References
[1] A. Ferrari, I.B. Brecht, G. Gatta, et al. Defining and listing very rare cancers of paediatric age: consensus of the Joint Action on Rare Cancers in cooperation with the European Cooperative Study Group for Pediatric Rare Tumors. Eur. J. Cancer 2019;110:120-126.
[2] D.A. Hill, J. Ivanovich, J.R. Priest, et al. DICER1 mutations in familial pleuropulmonary blastoma. Science 2009;325(5943):965.
[3] M. Seki, K. Yoshida, Y. Shiraishi, et al. Biallelic DICER1 mutations in sporadic pleuropulmonary blastoma. Cancer Res.2014;74(10):2742-2749.
[4] R. Shukrun, H. Golan, R. Caspi, et al. NCAM1/FGF module serves as a putative pleuropulmonary blastoma therapeutic target.Oncogenesis 2019;8(9):48.
[5] A.C. White, J. Xu, Y. Yin, et al. FGF9 and SHH signaling coordinate lung growth and development through regulation of distinct mesenchymal domains. Development 2006;133(8):1507-1517.
[6] S.S. Potter. Single-cell RNA sequencing for the study of development, physiology and disease. Nat Rev Nephrol2018;14(8):479-492.
[7] X. Ren, B. Kang, Z. Zhang. Understanding tumor ecosystems by single-cell sequencing: promises and limitations. Genome Biol.2018;19(1):211.
[8] S. Picelli. Single-cell RNA-sequencing: The future of genome biology is now. RNA Biol. 2017;14(5):637-650.
[9] F. Tang, C. Barbacioru, Y. Wang, et al. mRNA-Seq whole-transcriptome analysis of a single cell. Nature methods2009;6(5):377-382.
[10] W. Chung, H.H. Eum, H.O. Lee, et al. Single-cell RNA-seq enables comprehensive tumour and immune cell profiling in primary breast cancer. Nat Commun 2017;8:15081.
[11] A.P. Patel, I. Tirosh, J.J. Trombetta, et al. Single-cell RNA-seq highlights intratumoral heterogeneity in primary glioblastoma.Science 2014;344(6190):1396-1401.
[12] E. Valenzi, M. Bulik, T. Tabib, et al. Single-cell analysis reveals fibroblast heterogeneity and myofibroblasts in systemic sclerosis-associated interstitial lung disease. Ann. Rheum. Dis.2019;78(10):1379-1387.
[13] M. Venkatasubramanian, K. Chetal, D. Schnell, et al. Resolving single-cell heterogeneity from hundreds of thousands of cells through sequential hybrid clustering and NMF. Bioinformatics 2020;
[14] C. Trapnell. Defining cell types and states with single-cell genomics. Genome Res. 2015;25(10):1491-1498.
[15] C. Vokuhl, L. de Leon-Escapini, I. Leuschner. Strong Expression and Amplification of IGF1R in Pleuropulmonary Blastomas. Pediatr. Dev. Pathol. 2017;20(6):475-481.
[16] M. Lagha, A. Mayeuf-Louchart, T. Chang, et al. Itm2a is a Pax3 target gene, expressed at sites of skeletal muscle formation in vivo.PLoS One 2013;8(5):e63143.
[17] C. Prein, F. Beier. ECM signaling in cartilage development and endochondral ossification. Curr. Top. Dev. Biol. 2019;133:25-47.
[18] M.K. Yadav, M. Singhal, A. Bhatia, et al. Pleuropulmonary blastoma in adolescence: A rare tumor beyond first decade of life.Lung India 2015;32(3):281-284.
[19] Y.H. Messinger, D.R. Stewart, J.R. Priest, et al. Pleuropulmonary blastoma: a report on 350 central pathology-confirmed pleuropulmonary blastoma cases by the International Pleuropulmonary Blastoma Registry. Cancer 2015;121(2):276-285.
[20] P.S. Zammit. Function of the myogenic regulatory factors Myf5, MyoD, Myogenin and MRF4 in skeletal muscle, satellite cells and regenerative myogenesis. Semin. Cell Dev. Biol. 2017;72:19-32.
[21] M.A. Rudnicki, F. Le Grand, I. McKinnell, et al. The molecular regulation of muscle stem cell function. Cold Spring Harb. Symp. Quant. Biol. 2008;73:323-331.
[22] P. Zhao, E.P. Hoffman. Musculin isoforms and repression of MyoD in muscle regeneration. Biochem. Biophys. Res. Commun.2006;342(3):835-842.
[23] G.H. Lee, M.Y. Chang, C.H. Hsu, et al. Essential roles of basic helix-loop-helix transcription factors, Capsulin and Musculin, during craniofacial myogenesis of zebrafish. Cell. Mol. Life Sci.2011;68(24):4065-4078.
[24] L. Robb, L. Hartley, C.C. Wang, et al. musculin: a murine basic helix-loop-helix transcription factor gene expressed in embryonic skeletal muscle. Mech. Dev. 1998;76(1-2):197-201.
[25] E.J. Lee, J.H. Nam, I. Choi. Fibromodulin modulates myoblast differentiation by controlling calcium channel. Biochem. Biophys. Res. Commun. 2018;503(2):580-585.
[26] J.M. Venuti, J.H. Morris, J.L. Vivian, et al. Myogenin is required for late but not early aspects of myogenesis during mouse development. J. Cell Biol. 1995;128(4):563-576.
[27] A. Rawls, J.H. Morris, M. Rudnicki, et al. Myogenin’s functions do not overlap with those of MyoD or Myf-5 during mouse embryogenesis.Dev. Biol. 1995;172(1):37-50.
[28] H. Miraoui, P.J. Marie. Pivotal role of Twist in skeletal biology and pathology. Gene 2010;468(1-2):1-7.
[29] C.F. Liu, W.E. Samsa, G. Zhou, et al. Transcriptional control of chondrocyte specification and differentiation. Semin. Cell Dev. Biol. 2017;62:34-49.
[30] A. Tsuchiya, M. Yano, J. Tocharus, et al. Expression of mouse HtrA1 serine protease in normal bone and cartilage and its upregulation in joint cartilage damaged by experimental arthritis. Bone2005;37(3):323-336.
[31] L. Zeng, H. Kempf, L.C. Murtaugh, et al. Shh establishes an Nkx3.2/Sox9 autoregulatory loop that is maintained by BMP signals to induce somitic chondrogenesis. Genes Dev. 2002;16(15):1990-2005.
[32] H. Akiyama, M.C. Chaboissier, J.F. Martin, et al. The transcription factor Sox9 has essential roles in successive steps of the chondrocyte differentiation pathway and is required for expression of Sox5 and Sox6. Genes Dev. 2002;16(21):2813-2828.
[33] V. Lefebvre, P. Smits. Transcriptional control of chondrocyte fate and differentiation. Birth Defects Res C Embryo Today2005;75(3):200-212.
[34] H. Peters, B. Wilm, N. Sakai, et al. Pax1 and Pax9 synergistically regulate vertebral column development.Development 1999;126(23):5399-5408.
[35] H. Peters, A. Neubüser, K. Kratochwil, et al. Pax9-deficient mice lack pharyngeal pouch derivatives and teeth and exhibit craniofacial and limb abnormalities. Genes Dev.1998;12(17):2735-2747.
[36] V. Sivakamasundari, P. Kraus, W. Sun, et al. A developmental transcriptomic analysis of Pax1 and Pax9 in embryonic intervertebral disc development. Biol Open 2017;6(2):187-199.
[37] K. Yagami, J.Y. Suh, M. Enomoto-Iwamoto, et al. Matrix GLA protein is a developmental regulator of chondrocyte mineralization and, when constitutively expressed, blocks endochondral and intramembranous ossification in the limb. J. Cell Biol. 1999;147(5):1097-1108.
[38] G. Luo, P. Ducy, M.D. McKee, et al. Spontaneous calcification of arteries and cartilage in mice lacking matrix GLA protein.Nature 1997;386(6620):78-81.
[39] X. Li, P. Liu, W. Liu, et al. Dkk2 has a role in terminal osteoblast differentiation and mineralized matrix formation. Nat. Genet. 2005;37(9):945-952.
[40] H. Oh, J.H. Ryu, J. Jeon, et al. Misexpression of Dickkopf-1 in endothelial cells, but not in chondrocytes or hypertrophic chondrocytes, causes defects in endochondral ossification. J. Bone Miner. Res.2012;27(6):1335-1344.