DOK家族在急性髓系白血病中的预后作用
Prognostic Role of the DOK Family in Acute Myeloid Leukemia
DOI: 10.12677/ACM.2023.1371696, PDF,   
作者: 周心怡:延安大学附属医院,陕西 延安
关键词: 急性髓系白血病DOK家族Acute Myeloid Leukemia DOK Family
摘要: 急性髓系白血病是一种异质性恶性血液学系统,其特征是骨髓和外周血中的白血病细胞浸润,其发病率和相关死亡率迅速增加,在过去的30年中几乎翻了一番。估计2年和5年总生存率分别为32.0%和24.0%,明显低于其他白血病亚型。主要驱动突变,共发突变和复杂的基因–基因交互作用是白血病异质性原因,并影响患者生活质量。基因突变和表达谱可以帮助识别不同的预后亚组。然而,关于预后的标准指南缺乏共识,随着测序技术和生物信息学资源的发展,迫切需要发现和评估新的标记物,为诊断评估、生存预测和治疗方案提供可靠的临床指导。酪氨酸激酶(DOK)蛋白的下游是一个多基因的衔接子家族;其中一些是免疫细胞信号传导的关键负调节剂。然而,DOK家族在AML中的表达和临床意义很少被研究。
Abstract: Acute myeloid leukemia is a heterogeneous hematologic malignancy characterized by infiltration of leukemia cells in bone marrow and peripheral blood, with rapidly increasing morbidity and associ-ated mortality, which has nearly doubled over the past 30 years. The estimated 2-year and 5-year overall survival rates were 32.0% and 24.0%, respectively, significantly lower than those of other leukemia subtypes. Major driver mutations, co-occurring mutations, and complex gene-gene inter-actions contribute to leukemic heterogeneity and affect patient quality of life. Gene mutations and expression profiles can help identify different prognostic subgroups. However, there is a lack of consensus on standard guidelines for prognosis, and with the development of sequencing technolo-gy and bioinformatics resources, there is an urgent need to discover and evaluate new markers to provide reliable clinical guidance for diagnostic assessment, survival prediction, and treatment op-tions. The downstream tyrosine kinase (DOK) protein is a multigene bridging subfamily; some of them are key negative regulators of immune cell signaling. However, the expression and clinical significance of the DOK family in AML have rarely been studied.
文章引用:周心怡. DOK家族在急性髓系白血病中的预后作用[J]. 临床医学进展, 2023, 13(7): 12094-12099. https://doi.org/10.12677/ACM.2023.1371696

参考文献

[1] Mashima, R., Yamanashi, Y., Hishida, Y. and Tezuka, T. (2009) The Roles of Dok Family Adapters in Immunoreceptor Signaling. Immunological Reviews, 232, 273-285. [Google Scholar] [CrossRef
[2] Grimm, J., Sachs, M., Britsch, S., et al. (2001) Novel p62dok Family Members, dok-4 and dok-5, Are Substrates of the c-Ret Receptor Tyrosine Kinase and Mediate Neuronal Differentiation. Journal of Cell Biology, 154, 345-354. [Google Scholar] [CrossRef] [PubMed]
[3] Okada, K., Inoue, A., Okada, M., et al. (2006) The Muscle Protein Dok-7 Is Essential for Neuromuscular Synaptogenesis. Science, 312, 1802-1805. [Google Scholar] [CrossRef] [PubMed]
[4] Di Cristofano, A., Carpino, N., Dunant, N., et al. (1998) Molecular Cloning and Characterization of p56dok-2 Defines a New Family of RasGAP-Binding Proteins. Journal of Biological Chemistry, 273, 4827-4830. [Google Scholar] [CrossRef] [PubMed]
[5] Lemay, S., Davidson, D., Latour, S., et al. (2000) Dok-3, a Novel Adapter Molecule Involved in the Negative Regulation of Immunoreceptor Signaling. Molecular and Cellular Biology, 20, 2743-2754. [Google Scholar] [CrossRef
[6] He, P.F., Xu, Z.J., Zhou, J.D., et al. (2018) Methyla-tion-Associated DOK1 and DOK2 Down-Regulation: Potential Biomarkers for Predicting Adverse Prognosis in Acute Myeloid Leukemia. Journal of Cellular Physiology, 233, 6604-6614. [Google Scholar] [CrossRef] [PubMed]
[7] Zhang, L., Li, R., Hu, K., et al. (2019) Prognostic Role of DOK Family Adapters in Acute Myeloid Leukemia. Cancer Gene Therapy, 26, 305-312. [Google Scholar] [CrossRef] [PubMed]
[8] Yasuda, T., Bundo, K., Hino, A., et al. (2007) Dok-1 and Dok-2 Are Negative Regulators of T Cell Receptor Signaling. International Immunology, 19, 487-495. [Google Scholar] [CrossRef] [PubMed]
[9] Celis-Gutierrez, J., Boyron, M., Walzer, T., et al. (2014) Dok1 and Dok2 Proteins Regulate Natural Killer Cell Development and Function. EMBO Journal, 33, 1928-1940. [Google Scholar] [CrossRef] [PubMed]
[10] Laroche-Lefebvre, C., Yousefi, M., Daudelin, J.F., et al. (2016) Dok-1 and Dok-2 Regulate the Formation of Memory CD8+ T Cells. The Journal of Immunology, 197, 3618-3627. [Google Scholar] [CrossRef] [PubMed]
[11] 周瑜, 丁佑铭, 周文波. 酪氨酸激酶下游蛋白基因与肿瘤关系的研究进展[J]. 医学综述, 2016, 22(13): 2561-2564.
[12] Mihrshahi, R. and Brown, M.H. (2010) Downstream of Tyrosine Kinase 1 and 2 Play Opposing roles in CD200 Receptor Signaling. The Journal of Immunology, 185, 7216-7222. [Google Scholar] [CrossRef] [PubMed]
[13] Lum, E., Vigliotti, M., Banerjee, N., et al. (2013) Loss of DOK2 Induces Carboplatin Resistance in Ovarian Cancer via Suppression of Apoptosis. Gynecologic Oncology, 130, 369-376. [Google Scholar] [CrossRef] [PubMed]
[14] Niki, M., Di Cristofano, A., Zhao, M., et al. (2004) Role of Dok-1 and Dok-2 in Leukemia Suppression. Journal of Experimental Medicine, 200, 1689-1695. [Google Scholar] [CrossRef] [PubMed]
[15] Yasuda, T., Shirakata, M., Iwama, A., et al. (2004) Role of Dok-1 and Dok-2 in Myeloid Homeostasis and Suppression of Leukemia. Journal of Experimental Medicine, 200, 1681-1687. [Google Scholar] [CrossRef] [PubMed]
[16] Xu, J., Dong, X., Wang, R., et al. (2022) DOK2 Has Prognostic and Immunologic Significance in Adults with Acute Myeloid Leukemia: A Novel Immune-Related Therapeutic Target. Fron-tiers in Medicine (Lausanne), 9, Article ID: 842383. [Google Scholar] [CrossRef] [PubMed]
[17] Chandran, S.S. and Klebanoff, C.A. (2019) T Cell Receptor-Based Cancer Immunotherapy: Emerging Efficacy and Pathways of Resistance. Immunological Reviews, 290, 127-147. [Google Scholar] [CrossRef] [PubMed]
[18] Park, S., Chapuis, N., Tamburini, J., et al. (2010) Role of the PI3K/AKT and mTOR Signaling Pathways in Acute Myeloid Leukemia. Haema-tologica, 95, 819-828. [Google Scholar] [CrossRef] [PubMed]
[19] Nepstad, I., Hatfield, K.J., Gronningsaeter, I.S., et al. (2020) The PI3K-Akt-mTOR Signaling Pathway in Human Acute Myeloid Leukemia (AML) Cells. International Journal of Molecular Sciences, 21, 2907. [Google Scholar] [CrossRef] [PubMed]
[20] Cook, A.M., Li, L., Ho, Y., et al. (2014) Role of Altered Growth Factor Receptor-Mediated JAK2 Signaling in Growth and Maintenance of Human Acute Myeloid Leukemia Stem Cells. Blood, 123, 2826-2837. [Google Scholar] [CrossRef] [PubMed]
[21] Jia, M., Zhang, H., Wang, L., et al. (2021) Identification of Mast Cells as a Candidate Significant Target of Immunotherapy for Acute Myeloid Leukemia. Hematology, 26, 284-294. [Google Scholar] [CrossRef] [PubMed]
[22] Noviello, M., Manfredi, F., Ruggiero, E., et al. (2019) Bone Marrow Central Memory and Memory Stem T-Cell Exhaustion in AML Patients Relapsing after HSCT. Nature Com-munications, 10, Article No. 1065. [Google Scholar] [CrossRef] [PubMed]
[23] Crowder, R.J., Enomoto, H., Yang, M., et al. (2004) Dok-6, a Novel p62 Dok Family Member, Promotes Ret-Mediated Neurite Outgrowth. Journal of Biological Chemistry, 279, 42072-42081. [Google Scholar] [CrossRef
[24] Li, W., Shi, L., You, Y., et al. (2010) Downstream of Tyrosine Kinase/Docking Protein 6, as a Novel Substrate of Tropomyosin-Related Kinase C Receptor, Is Involved in Neurotrophin 3-Mediated Neurite Outgrowth in Mouse Cortex Neurons. BMC Biology, 8, Article No. 86. [Google Scholar] [CrossRef] [PubMed]
[25] Leong, S.H., Lwin, K.M., Lee, S.S., et al. (2017) Chromosomal Breaks at FRA18C: Association with Reduced DOK6 Expression, Altered Oncogenic Signaling and Increased Gastric Cancer Survival. NPJ Precision Oncology, 1, Article No. 9. [Google Scholar] [CrossRef] [PubMed]
[26] Kurotsuchi, A., Murakumo, Y., Jijiwa, M., et al. (2010) Analysis of DOK-6 Function in Downstream Signaling of RET in Human Neuroblastoma Cells. Cancer Science, 101, 1147-1155. [Google Scholar] [CrossRef] [PubMed]
[27] Sun, G.K., Tang, L.J., Zhou, J.D., et al. (2019) DOK6 Promoter Methylation Serves as a Potential Biomarker Affecting Prognosis in de Novo Acute Myeloid Leukemia. Cancer Medicine, 8, 6393-6402. [Google Scholar] [CrossRef] [PubMed]
[28] Gray, S.G., Stenfeldt, M.I. and De Meyts, P. (2003) The Insulin-Like Growth Factors and Insulin-Signalling Systems: An Appealing Target for Breast Cancer Thera-py? Hormone and Metabolic Research, 35, 857-871. [Google Scholar] [CrossRef] [PubMed]
[29] Blugeon, C., Le Crom, S., Richard, L., et al. (2011) Dok4 Is Involved in Schwann Cell Myelination and Axonal Interaction in Vitro. Glia, 59, 351-362. [Google Scholar] [CrossRef] [PubMed]
[30] Favre, C., Gerard, A., Clauzier, E., et al. (2003) DOK4 and DOK5: New Dok-Related Genes Expressed in Human T Cells. Genes & Immunity, 4, 40-45. [Google Scholar] [CrossRef] [PubMed]
[31] Guan, Y., Li, M., Qiu, Z., et al. (2022) Comprehensive Analysis of DOK Family Genes Expression, Immune Characteristics, and Drug Sensitivity in Human Tumors. Journal of Advanced Research, 36, 73-87. [Google Scholar] [CrossRef] [PubMed]
[32] Ohashi, T., Komatsu, S., Ichikawa, D., et al. (2017) Overexpression of PBK/TOPK Relates to Tumour Malignant Potential and Poor Outcome of Gastric Carcinoma. British Journal of Can-cer, 116, 218-226. [Google Scholar] [CrossRef] [PubMed]
[33] Ayllon, V. and O’Connor, R. (2007) PBK/TOPK Promotes Tumour Cell Proliferation through p38 MAPK Activity and Regulation of the DNA Damage Response. Oncogene, 26, 3451-3461. [Google Scholar] [CrossRef] [PubMed]
[34] Sun, H., Zhang, L., Shi, C., et al. (2015) TOPK Is Highly Expressed in Circulating Tumor Cells, Enabling Metastasis of Prostate Cancer. Oncotarget, 6, 12392-12404. [Google Scholar] [CrossRef] [PubMed]
[35] Huttlin, E.L., Ting, L., Bruckner, R.J., et al. (2015) The BioPlex Network: A Systematic Exploration of the Human Interactome. Cell, 162, 425-440. [Google Scholar] [CrossRef] [PubMed]