Abstract
The Catalogue of Somatic Mutations in Cancer (COSMIC) Cancer Gene Census (CGC) is an expert-curated description of the genes driving human cancer that is used as a standard in cancer genetics across basic research, medical reporting and pharmaceutical development. After a major expansion and complete re-evaluation, the 2018 CGC describes in detail the effect of 719 cancer-driving genes. The recent expansion includes functional and mechanistic descriptions of how each gene contributes to disease generation in terms of the key cancer hallmarks and the impact of mutations on gene and protein function. These functional characteristics depict the extraordinary complexity of cancer biology and suggest multiple cancer-related functions for many genes, which are often highly tissue-dependent or tumour stage-dependent. The 2018 CGC encompasses a second tier, describing an expanding list of genes (currently 145) from more recent cancer studies that show supportive but less detailed indications of a role in cancer.
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References
Futreal, P. A. et al. A census of human cancer genes. Nat. Rev. Cancer 4, 177–183 (2004). This publication describes the first version of the CGC, presenting 291 genes causally implicated in cancer and characterizing their alterations.
Department of Health & Social Care. Whole Genome Analysis — 100,000 Genomes Project Cancer Programme. Genomics England https://www.genomicsengland.co.uk/information-for-gmc-staff/cancer-programme/genome-analysis (2017).
Patel, M. N., Halling-Brown, M. D., Tym, J. E., Workman, P. & Al-Lazikani, B. Objective assessment of cancer genes for drug discovery. Nat. Rev. Drug Discov. 12, 35–50 (2013).
Koscielny, G. et al. Open Targets: a platform for therapeutic target identification and validation. Nucleic Acids Res. 45, D985–D994 (2017).
Ramos, A. H. et al. Oncotator: cancer variant annotation tool. Hum. Mutat. 36, E2423–E2429 (2015).
Van den Eynden, J., Fierro, A. C., Verbeke, L. P. & Marchal, K. SomInaClust: detection of cancer genes based on somatic mutation patterns of inactivation and clustering. BMC Bioinformatics 16, 125 (2015).
Schroeder, M. P., Rubio-Perez, C., Tamborero, D., Gonzalez-Perez, A. & Lopez-Bigas, N. OncodriveROLE classifies cancer driver genes in loss of function and activating mode of action. Bioinformatics 30, i549–i555 (2014).
Tamborero, D., Gonzalez-Perez, A. & Lopez-Bigas, N. OncodriveCLUST: exploiting the positional clustering of somatic mutations to identify cancer genes. Bioinformatics 29, 2238–2244 (2013).
Forbes, S. A. et al. COSMIC: somatic cancer genetics at high-resolution. Nucleic Acids Res. 45, D777–D783 (2017).
Forbes, S. A. et al. COSMIC: high-resolution cancer genetics using the catalogue of somatic mutations in cancer. Curr. Protoc. Hum. Genet. 91, 10.11.1–10.11.37 (2016). This publication describes COSMIC and provides protocols for access and data analysis.
Vogelstein, B. et al. Cancer genome landscapes. Science 339, 1546–1558 (2013). This review describes alterations to genes, and signalling and metabolic pathways driving cancer, identified through whole-genome sequencing of cancer samples.
Flaherty, K. T. et al. Inhibition of mutated, activated BRAF in metastatic melanoma. N. Engl. J. Med. 363, 809–819 (2010).
Yap, T. A., Sandhu, S. K., Carden, C. P. & de Bono, J. S. Poly(ADP-Ribose) polymerase (PARP) inhibitors: exploiting a synthetic lethal strategy in the clinic. CA Cancer J. Clin. 61, 31–49 (2011). This study describes the principles of PARP inhibitor-dependent synthetic lethality in BRCA-depleted cancers and its implications for cancer therapy.
Hanahan, D. & Weinberg, R. A. The hallmarks of cancer. Cell 100, 57–70 (2000).
Hanahan, D. & Weinberg, R. A. Hallmarks of cancer: the next generation. Cell 144, 646–674 (2011). This review describes an improved model of the hallmarks that define cancers and malignant transformation.
Mertens, F., Johansson, B., Fioretos, T. & Mitelman, F. The emerging complexity of gene fusions in cancer. Nat. Rev. Cancer 15, 371–381 (2015).
Cerveira, N. et al. TMPRSS2-ERG gene fusion causing ERG overexpression precedes chromosome copy number changes in prostate carcinomas and paired HGPIN lesions. Neoplasia 8, 826–832 (2006).
Tian, E. et al. In multiple myeloma, 14q32 translocations are non-random chromosomal fusions driving high expression levels of the respective partner genes. Genes Chromosomes Cancer 53, 549–557 (2014).
Zhao, X., Ghaffari, S., Lodish, H., Malashkevich, V. N. & Kim, P. S. Structure of the Bcr-Abl oncoprotein oligomerization domain. Nat. Struct. Biol. 9, 117–120 (2002).
Nakata, T., Yokota, T., Emi, M. & Minami, S. Differential expression of multiple isoforms of the ELKS mRNAs involved in a papillary thyroid carcinoma. Genes Chromosomes Cancer 35, 30–37 (2002).
Seong, K. M. et al. The histone acetyltransferase Myst2 regulates Nanog expression, and is involved in maintaining pluripotency and self-renewal of embryonic stem cells. FEBS Lett. 589, 941–950 (2015).
Sauer, T. et al. MYST2 acetyltransferase expression and histone H4 lysine acetylation are suppressed in AML. Exp. Hematol. 43, 794–802 (2015).
Gerlinger, M. et al. Genomic architecture and evolution of clear cell renal cell carcinomas defined by multiregion sequencing. Nat. Genet. 46, 225–233 (2014).
Wellcome Sanger Institute. Gene view — KAT7. COSMIC https://cancer.sanger.ac.uk/cosmic/gene/analysis?ln=KAT7 (2018).
Jones, D. T. W. et al. Tandem duplication producing a novel oncogenic BRAF fusion gene defines the majority of pilocytic astrocytomas. Cancer Res. 68, 8673–8677 (2008).
Awasthi, P., Foiani, M. & Kumar, A. ATM and ATR signaling at a glance. J. Cell Sci. 128, 4255–4262 (2015).
Hilton, B. A. et al. ATR plays a direct antiapoptotic role at mitochondria which is regulated by prolyl isomerase Pin1. Mol. Cell 60, 35–46 (2015).
Wellcome Sanger Institute. Gene view — ATR. COSMIC https://cancer.sanger.ac.uk/cosmic/gene/analysis?ln=ATR#tissue (2018).
Knudson, A. G. Mutation and cancer: statistical study of retinoblastoma. Proc. Natl Acad. Sci. USA 68, 820–823 (1971).
Adegbola, O. & Pasternack, G. R. Phosphorylated retinoblastoma protein complexes with pp32 and inhibits pp32-mediated apoptosis. J. Biol. Chem. 280, 15497–15502 (2005).
Indovina, P., Pentimalli, F., Casini, N., Vocca, I. & Giordano, A. RB1 dual role in proliferation and apoptosis: cell fate control and implications for cancer therapy. Oncotarget 6, 17873–17890 (2015).
Agerbaek, M., Alsner, J., Marcussen, N., Lundbeck, F. & von der Maase, H. Retinoblastoma protein expression is an independent predictor of both radiation response and survival in muscle-invasive bladder cancer. Br. J. Cancer 89, 298–304 (2003).
Bid, H. K., Roberts, R. D., Manchanda, P. K. & Houghton, P. J. RAC1: an emerging therapeutic option for targeting cancer angiogenesis and metastasis. Mol. Cancer Ther. 12, 1925–1934 (2013).
Singh, A. et al. Rac1b, a tumor associated, constitutively active Rac1 splice variant, promotes cellular transformation. Oncogene 23, 9369–9380 (2004).
Hofbauer, S. W. et al. Tiam1/Rac1 signals contribute to the proliferation and chemoresistance, but not motility, of chronic lymphocytic leukemia cells. Blood 123, 2181–2188 (2014).
Deshmukh, J., Pofahl, R. & Haase, I. Epidermal Rac1 regulates the DNA damage response and protects from UV-light-induced keratinocyte apoptosis and skin carcinogenesis. Cell Death Dis. 8, e2664 (2017).
Takiar, V., Ip, C. K. M., Gao, M., Mills, G. B. & Cheung, L. W. T. Neomorphic mutations create therapeutic challenges in cancer. Oncogene 36, 1607 (2016). This review describes the neomorphic mutations in cancer, including the best-known examples, and indicates potential therapeutic challenges associated with this class of mutations.
Hao, Y. et al. Gain of interaction with IRS1 by p110α helical domain mutants is crucial for their oncogenic functions. Cancer Cell 23, 583–593 (2013).
Pang, H. et al. Differential enhancement of breast cancer cell motility and metastasis by helical and kinase domain mutations of class IA PI3K. Cancer Res. 69, 8868–8876 (2009).
Dang, L. et al. Cancer-associated IDH1 mutations produce 2-hydroxyglutarate. Nature 462, 739 (2009).
Gagné, M. L., Boulay, K., Topisirovic, I., Huot, M.-É. & Mallette, F. A. Oncogenic activities of IDH1/2 mutations: from epigenetics to cellular signaling. Trends Cell Biol. 27, 738–752 (2017).
Ward, P. S. et al. The common feature of leukemia-associated IDH1 and IDH2 mutations is a neomorphic enzymatic activity that converts α-ketoglutarate to 2-hydroxyglutarate. Cancer Cell 17, 225–234 (2010).
Turcan, S. et al. IDH1 mutation is sufficient to establish the glioma hypermethylator phenotype. Nature 483, 479–483 (2012).
Schneider, G., Schmidt-Supprian, M., Rad, R. & Saur, D. Tissue-specific tumorigenesis: context matters. Nat. Rev. Cancer 17, 239–253 (2017). This article presents a perspective on the molecular, cellular, systemic and environmental determinants of organ-specific tumorigenesis and the mechanisms of context-specific oncogenic signalling outputs.
Tremblay, C. S. et al. Loss-of-function mutations of dynamin 2 promote T-ALL by enhancing IL-7 signalling. Leukemia 30, 1993–2001 (2016).
Xu, B. et al. The significance of dynamin 2 expression for prostate cancer progression, prognostication, and therapeutic targeting. Cancer Med. 3, 14–24 (2014).
Razidlo, G. L. et al. Dynamin 2 potentiates invasive migration of pancreatic tumor cells through stabilization of the Rac1 GEF Vav1. Dev. Cell 24, 573–585 (2013).
Denli, A. M., Tops, B. B. J., Plasterk, R. H. A., Ketting, R. F. & Hannon, G. J. Processing of primary microRNAs by the microprocessor complex. Nature 432, 231–235 (2004).
Torrezan, G. T. et al. Recurrent somatic mutation in DROSHA induces microRNA profile changes in Wilms tumour. Nat. Commun. 5, 4039 (2014). This work describes somatic mutations in the miRNA processing protein DROSHA, which drives cancer through genome-wide alteration of gene expression patterns.
Rakheja, D. et al. Somatic mutations in DROSHA and DICER1 impair microRNA biogenesis through distinct mechanisms in Wilms tumors. Nat. Commun. 2, 4802–4802 (2014).
Czubak, K. et al. High copy number variation of cancer-related microRNA genes and frequent amplification of DICER1 and DROSHA in lung cancer. Oncotarget 6, 23399–23416 (2015).
Wellcome Sanger Institute. Hallmarks of Cancer — DROSHA. COSMIC https://cancer.sanger.ac.uk/cosmic/census-page/DROSHA (2018).
Dwane, L., Gallagher, W. M., Ní Chonghaile, T. & O’Connor, D. P. The emerging role of non-traditional ubiquitination in oncogenic pathways. J. Biol. Chem. 292, 3543–3551 (2017).
Yamato, A. et al. Oncogenic activity of BIRC2 and BIRC3 mutants independent of nuclear factor-κB-activating potential. Cancer Sci. 106, 1137–1142 (2015).
Wang, D. et al. BIRC3 is a novel driver of therapeutic resistance in glioblastoma. Sci. Rep. 6, 21710 (2016).
Jeselsohn, R., Buchwalter, G., De Angelis, C., Brown, M. & Schiff, R. ESR1 mutations as a mechanism for acquired endocrine resistance in breast cancer. Nat. Rev. Clin. Oncol. 12, 573–583 (2015).
Liu, W. H. et al. MicroRNA-18a prevents estrogen receptor-alpha expression, promoting proliferation of hepatocellular carcinoma cells. Gastroenterology 136, 683–693 (2009).
Wu, X. et al. Nuclear TBLR1 as an ER corepressor promotes cell proliferation, migration and invasion in breast and ovarian cancer. Am. J. Cancer Res. 6, 2351–2360 (2016).
Daniels, G. et al. TBLR1 as an AR coactivator selectively activates AR target genes to inhibit prostate cancer growth. Endocr. Relat. Cancer 21, 127–142 (2014).
Cai, Y. et al. The NuRD complex cooperates with DNMTs to maintain silencing of key colorectal tumor suppressor genes. Oncogene 33, 2157–2168 (2014).
O’Shaughnessy, A. & Hendrich, B. CHD4 in the DNA-damage response and cell cycle progression: not so NuRDy now. Biochem. Soc. Trans. 41, 777–782 (2013).
Benyoucef, A. et al. UTX inhibition as selective epigenetic therapy against TAL1-driven T cell acute lymphoblastic leukemia. Genes Dev. 30, 508–521 (2016).
Van der Meulen, J., Speleman, F. & Van Vlierberghe, P. The H3K27me3 demethylase UTX in normal development and disease. Epigenetics 9, 658–668 (2014).
Huang, H. et al. TET1 plays an essential oncogenic role in MLL-rearranged leukemia. Proc. Natl Acad. Sci. USA 110, 11994–11999 (2013).
Neri, F. et al. TET1 is a tumour suppressor that inhibits colon cancer growth by derepressing inhibitors of the WNT pathway. Oncogene 34, 4168 (2014).
Godoy, A. S. et al. Altered corepressor SMRT expression and recruitment to target genes as a mechanism that change the response to androgens in prostate cancer progression. Biochem. Biophys. Res. Commun. 423, 564–570 (2012).
Privalsky, M. L. The role of corepressors in transcriptional regulation by nuclear hormone receptors. Annu. Rev. Physiol. 66, 315–360 (2004).
Blackmore, J. K. et al. The SMRT coregulator enhances growth of estrogen receptor-α-positive breast cancer cells by promotion of cell cycle progression and inhibition of apoptosis. Endocrinology 155, 3251–3261 (2014).
Yu, J., Li, Y., Ishizuka, T., Guenther, M. G. & Lazar, M. A. A. SANT motif in the SMRT corepressor interprets the histone code and promotes histone deacetylation. EMBO J. 22, 3403–3410 (2003).
Bhaskara, S. et al. Hdac3 is essential for the maintenance of chromatin structure and genome stability. Cancer Cell 18, 436–447 (2010).
Song, L. et al. Alteration of SMRT tumor suppressor function in transformed non-Hodgkin lymphomas. Cancer Res. 65, 4554–4561 (2005).
Scafoglio, C., Smolka, M., Zhou, H., Perissi, V. & Rosenfeld, M. G. The co-repressor SMRT delays DNA damage-induced caspase activation by repressing pro-apoptotic genes and modulating the dynamics of checkpoint kinase 2 activation. PLOS ONE 8, e59986 (2013).
Manandhar, M., Boulware, K. S. & Wood, R. D. The ERCC1 and ERCC4 (XPF) genes and gene products. Gene 569, 153–161 (2015).
Emmert, S., Schneider, T. D., Khan, S. G. & Kraemer, K. H. The human XPG gene: gene architecture, alternative splicing and single nucleotide polymorphisms. Nucleic Acids Res. 29, 1443–1452 (2001).
Hartung, M. L. et al. H. pylori-induced DNA strand breaks are introduced by nucleotide excision repair endonucleases and promote NF-κB target gene expression. Cell Rep. 13, 70–79 (2015). This article describes how the infection of gastric epithelium cells by Helicobacter pylori may lead to generation of potentially oncogenic DNA double-strand breaks by nucleases normally involved in DNA repair.
Le May, N., Fradin, D., Iltis, I., Bougnères, P. & Egly, J.-M. XPG and XPF endonucleases trigger chromatin looping and DNA demethylation for accurate expression of activated genes. Mol. Cell 47, 622–632 (2012).
Bernardo, G. M. & Keri, R. A. FOXA1: a transcription factor with parallel functions in development and cancer. Biosci. Rep. 32, 113–130 (2012).
Yamaguchi, N. et al. FoxA1 as a lineage-specific oncogene in luminal type breast cancer. Biochem. Biophys. Res. Commun. 365, 711–717 (2008).
Grasso, C. S. et al. The mutational landscape of lethal castrate resistant prostate cancer. Nature 487, 239–243 (2012).
Jin, H.-J., Zhao, J. C., Ogden, I., Bergan, R. & Yu, J. Androgen receptor-independent function of FoxA1 in prostate cancer metastasis. Cancer Res. 73, 3725–3736 (2013).
Song, Y., Washington, M. K. & Crawford, H. C. Loss of FOXA1/2 is essential for the epithelial-to-mesenchymal transition in pancreatic cancer. Cancer Res. 70, 2115–2125 (2010).
Bernardo, G. M. et al. FOXA1 represses the molecular phenotype of basal breast cancer cells. Oncogene 32, 554–563 (2013).
Zhan, T., Rindtorff, N. & Boutros, M. Wnt signaling in cancer. Oncogene 36, 1461–1473 (2017).
Hanson, C. A. & Miller, J. R. Non-traditional roles for the adenomatous polyposis coli (APC) tumor suppressor protein. Gene 361, 1–12 (2005).
Wellcome Sanger Institute. Gene view — APC. COSMIC https://cancer.sanger.ac.uk/cosmic/gene/analysis?ln=APC#tissue (2018).
Nagata, S. Fas ligand-induced apoptosis. Annu. Rev. Genet. 33, 29–55 (1999).
Yang, Y. et al. Fas signaling promotes gastric cancer metastasis through STAT3-dependent upregulation of fascin. PLOS ONE 10, e0125132 (2015).
Chen, L. et al. CD95/Fas promotes tumour growth. Nature 465, 492–496 (2010).
Ceppi, P. et al. CD95 and CD95L promote and protect cancer stem cells. Nat. Commun. 5, 5238–5238 (2014).
Mullan, P. B., Quinn, J. E. & Harkin, D. P. The role of BRCA1 in transcriptional regulation and cell cycle control. Oncogene 25, 5854 (2006).
Rodriguez, J. A., Au, W. W. Y. & Henderson, B. R. Cytoplasmic mislocalization of BRCA1 caused by cancer-associated mutations in the BRCT domain. Exp. Cell Res. 293, 14–21 (2004).
Santivasi, W. L. et al. Association between cytosolic expression of BRCA1 and metastatic risk in breast cancer. Br. J. Cancer 113, 453–459 (2015).
Shimizu, Y. et al. BRCA1-IRIS overexpression promotes formation of aggressive breast cancers. PLOS ONE 7, e34102 (2012).
Chen, H. et al. Requirement for BUB1B/BUBR1 in tumor progression of lung adenocarcinoma. Genes Cancer 6, 106–118 (2015).
Matsuura, S. et al. Monoallelic BUB1B mutations and defective mitotic-spindle checkpoint in seven families with premature chromatid separation (PCS) syndrome. Am. J. Med. Genet. A 140, 358–367 (2006).
Kapanidou, M., Lee, S. & Bolanos-Garcia, V. M. BubR1 kinase: protection against aneuploidy and premature aging. Trends Mol. Med. 21, 364–372 (2015).
Chao, C.-H. et al. DDX3, a DEAD box RNA helicase with tumor growth-suppressive property and transcriptional regulation activity of the p21waf1/cip1 promoter, is a candidate tumor suppressor. Cancer Res. 66, 6579–6588 (2006).
Chen, H. H., Yu, H. I., Cho, W. C. & Tarn, W. Y. DDX3 modulates cell adhesion and motility and cancer cell metastasis via Rac1-mediated signaling pathway. Oncogene 34, 2790 (2014).
Botlagunta, M. et al. Oncogenic role of DDX3 in breast cancer biogenesis. Oncogene 27, 3912–3922 (2008).
Gan, W. et al. SPOP promotes ubiquitination and degradation of the ERG oncoprotein to suppress prostate cancer progression. Mol. Cell 59, 917–930 (2015).
Zhao, W., Zhou, J., Deng, Z., Gao, Y. & Cheng, Y. SPOP promotes tumor progression via activation of beta-catenin/TCF4 complex in clear cell renal cell carcinoma. Int. J. Oncol. 49, 1001–1008 (2016).
Delbridge, A. R. D., Valente, L. J. & Strasser, A. The role of the apoptotic machinery in tumor suppression. Cold Spring Harb. Perspect. Biol. 4, a008789 (2012).
Labi, V. & Erlacher, M. How cell death shapes cancer. Cell Death Dis. 6, e1675 (2015). This review describes the role of apoptosis as an anticancer defence mechanism but also as a process fuelling evolution of cancer and promoting the expansion of more aggressive subclones.
Pérez-Garijo, A. When dying is not the end: apoptotic caspases as drivers of proliferation. Semin. Cell Dev. Biol. https://doi.org/10.1016/j.semcdb.2017.11.036 (2017).
Bandopadhayay, P. et al. MYB-QKI rearrangements in angiocentric glioma drive tumorigenicity through a tripartite mechanism. Nat. Genet. 48, 273–282 (2016).
Steidl, C. et al. MHC class II transactivator CIITA is a recurrent gene fusion partner in lymphoid cancers. Nature 471, 377–381 (2011).
Lin, A. et al. BRAF alterations in primary glial and glioneuronal neoplasms of the central nervous system with identification of 2 novel KIAA1549:BRAF fusion variants. J. Neuropathol. Exp. Neurol. 71, 66–72 (2012).
Wellcome Sanger Institute. Hallmarks of Cancer — PTEN. COSMIC https://cancer.sanger.ac.uk/cosmic/census-page/PTEN (2018).
Acknowledgements
The authors would like to thank J. Tate, who created the web pages presenting the functional descriptions of cancer genes. They also thank C. Rye, N. Bindal and C. Ramshaw as well as the COSMIC and Open Targets teams for testing and improving these pages. This work was supported by the Wellcome Trust (grant 206194) and by Open Targets (grant OTAR007).
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Nature Reviews Cancer thanks F. Ciccarelli, J. Korbel and the other anonymous reviewer(s) for their contribution to the peer review of this work.
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Z.S. researched data for the article, substantially contributed to the discussion of content and wrote, reviewed and edited the article. S.B., C.G.C. and S.A.W. researched data and reviewed and edited the article. I.D. substantially contributed to the discussion of content and reviewed and edited the article. S.A.F. substantially contributed to the discussion of content and wrote, reviewed and edited the article.
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COSMIC Cancer Gene Census: https://cancer.sanger.ac.uk/censusCOSMIC Database: https://cancer.sanger.ac.uk/cosmic
Glossary
- Synthetic lethality
-
A mechanism using a combination of genetic and induced effects (for example, by a therapeutic agent) working together to induce cell death, where any single one of these effects is non-lethal.
- Gain of function
-
A type of mutation resulting in an altered gene product with intensified activity or with a new biological function (neomorphic mutation).
- Loss of function
-
A type of mutation resulting in an altered gene product with lower or no biological function.
- Nucleotide excision repair
-
(NER). A DNA repair mechanism that removes DNA damage induced by ultraviolet light — mostly thymine dimers — and uses the complementary undamaged strand as a template to repair the damage.
- Wilms tumour
-
Another name for nephroblastoma, a malignant embryonal neoplasm of the kidney.
- Epithelial-to-mesenchymal transition
-
(EMT). A process in which epithelial cells lose cell polarity and cell–cell adhesion with accompanying increases in migratory and invasive capacities; EMT occurs during embryogenesis, fibrosis and wound healing but may also be an early event in cancer metastasis.
- Anoikis
-
A form of programmed cell death triggered in anchorage-dependent cells by detachment of the cell from the extracellular matrix.
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Sondka, Z., Bamford, S., Cole, C.G. et al. The COSMIC Cancer Gene Census: describing genetic dysfunction across all human cancers. Nat Rev Cancer 18, 696–705 (2018). https://doi.org/10.1038/s41568-018-0060-1
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DOI: https://doi.org/10.1038/s41568-018-0060-1
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