[1] |
Yamaguchi Y, Hearing VJ. Melanocytes and their diseases. Cold Spring Harb Perspect Med, 2014; 4, a017046. doi: 10.1101/cshperspect.a017046 |
[2] |
Lin JY, Fisher DE. Melanocyte biology and skin pigmentation. Nature, 2007; 445, 843−50. doi: 10.1038/nature05660 |
[3] |
Mort RL, Jackson IJ, Patton EE. The melanocyte lineage in development and disease. Development, 2015; 142, 1387. doi: 10.1242/dev.123729 |
[4] |
Shahbazi A, Zargar SJ, Aghdami N, et al. The story of melanocyte: a long way from bench to bedside. Cell Tissue Bank, 2024; 25, 143−57. doi: 10.1007/s10561-023-10081-5 |
[5] |
Patton EE, Mueller KL, Adams DJ, et al. Melanoma models for the next generation of therapies. Cancer Cell, 2021; 39, 610−31. doi: 10.1016/j.ccell.2021.01.011 |
[6] |
Rebecca VW, Somasundaram R, Herlyn M. Pre-clinical modeling of cutaneous melanoma. Nat Commun, 2020; 11, 2858. doi: 10.1038/s41467-020-15546-9 |
[7] |
Saleh J. Murine models of melanoma. Pathol Res Pract, 2018; 214, 1235−8. doi: 10.1016/j.prp.2018.07.008 |
[8] |
Happle R. What is a nevus: a proposed definition of a common medical term. Dermatology, 1995; 191, 1−5. doi: 10.1159/000246468 |
[9] |
Roh MR, Eliades P, Gupta S, et al. Genetics of melanocytic nevi. Pigment Cell Melanoma Res, 2015; 28, 661−72. doi: 10.1111/pcmr.12412 |
[10] |
Lin WM, Luo S, Muzikansky A, et al. Outcome of patients with de novo versus nevus-associated melanoma. J Am Acad Dermatol, 2015; 72, 54−8. doi: 10.1016/j.jaad.2014.09.028 |
[11] |
Michaloglou C, Vredeveld LCW, Soengas MS, et al. BRAFE600-associated senescence-like cell cycle arrest of human naevi. Nature, 2005; 436, 720−4. doi: 10.1038/nature03890 |
[12] |
Pollock PM, Harper UL, Hansen KS, et al. High frequency of BRAF mutations in nevi. Nat Genet, 2003; 33, 19−20. doi: 10.1038/ng1054 |
[13] |
Centeno PP, Pavet V, Marais R. The journey from melanocytes to melanoma. Nat Rev Cancer, 2023; 23, 372−90. doi: 10.1038/s41568-023-00565-7 |
[14] |
Shain AH, Yeh I, Kovalyshyn I, et al. The genetic evolution of melanoma from precursor lesions. N Engl J Med, 2015; 373, 1926−36. doi: 10.1056/NEJMoa1502583 |
[15] |
Miller AJ, Mihm MC Jr. Melanoma. N Engl J Med, 2006; 355, 51−65. doi: 10.1056/NEJMra052166 |
[16] |
Curtin JA, Fridlyand J, Kageshita T, et al. Distinct sets of genetic alterations in melanoma. N Engl J Med, 2005; 353, 2135−47. doi: 10.1056/NEJMoa050092 |
[17] |
Castro-Pérez E, Singh M, Sadangi S, et al. Connecting the dots: melanoma cell of origin, tumor cell plasticity, trans-differentiation, and drug resistance. Pigment Cell Melanoma Res, 2023; 36, 330−47. doi: 10.1111/pcmr.13092 |
[18] |
Damsky WE, Bosenberg M. Melanocytic nevi and melanoma: unraveling a complex relationship. Oncogene, 2017; 36, 5771−92. doi: 10.1038/onc.2017.189 |
[19] |
Nascentes Melo LM, Kumar S, Riess V, et al. Advancements in melanoma cancer metastasis models. Pigment Cell Melanoma Res, 2023; 36, 206−23. doi: 10.1111/pcmr.13078 |
[20] |
Dessinioti C, Befon A, Stratigos AJ. The association of nevus-associated melanoma with common or dysplastic melanocytic nevus: a systematic review and meta-analysis. Cancers (Basel), 2023; 15, 856. doi: 10.3390/cancers15030856 |
[21] |
Aktary Z, Raymond JH, Pouteaux M, et al. Derivation and use of cell lines from mouse models of melanoma. J Invest Dermatol, 2023; 143, 538-44. e2. |
[22] |
Michaloglou C, Vredeveld LCW, Mooi WJ, et al. BRAFE600 in benign and malignant human tumours. Oncogene, 2008; 27, 877−95. doi: 10.1038/sj.onc.1210704 |
[23] |
Conde-Perez A, Larue L. Human relevance of NRAS/BRAF mouse melanoma models. Eur J Cell Biol, 2014; 93, 82−6. doi: 10.1016/j.ejcb.2013.10.010 |
[24] |
Cantwell-Dorris ER, O'Leary JJ, Sheils OM. BRAFV600E: implications for carcinogenesis and molecular therapy. Mol Cancer Ther, 2011; 10, 385−94. doi: 10.1158/1535-7163.MCT-10-0799 |
[25] |
Pritchard C, Carragher L, Aldridge V, et al. Mouse models for BRAF-induced cancers. Biochem Soc Trans, 2007; 35, 1329−33. doi: 10.1042/BST0351329 |
[26] |
The Cancer Genome Atlas Network. Genomic classification of cutaneous melanoma. Cell, 2015; 161, 1681−96. doi: 10.1016/j.cell.2015.05.044 |
[27] |
Lavoie H, Therrien M. Regulation of RAF protein kinases in ERK signalling. Nat Rev Mol Cell Biol, 2015; 16, 281−98. doi: 10.1038/nrm3979 |
[28] |
Poulikakos PI, Sullivan RJ, Yaeger R. Molecular pathways and mechanisms of BRAF in cancer therapy. Clin Cancer Res, 2022; 28, 4618−28. doi: 10.1158/1078-0432.CCR-21-2138 |
[29] |
Ullah R, Yin Q, Snell AH, et al. RAF-MEK-ERK pathway in cancer evolution and treatment. Semin Cancer Biol, 2022; 85, 123−54. doi: 10.1016/j.semcancer.2021.05.010 |
[30] |
Yaeger R, Corcoran RB. Targeting alterations in the RAF-MEK pathway. Cancer Discov, 2019; 9, 329−41. doi: 10.1158/2159-8290.CD-18-1321 |
[31] |
Janardhan HP, Saheera S, Jung R, et al. Vascular and lymphatic malformations: perspectives from human and vertebrate studies. Circ Res, 2021; 129, 131−5. doi: 10.1161/CIRCRESAHA.121.319587 |
[32] |
Rezaei Adariani S, Buchholzer M, Akbarzadeh M, et al. Structural snapshots of RAF kinase interactions. Biochem Soc Trans, 2018; 46, 1393−406. doi: 10.1042/BST20170528 |
[33] |
Scheffzek K, Shivalingaiah G. Ras-specific GTPase-activating proteins—structures, mechanisms, and interactions. Cold Spring Harb Perspect Med, 2019; 9, a031500 . doi: 10.1101/cshperspect.a031500 |
[34] |
Karoulia Z, Gavathiotis E, Poulikakos PI. New perspectives for targeting RAF kinase in human cancer. Nat Rev Cancer, 2017; 17, 676−91. doi: 10.1038/nrc.2017.79 |
[35] |
Sanchez-Vega F, Mina M, Armenia J, et al. Oncogenic signaling pathways in the cancer genome atlas. Cell, 2018; 173, 321-37. e10. |
[36] |
Holderfield M, Deuker MM, McCormick F, et al. Targeting RAF kinases for cancer therapy: BRAF-mutated melanoma and beyond. Nat Rev Cancer, 2014; 14, 455−67. doi: 10.1038/nrc3760 |
[37] |
Juliana V, Bruno S. Bridging the gap between testing and clinics exploring alternative pre-clinical models in melanoma research. Adv Drug Deliv Rev, 2025; 208. doi: 10.1016/j.addr.2024.115295 |
[38] |
Poulikakos PI, Persaud Y, Janakiraman M, et al. RAF inhibitor resistance is mediated by dimerization of aberrantly spliced BRAF(V600E). Nature, 2011; 480, 387−90. doi: 10.1038/nature10662 |
[39] |
Darp R, Vittoria MA, Ganem NJ, et al. Oncogenic BRAF induces whole-genome doubling through suppression of cytokinesis. Nat Commun, 2022; 13, 4109. doi: 10.1038/s41467-022-31899-9 |
[40] |
Montal E, Lumaquin D, Ma YL, et al. Modeling the effects of genetic- and diet-induced obesity on melanoma progression in zebrafish. Dis Model Mech, 2023; 16, dmm049671. doi: 10.1242/dmm.049671 |
[41] |
Radomir MS, Tae-Kang K, Zorica J, et al. Malignant melanoma: an overview, new perspectives, and vitamin D signaling. Cancers (Basel), 2024; 16. doi: 10.3390/cancers16122262 |
[42] |
Wellbrock C, Karasarides M, Marais R. The RAF proteins take centre stage. Nat Rev Mol Cell Biol, 2004; 5, 875−85. doi: 10.1038/nrm1498 |
[43] |
Maria C, Milena C, Panagiotis P, et al. Heterogeneous pathogenesis of melanoma: BRAF mutations and beyond. Crit Rev Oncol Hematol, 2024; 201. |
[44] |
Osborne JK, Zaganjor E, Cobb MH. Signal control through Raf: in sickness and in health. Cell Res, 2012; 22, 14−22. doi: 10.1038/cr.2011.193 |
[45] |
Hyesung J, Emre T, Michael J E. Signaling from RAS to RAF: The Molecules and Their Mechanisms. Annu Rev Biochem, 2024. doi: 10.1146/annurev-biochem-052521-040754 |
[46] |
Lavoie H, Gagnon J, Therrien M. ERK signalling: a master regulator of cell behaviour, life and fate. Nat Rev Mol Cell Biol, 2020; 21, 607−32. doi: 10.1038/s41580-020-0255-7 |
[47] |
Heppner DE, Eck MJ. A structural perspective on targeting the RTK/Ras/MAP kinase pathway in cancer. Protein Sci, 2021; 30, 1535−53. doi: 10.1002/pro.4125 |
[48] |
Simanshu DK, Nissley DV, Mccormick F. RAS proteins and their regulators in human disease. Cell, 2017; 170, 17−33. doi: 10.1016/j.cell.2017.06.009 |
[49] |
Kim JS, Lee C, Foxworth A, et al. B-Raf is dispensable for K-Ras-mediated oncogenesis in human cancer cells. Cancer Res, 2004; 64, 1932−7. doi: 10.1158/0008-5472.CAN-03-3862 |
[50] |
Guo YJ, Pan WW, Liu SB, et al. ERK/MAPK signalling pathway and tumorigenesis (review). Exp Ther Med, 2020; 19, 1997−2007. |
[51] |
Davies H, Bignell GR, Cox C, et al. Mutations of the BRAF gene in human cancer. Nature, 2002; 417, 949−54. doi: 10.1038/nature00766 |
[52] |
Joselow A, Lynn D, Terzian T, et al. Senescence-like phenotypes in human nevi. In: Nikiforov MA. Oncogene-Induced Senescence. Humana Press. 2017, 175-84. |
[53] |
Mooi WJ, Peeper DS. Oncogene-induced cell senescence—halting on the road to cancer. N Engl J Med, 2006; 355, 1037−46. doi: 10.1056/NEJMra062285 |
[54] |
Haferkamp S, Rizos H. Oncogene-induced senescence pathways in melanocytes. Cell Cycle, 2010; 9, 4778−9. doi: 10.4161/cc.9.24.14248 |
[55] |
Chandeck C, Mooi WJ. Oncogene-induced cellular senescence. Adv Anat Pathol, 2010; 17, 42−8. doi: 10.1097/PAP.0b013e3181c66f4e |
[56] |
Wellbrock C, Arozarena I. Microphthalmia-associated transcription factor in melanoma development and MAP-kinase pathway targeted therapy. Pigment Cell Melanoma Res, 2015; 28, 390−406. doi: 10.1111/pcmr.12370 |
[57] |
Wu M, Hemesath T, Takemoto CM, et al. c-Kit triggers dual phosphorylations, which couple activation and degradation of the essential melanocyte factor Mi. Genes Dev, 2000; 14, 301−12. doi: 10.1101/gad.14.3.301 |
[58] |
Hemesath TJ, Price E, Takemoto C, et al. MAP kinase links the transcription factor Microphthalmia to c-Kit signalling in melanocytes. Nature, 1998; 391, 298−301. doi: 10.1038/34681 |
[59] |
Ngeow KC, Friedrichsen HJ, Li LX, et al. BRAF/MAPK and GSK3 signaling converges to control MITF nuclear export. Proc Natl Acad Sci U S A, 2018; 115, E8668−77. |
[60] |
Todd JR, Scurr LL, Becker TM, et al. The MAPK pathway functions as a redundant survival signal that reinforces the PI3K cascade in c-Kit mutant melanoma. Oncogene, 2014; 33, 236−45. doi: 10.1038/onc.2012.562 |
[61] |
Liu F, Singh A, Yang Z, et al. MiTF links Erk1/2 kinase and p21CIP1/WAF1 activation after UVC radiation in normal human melanocytes and melanoma cells. Mol Cancer, 2010; 9, 214. doi: 10.1186/1476-4598-9-214 |
[62] |
Tachibana M. MITF: a stream flowing for pigment cells. Pigment Cell Res, 2000; 13, 230−40. doi: 10.1034/j.1600-0749.2000.130404.x |
[63] |
Huang WJ, Hickson LJ, Eirin A, et al. Cellular senescence: the good, the bad and the unknown. Nat Rev Nephrol, 2022; 18, 611−27. |
[64] |
Meloche S, Pouysségur J. The ERK1/2 mitogen-activated protein kinase pathway as a master regulator of the G1- to S-phase transition. Oncogene, 2007; 26, 3227−39. doi: 10.1038/sj.onc.1210414 |
[65] |
Xu YX, Li N, Xiang R, et al. Emerging roles of the p38 MAPK and PI3K/AKT/mTOR pathways in oncogene-induced senescence. Trends Biochem Sci, 2014; 39, 268−76. doi: 10.1016/j.tibs.2014.04.004 |
[66] |
Canovas B, Nebreda AR. Diversity and versatility of p38 kinase signalling in health and disease. Nat Rev Mol Cell Biol, 2021; 22, 346−66. doi: 10.1038/s41580-020-00322-w |
[67] |
McNeal AS, Belote RL, Zeng HL, et al. BRAFV600E induces reversible mitotic arrest in human melanocytes via microrna-mediated suppression of AURKB. eLife, 2021; 10, e70385. doi: 10.7554/eLife.70385 |
[68] |
Bai X, Fisher DE, Flaherty KT. Cell-state dynamics and therapeutic resistance in melanoma from the perspective of MITF and IFNγ pathways. Nat Rev Clin Oncol, 2019; 16, 549−62. doi: 10.1038/s41571-019-0204-6 |
[69] |
Ballotti R, Cheli Y, Bertolotto C. The complex relationship between MITF and the immune system: a Melanoma ImmunoTherapy (response) Factor? Mol Cancer, 2020; 19, 170. |
[70] |
Goding CR, Arnheiter H. MITF-the first 25 years. Genes Dev, 2019; 33, 983−1007. doi: 10.1101/gad.324657.119 |
[71] |
Bertolotto C, Lesueur F, Giuliano S, et al. A SUMOylation-defective MITF germline mutation predisposes to melanoma and renal carcinoma. Nature, 2011; 480, 94−8. doi: 10.1038/nature10539 |
[72] |
Yokoyama S, Woods SL, Boyle GM, et al. A novel recurrent mutation in MITF predisposes to familial and sporadic melanoma. Nature, 2011; 480, 99−103. doi: 10.1038/nature10630 |
[73] |
Bonet C, Luciani F, Ottavi JF, et al. Deciphering the role of oncogenic MITFE318K in senescence delay and melanoma progression. J Natl Cancer Inst, 2017; 109, djw340. |
[74] |
Ballotti R, Bertolotto C. Deregulated MITF sumoylation: a route to melanoma. Mol Cell Oncol, 2017; 4, e1331154. doi: 10.1080/23723556.2017.1331154 |
[75] |
Estrada C, Mirabal-Ortega L, Méry L, et al. MITF activity is regulated by a direct interaction with RAF proteins in melanoma cells. Commun Biol, 2022; 5, 101. doi: 10.1038/s42003-022-03049-w |
[76] |
Smith MP, Rana S, Ferguson J, et al. A PAX3/BRN2 rheostat controls the dynamics of BRAF mediated MITF regulation in MITFhigh/AXLlow melanoma. Pigment Cell Melanoma Res, 2019; 32, 280−91. doi: 10.1111/pcmr.12741 |
[77] |
Chen JY, Hug C, Reyes J, et al. Multi-range ERK responses shape the proliferative trajectory of single cells following oncogene induction. Cell Rep, 2023; 42, 112252 . doi: 10.1016/j.celrep.2023.112252 |
[78] |
Fane ME, Chhabra Y, Spoerri L, et al. Reciprocal regulation of BRN2 and NOTCH1/2 signaling synergistically drives melanoma cell migration and invasion. J Invest Dermatol, 2022; 142, 1845−57. doi: 10.1016/j.jid.2020.12.039 |
[79] |
Fane ME, Chhabra Y, Smith AG, et al. BRN2, a POUerful driver of melanoma phenotype switching and metastasis. Pigment Cell Melanoma Res, 2019; 32, 9−24. doi: 10.1111/pcmr.12710 |
[80] |
He SH, Sharpless NE. Senescence in health and disease. Cell, 2017; 169, 1000−11. doi: 10.1016/j.cell.2017.05.015 |
[81] |
Roy AL, Sierra F, Howcroft K, et al. A blueprint for characterizing senescence. Cell, 2020; 183, 1143−6. doi: 10.1016/j.cell.2020.10.032 |
[82] |
Behr LC, Simm A, Kluttig A, et al. 60 years of healthy aging: on definitions, biomarkers, scores and challenges. Age Res Rev, 2023; 88, 101934. doi: 10.1016/j.arr.2023.101934 |
[83] |
Ruiz-Vega R, Chen CF, Razzak E, et al. Dynamics of nevus development implicate cell cooperation in the growth arrest of transformed melanocytes. eLife, 2020; 9, e61026. doi: 10.7554/eLife.61026 |
[84] |
Hernandez-Segura A, Nehme J, Demaria M. Hallmarks of cellular senescence. Trends Cell Biol, 2018; 28, 436−53. doi: 10.1016/j.tcb.2018.02.001 |
[85] |
Sharpless NE, Sherr CJ. Forging a signature of in vivo senescence. Nat Rev Cancer, 2015; 15, 397−408. doi: 10.1038/nrc3960 |
[86] |
Calcinotto A, Kohli J, Zagato E, et al. Cellular senescence: aging, cancer, and injury. Physiol Rev, 2019; 99, 1047−78. doi: 10.1152/physrev.00020.2018 |
[87] |
González-Gualda E, Baker AG, Fruk L, et al. A guide to assessing cellular senescence in vitro and in vivo. FEBS J, 2021; 288, 56−80. doi: 10.1111/febs.15570 |
[88] |
Herranz N, Gil J. Mechanisms and functions of cellular senescence. J Clin Invest, 2018; 128, 1238−46. doi: 10.1172/JCI95148 |
[89] |
Muñoz-Espín D, Serrano M. Cellular senescence: from physiology to pathology. Nat Rev Mol Cell Biol, 2014; 15, 482−96. doi: 10.1038/nrm3823 |
[90] |
Kumari R, Jat P. Mechanisms of cellular senescence: cell cycle arrest and senescence associated secretory phenotype. Front Cell Dev Biol, 2021; 9, 645593. doi: 10.3389/fcell.2021.645593 |
[91] |
Gorgoulis V, Adams PD, Alimonti A, et al. Cellular senescence: defining a path forward. Cell, 2019; 179, 813−27. doi: 10.1016/j.cell.2019.10.005 |
[92] |
Okamoto T, Sanda T, Asamitsu K. NF-κB signaling and carcinogenesis. Curr Pharm Des, 2007; 13, 447−62. doi: 10.2174/138161207780162944 |
[93] |
Dorothy C B. Review: Are moles senescent? Pigment Cell Melanoma Res, 2024; 37. |
[94] |
Ruiz J, Hyde M, Perry A, et al. Genomic evaluation of clinically ambiguous pigmented lesions. J Clin Aesthet Dermatol, 2023; 16, 44−5. |
[95] |
Maher NG, Scolyer RA, Colebatch AJ. Biology and genetics of acquired and congenital melanocytic naevi. Pathology, 2023; 55, 169−77. |
[96] |
Urso C. Melanocytic skin neoplasms: what lesson from genomic aberrations? Am J Dermatopathol, 2019; 41, 623-9. |
[97] |
Wang XJ, Ramos R, Phan AQ, et al. Signalling by senescent melanocytes hyperactivates hair growth. Nature, 2023; 618, 808−17. doi: 10.1038/s41586-023-06172-8 |
[98] |
Zia A, Litvin Y, Voskoboynik R, et al. Transcriptome analysis identifies oncogenic tissue remodeling during progression from common nevi to early melanoma. Am J Pathol, 2023; 193, 995−1004. doi: 10.1016/j.ajpath.2023.03.016 |
[99] |
Yuan T, Lu XH, Tang B, et al. Differences in clinical characteristics and lesion proteomics between inflammatory linear verrucous epidermal nevus and local verrucous epidermal nevus. J Proteomics, 2022; 260, 104554. doi: 10.1016/j.jprot.2022.104554 |
[100] |
Varum S, Baggiolini A, Zurkirchen L, et al. Yin Yang 1 orchestrates a metabolic program required for both neural crest development and melanoma formation. Cell Stem Cell, 2019; 24, 637-53. e9. |
[101] |
Muse ME, Schaider H, Oey H, et al. Distinct HOX gene family DNA methylation profiles in histologically normal skin dependent on dermoscopic pattern of adjacent nevi. J Invest Dermatol, 2023; 143, 1830-4. e6. |
[102] |
Zaremba A, Jansen P, Murali R, et al. Genetic and methylation profiles distinguish benign, malignant and spitzoid melanocytic tumors. Int J Cancer, 2022; 151, 1542−54. doi: 10.1002/ijc.34187 |
[103] |
Muse ME, Bergman DT, Salas LA, et al. Genome-scale DNA methylation analysis identifies repeat element alterations that modulate the genomic stability of melanocytic nevi. J Invest Dermatol, 2022; 142, 1893-902. e7. |
[104] |
Huang JM, Chikeka I, Hornyak TJ. Melanocytic nevi and the genetic and epigenetic control of oncogene-induced senescence. Dermatol Clin, 2017; 35, 85−93. |
[105] |
Shain AH, Bastian BC. From melanocytes to melanomas. Nat Rev Cancer, 2016; 16, 345−58. doi: 10.1038/nrc.2016.37 |
[106] |
Veronique C, Evelien V, Sofie DS, et al. Clinicopathologically Defined Naevus Subtypes and Melanoma Risk. J Invest Dermatol, 2024. |
[107] |
Hill VK, Gartner JJ, Samuels Y, et al. The genetics of melanoma: recent advances. Annu Rev Genomics Hum Genet, 2013; 14, 257−79. doi: 10.1146/annurev-genom-091212-153429 |
[108] |
Goel VK, Ibrahim N, Jiang G, et al. Melanocytic nevus-like hyperplasia and melanoma in transgenic BRAFV600E mice. Oncogene, 2009; 28, 2289−98. doi: 10.1038/onc.2009.95 |
[109] |
Dhomen N, Reis-Filho JS, Da Rocha Dias S, et al. Oncogenic Braf induces melanocyte senescence and melanoma in mice. Cancer Cell, 2009; 15, 294−303. doi: 10.1016/j.ccr.2009.02.022 |
[110] |
Patton E, Widlund HR, Kutok JL, et al. BRAF mutations are sufficient to promote nevi formation and cooperate with p53 in the genesis of melanoma. Curr Biol, 2005; 15, 249−54. doi: 10.1016/j.cub.2005.01.031 |
[111] |
Ran RS, Li LX, Shi ZY, et al. Disruption of tp53 leads to cutaneous nevus and melanoma formation in Xenopus tropicalis. Mol Oncol, 2022; 16, 3554−67. doi: 10.1002/1878-0261.13301 |
[112] |
Wang JY, Doudna JA. CRISPR technology: a decade of genome editing is only the beginning. Science, 2023; 379, eadd8643. doi: 10.1126/science.add8643 |
[113] |
Chen PJ, Liu DR. Prime editing for precise and highly versatile genome manipulation. Nat Rev Genet, 2023; 24, 161−77. doi: 10.1038/s41576-022-00541-1 |
[114] |
Lampe GD, King RT, Halpin-Healy TS, et al. Targeted DNA integration in human cells without double-strand breaks using CRISPR-associated transposases. Nat Biotechnol, 2024; 42, 87−98. doi: 10.1038/s41587-023-01748-1 |
[115] |
Qin W, Cho KF, Cavanagh PE, et al. Deciphering molecular interactions by proximity labeling. Nat Methods, 2021; 18, 133−43. doi: 10.1038/s41592-020-01010-5 |
[116] |
Badia-I-Mompel P, Wessels L, Müller-Dott S, et al. Gene regulatory network inference in the era of single-cell multi-omics. Nat Rev Genet, 2023; 24, 739−54. doi: 10.1038/s41576-023-00618-5 |
[117] |
Bahar E, Kim HJ, Kim DR. Targeting the RAS/RAF/MAPK pathway for cancer therapy: from mechanism to clinical studies. Signal Transduct Target Ther, 2023; 8, 455. doi: 10.1038/s41392-023-01705-z |
[118] |
Aphrothiti JH, Chen ZY, Neal R, et al. BRAF — a tumour-agnostic drug target with lineage-specific dependencies. Nat Rev Clin Oncol, 2024; 21, 224−47. doi: 10.1038/s41571-023-00852-0 |