell Biol. doi: 10.1038/ncb1482 – ident: ref_77 doi: 10.1046/j.1365-2141.2003.04355.x – volume: 348 start-page: 648 year: 2015 ident: ref_40 article-title: Human genomics. The Genotype-Tissue Expression (GTEx) pilot analysis: Multitissue gene regulation in humans publication-title: Science doi: 10.1126/science.1262110 – volume: 33 start-page: 171 year: 2008 ident: ref_46 article-title: Are the IKKs and IKK-related kinases TBK1 and IKK-epsilon similarly activated? publication-title: Trends Biochem. Sci. doi: 10.1016/j.tibs.2008.01.002 – volume: 136 start-page: 561 year: 2006 ident: ref_66 article-title: Nutrients regulate the colonic vitamin D system in mice: Relevance for human colon malignancy publication-title: J. Nutr. doi: 10.1093/jn/136.3.561 – volume: 7 start-page: 59029 year: 2016 ident: ref_76 article-title: A common variant within the HNF1B gene is associated with overall survival of multiple myeloma patients: Results from the IMMEnSE consortium and meta-analysis publication-title: Oncotarget doi: 10.18632/oncotarget.10665 – volume: 186 start-page: 5313 year: 2011 ident: ref_22 article-title: Temporal regulation of intracellular organelle homeostasis in T lymphocytes by autophagy publication-title: J. Immunol. doi: 10.4049/jimmunol.1002404 – volume: 45 start-page: 1238 year: 2013 ident: ref_43 article-title: Systematic identification of trans eQTLs as putative drivers of known disease associations publication-title: Nat. Genet. doi: 10.1038/ng.2756 – volume: 41 start-page: 677 year: 2009 ident: ref_64 article-title: Genome-wide association study of blood pressure and hypertension publication-title: Nat. Genet. doi: 10.1038/ng.384 – volume: 119 start-page: 109434 year: 2019 ident: ref_58 article-title: The mechanism of SP1/p300 complex promotes proliferation of multiple myeloma cells through regulating IQGAP1 transcription publication-title: Biomed. Pharmacother. doi: 10.1016/j.biopha.2019.109434 – volume: 189 start-page: 15 year: 2012 ident: ref_19 article-title: Autophagy: An emerging immunological paradigm publication-title: J. Immunol. doi: 10.4049/jimmunol.1102108 – volume: 15 start-page: e538 year: 2014 ident: ref_78 article-title: International Myeloma Working Group updated criteria for the diagnosis of multiple myeloma publication-title: Lancet Oncol. doi: 10.1016/S1470-2045(14)70442-5 – volume: 167 start-page: 1099 year: 2016 ident: ref_83 article-title: A Functional Genomics Approach to Understand Variation in Cytokine Production in Humans publication-title: Cell doi: 10.1016/j.cell.2016.10.017 – volume: 455 start-page: 396 year: 2008 ident: ref_23 article-title: Autophagy in thymic epithelium shapes the T-cell repertoire and is essential for tolerance publication-title: Nature doi: 10.1038/nature07208 – volume: 2016 start-page: 7870590 year: 2016 ident: ref_52 article-title: Plasma Levels of Monocyte Chemotactic Protein-1 Are Associated with Clinical Features and Angiogenesis in Patients with Multiple Myeloma publication-title: Biomed. Res. Int. doi: 10.1155/2016/7870590 – volume: 190 start-page: 2966 year: 2013 ident: ref_71 article-title: Myeloma is characterized by stage-specific alterations in DNA methylation that occur early during myelomagenesis publication-title: J. Immunol. doi: 10.4049/jimmunol.1202493 – volume: 9 start-page: 1004 year: 2008 ident: ref_13 article-title: Autophagic cell death: The story of a misnomer publication-title: Nat. Rev. Mol. Cell Biol. doi: 10.1038/nrm2529 – volume: 304 start-page: 1500 year: 2004 ident: ref_14 article-title: Regulation of an ATG7-beclin 1 program of autophagic cell death by caspase-8 publication-title: Science doi: 10.1126/science.1096645 – volume: 42 start-page: 897 year: 2014 ident: ref_29 article-title: An imbalance between Beclin-1 and p62 expression promotes the proliferation of myeloma cells through autophagy regulation publication-title: Exp. Hematol. doi: 10.1016/j.exphem.2014.06.005 – volume: 17 start-page: 100253 year: 2019 ident: ref_49 article-title: The role of CXCR4 in multiple myeloma: Cells’ journey from bone marrow to beyond publication-title: J. Bone Oncol. doi: 10.1016/j.jbo.2019.100253 – volume: 40 start-page: e108863 year: 2021 ident: ref_30 article-title: Autophagy in major human diseases publication-title: EMBO J. doi: 10.15252/embj.2021108863 – volume: 28 start-page: 2613 year: 2008 ident: ref_67 article-title: Vitamin D and Wnt/beta-catenin pathway in colon cancer: Role and regulation of DICKKOPF genes publication-title: Anticancer Res. – ident: ref_56 doi: 10.3390/cancers13102326 – volume: 71 start-page: 1567 year: 2013 ident: ref_27 article-title: Preventing the autophagic survival response by inhibition of calpain enhances the cytotoxic activity of bortezomib in vitro and in vivo publication-title: Cancer Chemother. Pharmacol. doi: 10.1007/s00280-013-2156-3 – volume: 95 start-page: 1869 year: 2000 ident: ref_72 article-title: Germline CDKN2A mutation implicated in predisposition to multiple myeloma publication-title: Blood doi: 10.1182/blood.V95.5.1869.005k09_1869_1871 – volume: 59 start-page: 97 year: 2017 ident: ref_24 article-title: Targeting autophagy in multiple myeloma publication-title: Leuk. Res. doi: 10.1016/j.leukres.2017.06.002 – volume: 10 start-page: 4316 year: 2020 ident: ref_82 article-title: NFKB2 polymorphisms associate with the risk of developing rheumatoid arthritis and response to TNF inhibitors: Results from the REPAIR consortium publication-title: Sci. Rep. doi: 10.1038/s41598-020-61331-5 – volume: 17 start-page: 2474 year: 2016 ident: ref_84 article-title: Differential Effects of Environmental and Genetic Factors on T and B Cell Immune Traits publication-title: Cell Rep. doi: 10.1016/j.celrep.2016.10.053 – volume: 18 start-page: 5310 year: 2019 ident: ref_37 article-title: A predicted risk score based on the expression of 16 autophagy-related genes for multiple myeloma survival publication-title: Oncol. Lett. – volume: 3 start-page: 365 year: 2010 ident: ref_65 article-title: Association of genetic risk variants with expression of proximal genes identifies novel susceptibility genes for cardiovascular disease publication-title: Circ. Cardiovasc. Genet. doi: 10.1161/CIRCGENETICS.110.948935 – volume: 65 start-page: 3828 year: 2005 ident: ref_8 article-title: Mitochondrial-mediated disregulation of Ca2+ is a critical determinant of Velcade (PS-341/bortezomib) cytotoxicity in myeloma cell lines publication-title: Cancer Res. doi: 10.1158/0008-5472.CAN-04-3684 – volume: 4 start-page: 2789 year: 2020 ident: ref_69 article-title: Coinherited genetics of multiple myeloma and its precursor, monoclonal gammopathy of undetermined significance publication-title: Blood Adv. doi: 10.1182/bloodadvances.2020001435 – volume: 26 start-page: 2190 year: 2010 ident: ref_80 article-title: METAL: Fast and efficient meta-analysis of genomewide association scans publication-title: Bioinformatics doi: 10.1093/bioinformatics/btq340 – volume: 8 start-page: 1974 year: 2009 ident: ref_5 article-title: Effect of autophagy on multiple myeloma cell viability publication-title: Mol. Cancer Ther. doi: 10.1158/1535-7163.MCT-08-1177 – volume: 107 start-page: 1092 year: 2006 ident: ref_9 article-title: Antimyeloma activity of heat shock protein-90 inhibition publication-title: Blood doi: 10.1182/blood-2005-03-1158 – volume: 88 start-page: 855 year: 2003 ident: ref_53 article-title: Chemokine receptor CCR2 is expressed by human multiple myeloma cells and mediates migration to bone marrow stromal cell-produced monocyte chemotactic proteins MCP-1, -2 and -3 publication-title: Br. J. Cancer doi: 10.1038/sj.bjc.6600833 – volume: 11 start-page: 1350 year: 2018 ident: ref_26 article-title: Autophagy: A New Mechanism of Prosurvival and Drug Resistance in Multiple Myeloma publication-title: Transl. Oncol. doi: 10.1016/j.tranon.2018.08.014 – volume: 10 start-page: 228 year: 2022 ident: ref_36 article-title: Autophagy-related genes are potential diagnostic biomarkers for dermatomyositis publication-title: Ann. Transl. Med. doi: 10.21037/atm-22-70 – volume: 30 start-page: 611 year: 2012 ident: ref_17 article-title: Autophagy and the immune system publication-title: Annu. Rev. Immunol. doi: 10.1146/annurev-immunol-020711-074948 – volume: 24 start-page: 21 year: 2012 ident: ref_18 article-title: Autophagy as an innate immunity paradigm: Expanding the scope and repertoire of pattern recognition receptors publication-title: Curr. Opin. Immunol. doi: 10.1016/j.coi.2011.10.006 – volume: 46 start-page: 588 year: 2014 ident: ref_60 article-title: Pan-cancer genetic analysis identifies PARK2 as a master regulator of G1/S cyclins publication-title: Nat. Genet. doi: 10.1038/ng.2981 – volume: 45 start-page: 1215 year: 2004 ident: ref_44 article-title: Expression of HOXA genes in patients with multiple myeloma publication-title: Leuk. Lymphoma doi: 10.1080/10428190310001625836 – volume: 501 start-page: 506 year: 2013 ident: ref_41 article-title: Transcriptome and genome sequencing uncovers functional variation in humans publication-title: Nature doi: 10.1038/nature12531 – volume: 32 start-page: 1295 year: 2018 ident: ref_57 article-title: Targeting MYC in multiple myeloma publication-title: Leukemia doi: 10.1038/s41375-018-0036-x – volume: 100 start-page: 459 year: 1998 ident: ref_74 article-title: T-helper phenotypes in the blood of myeloma patients on ECOG phase III trials E9486/E3A93 publication-title: Br. J. Haematol. doi: 10.1046/j.1365-2141.1998.00609.x – ident: ref_73 doi: 10.1186/s12885-017-3715-5 – volume: 6 start-page: 41535 year: 2015 ident: ref_25 article-title: Mechanisms for autophagy modulation by isoprenoid biosynthetic pathway inhibitors in multiple myeloma cells publication-title: Oncotarget doi: 10.18632/oncotarget.6365 – volume: 186 start-page: 2201 year: 2011 ident: ref_11 article-title: A role for autophagic protein beclin 1 early in lymphocyte development publication-title: J. Immunol. doi: 10.4049/jimmunol.1002223 – volume: 9 start-page: 2616 year: 2020 ident: ref_35 article-title: Autophagy-related genes are potential diagnostic and prognostic biomarkers in prostate cancer publication-title: Transl. Androl. Urol. doi: 10.21037/tau-20-498 – volume: 44 start-page: 58 year: 2011 ident: ref_63 article-title: Common variation at 3p22.1 and 7p15.3 influences multiple myeloma risk publication-title: Nat. Genet. doi: 10.1038/ng.993 – ident: ref_79 doi: 10.1371/journal.pgen.1000529 – volume: 75 start-page: 1189 year: 2010 ident: ref_62 article-title: A comprehensive analysis of deletions, multiplications, and copy number variations in PARK2 publication-title: Neurology doi: 10.1212/WNL.0b013e3181f4d832 – volume: 32 start-page: 42 year: 2015 ident: ref_42 article-title: Circulating serum levels of IL-20 in multiple myeloma patients: Its significance in angiogenesis and disease activity publication-title: Med. Oncol. doi: 10.1007/s12032-015-0488-z – volume: 28 start-page: 2075 year: 2014 ident: ref_3 article-title: Preserved levels of uninvolved immunoglobulins are independently associated with favorable outcome in patients with symptomatic multiple myeloma publication-title: Leukemia doi: 10.1038/leu.2014.110 – ident: ref_50 doi: 10.3390/jcm11102913 – volume: 364 start-page: 1046 year: 2011 ident: ref_1 article-title: Multiple myeloma publication-title: N. Engl. J. Med. doi: 10.1056/NEJMra1011442 – volume: 104 start-page: 7516 year: 2007 ident: ref_54 article-title: Targeting the beta-catenin/TCF transcriptional complex in the treatment of multiple myeloma publication-title: Proc. Natl. Acad. Sci. USA doi: 10.1073/pnas.0610299104 – volume: 100 start-page: 9946 year: 2003 ident: ref_7 article-title: Proteasome inhibitors disrupt the unfolded protein response in myeloma cells publication-title: Proc. Natl. Acad. Sci. USA doi: 10.1073/pnas.1334037100 – volume: 584 start-page: 1386 year: 2010 ident: ref_61 article-title: Parkin-mediated selective mitochondrial autophagy, mitophagy: Parkin purges damaged organelles from the vital mitochondrial network publication-title: FEBS Lett. doi: 10.1016/j.febslet.2010.02.060 – volume: 10 start-page: 2759 year: 2019 ident: ref_51 article-title: More Than Just Attractive: How CCL2 Influences Myeloid Cell Behavior Beyond Chemotaxis publication-title: Front. Immunol. doi: 10.3389/fimmu.2019.02759 – volume: 170 start-page: 3125 year: 2003 ident: ref_55 article-title: Identification of a functionally impaired positive regulatory domain I binding factor 1 transcription repressor in myeloma cell lines publication-title: J. Immunol. doi: 10.4049/jimmunol.170.6.3125 – volume: 13 start-page: 197 year: 2022 ident: ref_32 article-title: NEDD4L binds the proteasome and promotes autophagy and bortezomib sensitivity in multiple myeloma publication-title: Cell Death Dis. doi: 10.1038/s41419-022-04629-8 – volume: 150 start-page: 2046 year: 2009 ident: ref_68 article-title: 1Alpha,25-dihydroxyvitamin D3 reduces c-Myc expression, inhibiting proliferation and causing G1 accumulation in C4-2 prostate cancer cells publication-title: Endocrinology doi: 10.1210/en.2008-1395 – volume: 78 start-page: 21 year: 2003 ident: ref_2 article-title: Review of 1027 patients with newly diagnosed multiple myeloma publication-title: Mayo Clin. Proc. doi: 10.4065/78.1.21 – volume: 9 start-page: 3707 year: 2018 ident: ref_38 article-title: Identification of multiple risk loci and regulatory mechanisms influencing susceptibility to multiple myeloma publication-title: Nat. Commun. doi: 10.1038/s41467-018-04989-w – volume: 5 start-page: 690 year: 2009 ident: ref_15 article-title: Nix directly binds to GABARAP: A possible crosstalk between apoptosis and autophagy publication-title: Autophagy doi: 10.4161/auto.5.5.8494 – volume: 38 start-page: 729 year: 2013 ident: ref_20 article-title: Anticancer chemotherapy-induced intratumoral recruitment and differentiation of antigen-presenting cells publication-title: Immunity doi: 10.1016/j.immuni.2013.03.003 – volume: 27 start-page: 202 year: 2013 ident: ref_4 article-title: Prognostic utility of intact immunoglobulin Ig’kappa/Ig’lambda ratios in multiple myeloma patients publication-title: Leukemia doi: 10.1038/leu.2012.159 – volume: 107 start-page: 4907 year: 2006 ident: ref_6 article-title: Proteasome inhibitors induce a terminal unfolded protein response in multiple myeloma cells publication-title: Blood doi: 10.1182/blood-2005-08-3531 – volume: 108 start-page: 3441 year: 2006 ident: ref_10 article-title: Aggresome induction by proteasome inhibitor bortezomib and alpha-tubulin hyperacetylation by tubulin deacetylase (TDAC) inhibitor LBH589 are synergistic in myeloma cells publication-title: Blood doi: 10.1182/blood-2006-04-016055 – volume: 6 start-page: 1221 year: 2004 ident: ref_12 article-title: Role of Bcl-2 family proteins in a non-apoptotic programmed cell death dependent on autophagy genes publication-title: Nat. Cell Biol. doi: 10.1038/ncb1192 – ident: ref_75 doi: 10.1371/journal.pone.0010693 – volume: 7 start-page: 12050 year: 2016 ident: ref_39 article-title: Genome-wide association study identifies multiple susceptibility loci for multiple myeloma publication-title: Nat. Commun. doi: 10.1038/ncomms12050 – volume: 3 start-page: e102 year: 2013 ident: ref_47 article-title: Multiple myeloma is affected by multiple and heterogeneous somatic mutations in adhesion- and receptor tyrosine kinase signaling molecules publication-title: Blood Cancer J. doi: 10.1038/bcj.2012.47 – volume: 114 start-page: 519 year: 2016 ident: ref_59 article-title: Chetomin, targeting HIF-1alpha/p300 complex, exhibits antitumour activity in multiple myeloma publication-title: Br. J. Cancer doi: 10.1038/bjc.2016.20 – ident: ref_34 doi: 10.3390/jcm9020552 – volume: 102 start-page: 7922 year: 2005 ident: ref_21 article-title: Autophagy promotes MHC class II presentation of peptides from intracellular source proteins publication-title: Proc. Natl. Acad. Sci. USA doi: 10.1073/pnas.0501190102 – volume: 10 start-page: 1380 year: 2014 ident: ref_28 article-title: Combined autophagy and proteasome inhibition: A phase 1 trial of hydroxychloroquine and bortezomib in patients with relapsed/refractory myeloma publication-title: Autophagy doi: 10.4161/auto.29264 – volume: 5 start-page: 12358 year: 2014 ident: ref_33 article-title: Bortezomib induces AMPK-dependent autophagosome formation uncoupled from apoptosis in drug resistant cells publication-title: Oncotarget doi: 10.18632/oncotarget.2590 – volume: 4 start-page: 491 year: 2003 ident: ref_45 article-title: IKKepsilon and TBK1 are essential components of the IRF3 signaling pathway publication-title: Nat. Immunol. doi: 10.1038/ni921 – volume: 39 start-page: 211 year: 2013 ident: ref_16 article-title: Autophagy and cellular immune responses publication-title: Immunity doi: 10.1016/j.immuni.2013.07.017 – volume: 10 start-page: 5480 year: 2019 ident: ref_48 article-title: The role of CD24 in multiple myeloma tumorigenicity and effects of the microenvironment on its expression publication-title: Oncotarget doi: 10.18632/oncotarget.27190 |
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| Snippet | Functional data used in this project have been meticulously catalogued and archived in the BBMRI-NL data infrastructure (https://hfgp.bbmri.nl/, accessed on 12... Multiple myeloma (MM) arises following malignant proliferation of plasma cells in the bone marrow, that secrete high amounts of specific monoclonal... We investigated the influence of autophagy-related variants in modulating Multiple Myeloma (MM) risk through a meta-analysis of germline genetic data on 234... Simple SummaryWe investigated the influence of autophagy-related variants in modulating Multiple Myeloma (MM) risk through a meta-analysis of germline genetic... |
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| SubjectTerms | Analysis Apoptosis Autofàgia Autophagy autophagy; genetic susceptibility; genetic variants; multiple myeloma B cells Biological Factors::Biomarkers [CHEMICALS AND DRUGS] Biomarkers Bone marrow Cancer Cells Cell Physiological Phenomena::Cell Death::Autophagy [PHENOMENA AND PROCESSES] Development and progression Disease susceptibility enfermedades hematológicas y linfáticas::enfermedades hematológicas::trastornos de las proteínas sanguíneas::paraproteinemias::enfermedades hematológicas y linfáticas::enfermedades hematológicas::mieloma múltiple [ENFERMEDADES] factores biológicos::biomarcadores [COMPUESTOS QUÍMICOS Y DROGAS] fenómenos fisiológicos celulares::muerte celular::autofagia [FENÓMENOS Y PROCESOS] Genes Genetic aspects Genetic polymorphisms Genetic susceptibility Genetic variants Hemic and Lymphatic Diseases::Hematologic Diseases::Blood Protein Disorders::Paraproteinemias::Hemic and Lymphatic Diseases::Hematologic Diseases::Multiple Myeloma [DISEASES] Humans Immune response Immunoglobulin M Immunoglobulins Independent study Leukocytes Leukocytes, Mononuclear Leukocytes, Mononuclear - pathology Life Sciences Marcadors bioquímics Medical prognosis Meta-analysis Mieloma múltiple - Aspectes genètics Mononuclear/pathology Multiple myeloma Multiple Myeloma - genetics Multiple Myeloma - pathology multiple myeloma; autophagy; genetic variants; genetic susceptibility Other subheadings::Other subheadings::/genetics [Other subheadings] Otros calificadores::Otros calificadores::/genética [Otros calificadores] Proteins Radboud University Medical Center Radboudumc 4: lnfectious Diseases and Global Health Internal Medicine |
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| Title | Polymorphisms within Autophagy-Related Genes as Susceptibility Biomarkers for Multiple Myeloma: A Meta-Analysis of Three Large Cohorts and Functional Characterization |
| URI | https://cir.nii.ac.jp/crid/1871991017700473856 http://hdl.handle.net/1822/85628 https://www.ncbi.nlm.nih.gov/pubmed/37239846 https://www.proquest.com/docview/2819457799 https://www.proquest.com/docview/2820021879 https://cnrs.hal.science/hal-04914042 https://pubmed.ncbi.nlm.nih.gov/PMC10218542 |
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