References
- Arber DA, Orazi A, Hasserjian R, et al. The 2016 revision to the World Health Organization classification of myeloid neoplasms and acute leukemia. Blood. 2016;127(20):2391–2405.
- Mangaonkar AA, Patnaik MM. Advances in chronic myelomonocytic leukemia and future prospects: lessons learned from precision genomics. Adv Cell Gene Ther. 2019;2(2):e48.
- Patnaik MM, Tefferi A. Chronic myelomonocytic leukemia: 2020 update on diagnosis, risk stratification and management. Am J Hematol. 2020;95(1):97–115.
- Carr RM, Vorobyev D, Lasho T, et al. RAS mutations drive proliferative chronic myelomonocytic leukemia via a KMT2A-PLK1 axis. Nat Commun. 2021;12(1):2901.
- Merlevede J, Droin N, Qin T, et al. Mutation allele burden remains unchanged in chronic myelomonocytic leukaemia responding to hypomethylating agents. Nat Commun. 2016;7:10767.
- Coston T, Pophali P, Vallapureddy R, et al. Suboptimal response rates to hypomethylating agent therapy in chronic myelomonocytic leukemia; a single institutional study of 121 patients. Am J Hematol. 2019;94:767–779.
- Moran-Crusio K, Reavie L, Shih A, et al. Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation. Cancer Cell. 2011;20(1):11–24.
- Abdel-Wahab O, Adli M, LaFave LM, et al. ASXL1 mutations promote myeloid transformation through loss of PRC2-mediated gene repression. Cancer Cell. 2012;22(2):180–193.
- Tefferi A, Pardanani A, Lim KH, et al. TET2 mutations and their clinical correlates in polycythemia vera, essential thrombocythemia and myelofibrosis. Leukemia. 2009;23(5):905–911.
- Smeets MF, Tan SY, Xu JJ, et al. Srsf2P95H initiates myeloid bias and myelodysplastic/myeloproliferative syndrome from hemopoietic stem cells . Blood. 2018;132(6):608–621.
- Thanopoulou E, Cashman J, Kakagianne T, et al. Engraftment of NOD/SCID-beta2 microglobulin null mice with multilineage neoplastic cells from patients with myelodysplastic syndrome. Blood. 2004;103(11):4285–4293.
- Nilsson L, Astrand-Grundström I, Anderson K, et al. Involvement and functional impairment of the CD34(+)CD38(–)thy-1(+) hematopoietic stem cell pool in myelodysplastic syndromes with trisomy 8. Blood. 2002;100(1):259–267.
- Yoshimi A, Balasis ME, Vedder A, et al. Robust patient-derived xenografts of MDS/MPN overlap syndromes capture the unique characteristics of CMML and JMML. Blood. 2017;130(4):397–407.
- Zhang Y, He L, Selimoglu-Buet D, et al. Engraftment of chronic myelomonocytic leukemia cells in immunocompromised mice supports disease dependency on cytokines. Blood Adv. 2017;1(14):972–979.
- Sevin M, Debeurme F, Laplane L, et al. Cytokine-like protein 1-induced survival of monocytes suggests a combined strategy targeting MCL1 and MAPK in CMML. Blood. 2021;137(24):3390–3402.
- Young K, Eudy E, Bell R, et al. Decline in IGF1 in the bone marrow microenvironment initiates hematopoietic stem cell aging. Cell Stem Cell. 2021;28(8):1473–1482.e7.
- Trowbridge JJ, Starczynowski DT. Innate immune pathways and inflammation in hematopoietic aging, clonal hematopoiesis, and MDS. J Exp Med. 2021;218:e20201544.
- Cazzola M. Myelodysplastic syndromes. N Engl J Med. 2020;383(14):1358–1374.
- Muto T, Walker CS, Choi K, et al. Adaptive response to inflammation contributes to sustained myelopoiesis and confers a competitive advantage in myelodysplastic syndrome HSCs. Nat Immunol. 2020;21(5):535–545.
- SanMiguel JM, Young K, Trowbridge JJ. Hand in hand: intrinsic and extrinsic drivers of aging and clonal hematopoiesis. Exp Hematol. 2020;91:1–9.
- Williams N, Lee J, Mitchell E, et al. Life histories of myeloproliferative neoplasms inferred from phylogenies. Nature. 2022;602(7895):162–168.
- Van Egeren D, Escabi J, Nguyen M, et al. Reconstructing the lineage histories and differentiation trajectories of individual cancer cells in myeloproliferative neoplasms. Cell Stem Cell. 2021;28(3):514–523.e9.
- Wong WH, Bhatt S, Trinkaus K, et al. Engraftment of rare, pathogenic donor hematopoietic mutations in unrelated hematopoietic stem cell transplantation. Sci Transl Med. 2020;12:eaax6249.
- Adelman ER, Huang HT, Roisman A, et al. Aging human hematopoietic stem cells manifest profound epigenetic reprogramming of enhancers that may predispose to leukemia. Cancer Discov. 2019;9(8):1080–1101.
- Kovtonyuk LV, Fritsch K, Feng X, et al. Inflamm-aging of hematopoiesis, hematopoietic stem cells, and the bone marrow microenvironment. Front Immunol. 2016;7:502.
- Yamashita M, Passegué E. TNF-α coordinates hematopoietic stem cell survival and myeloid regeneration. Cell Stem Cell. 2019;25(3):357–372.e7.
- Frisch BJ, Hoffman CM, Latchney SE, et al. Aged marrow macrophages expand platelet-biased hematopoietic stem cells via interleukin1B. JCI Insight. 2019;4(10):5.
- Cook EK, Izukawa T, Young S, et al. Comorbid and inflammatory characteristics of genetic subtypes of clonal hematopoiesis. Blood Adv. 2019;3(16):2482–2486.
- Grignano E, Mekinian A, Braun T, et al. Autoimmune and inflammatory diseases associated with chronic myelomonocytic leukemia: a series of 26 cases and literature review. Leuk Res. 2016;47:136–141.
- Zahid MF, Barraco D, Lasho TL, et al. Spectrum of autoimmune diseases and systemic inflammatory syndromes in patients with chronic myelomonocytic leukemia. Leuk Lymphoma. 2017;58(6):1488–1493.
- Sallman DA, List A. The central role of inflammatory signaling in the pathogenesis of myelodysplastic syndromes. Blood. 2019;133(10):1039–1048.
- Akira S, Takeda K. Toll-like receptor signalling. Nat Rev Immunol. 2004;4(7):499–511.
- Gañán-Gómez I, Wei Y, Starczynowski DT, et al. Deregulation of innate immune and inflammatory signaling in myelodysplastic syndromes. Leukemia. 2015;29(7):1458–1469.
- Niyongere S, Lucas N, Zhou JM, et al. Heterogeneous expression of cytokines accounts for clinical diversity and refines prognostication in CMML. Leukemia. 2019;33(1):205–216.
- Geissler K, Ohler L, Födinger M, et al. Interleukin 10 inhibits growth and granulocyte/macrophage colony-stimulating factor production in chronic myelomonocytic leukemia cells. J Exp Med. 1996;184(4):1377–1384.
- Zhang Q, Zhao K, Shen Q, et al. Tet2 is required to resolve inflammation by recruiting Hdac2 to specifically repress IL-6. Nature. 2015;525(7569):389–393.
- Lee SC, North K, Kim E, et al. Synthetic lethal and convergent biological effects of cancer-associated spliceosomal gene mutations. Cancer Cell. 2018;34(2):225–241.e8.
- Smith MA, Choudhary GS, Pellagatti A, et al. U2AF1 mutations induce oncogenic IRAK4 isoforms and activate innate immune pathways in myeloid malignancies. Nat Cell Biol. 2019;21(5):640–650.
- Basiorka AA, McGraw KL, Eksioglu EA, et al. The NLRP3 inflammasome functions as a driver of the myelodysplastic syndrome phenotype. Blood. 2016;128(25):2960–2975.
- Barreyro L, Chlon TM, Starczynowski DT. Chronic immune response dysregulation in MDS pathogenesis. Blood. 2018;132(15):1553–1560.
- Martin TD, Patel RS, Cook DR, et al. The adaptive immune system is a major driver of selection for tumor suppressor gene inactivation. Science. 2021;373(6561):1327–1335.
- Yang H, Bueso-Ramos C, DiNardo C, et al. Expression of PD-L1, PD-L2, PD-1 and CTLA4 in myelodysplastic syndromes is enhanced by treatment with hypomethylating agents. Leukemia. 2014;28(6):1280–1288.
- Mangaonkar AA, Reichard KK, Binder M, et al. Bone marrow dendritic cell aggregates associate with systemic immune dysregulation in chronic myelomonocytic leukemia. Blood Adv. 2020;4(21):5425–5430.
- You X, Liu F, Binder M, et al. Asxl1 loss cooperates with oncogenic Nras in mice to reprogram immune microenvironment and drive leukemic transformation. Blood. 2022;139(7):1066–1079.
- Lucas N, Duchmann M, Rameau P, et al. Biology and prognostic impact of clonal plasmacytoid dendritic cells in chronic myelomonocytic leukemia. Leukemia. 2019;33(10):2466–2480.
- Pemmaraju N, Lane AA, Sweet KL, et al. Tagraxofusp in blastic plasmacytoid dendritic-cell neoplasm. N Engl J Med. 2019;380(17):1628–1637.
- Patnaik MM, Mughal TI, Brooks C, et al. Targeting CD123 in hematologic malignancies: identifying suitable patients for targeted therapy. Leuk Lymphoma. 2021;62:1–19.
- Munn DH, Sharma MD, Hou D, et al. Expression of indoleamine 2,3-dioxygenase by plasmacytoid dendritic cells in tumor-draining lymph nodes. J Clin Invest. 2004;114(2):280–290.
- Munn DH, Sharma MD, Lee JR, et al. Potential regulatory function of human dendritic cells expressing indoleamine 2,3-dioxygenase. Science. 2002;297(5588):1867–1870.
- Mellor AL, Munn DH. IDO expression by dendritic cells: tolerance and tryptophan catabolism. Nat Rev Immunol. 2004;4(10):762–774.
- Brandacher G, Perathoner A, Ladurner R, et al. Prognostic value of indoleamine 2,3-dioxygenase expression in colorectal cancer: effect on tumor-infiltrating T cells. Clin Cancer Res. 2006;12(4):1144–1151.
- Ino K, Yoshida N, Kajiyama H, et al. Indoleamine 2,3-dioxygenase is a novel prognostic indicator for endometrial cancer. Br J Cancer. 2006;95(11):1555–1561.
- Riesenberg R, Weiler C, Spring O, et al. Expression of indoleamine 2,3-dioxygenase in tumor endothelial cells correlates with long-term survival of patients with renal cell carcinoma. Clin Cancer Res. 2007;13(23):6993–7002.
- Pan K, Wang H, Chen MS, et al. Expression and prognosis role of indoleamine 2,3-dioxygenase in hepatocellular carcinoma. J Cancer Res Clin Oncol. 2008;134(11):1247–1253.
- Mangaonkar A, Mondal AK, Fulzule S, et al. A novel immunohistochemical score to predict early mortality in acute myeloid leukemia patients based on indoleamine 2,3 dioxygenase expression. Sci Rep. 2017;7(1):12892.
- Folgiero V, Goffredo BM, Filippini P, et al. Indoleamine 2,3-dioxygenase 1 (IDO1) activity in leukemia blasts correlates with poor outcome in childhood acute myeloid leukemia. Oncotarget. 2014;5(8):2052–2064.
- Chamuleau ME, van de Loosdrecht AA, Hess CJ, et al. High INDO (indoleamine 2,3-dioxygenase) mRNA level in blasts of acute myeloid leukemic patients predicts poor clinical outcome. Haematologica. 2008;93(12):1894–1898.
- Kunimoto H, Meydan C, Nazir A, et al. Cooperative epigenetic remodeling by TET2 loss and NRAS mutation drives myeloid transformation and MEK inhibitor sensitivity. Cancer Cell. 2018;33(1):44–59.e8.
- Hunter AM, Newman H, Dezern AE, et al. Integrated human and murine clinical study establishes clinical efficacy of ruxolitinib in chronic myelomonocytic leukemia. Clin Cancer Res. 2021;27(22):6095–6105.
- O'Connell CL, Kropf PL, Punwani N, et al. Phase I results of a multicenter clinical trial combining guadecitabine, a DNA methyltransferase inhibitor, with atezolizumab, an immune checkpoint inhibitor, in patients with relapsed or refractory myelodysplastic syndrome or chronic myelomonocytic leukemia. Blood. 2018;132(Suppl. 1):1811.
- Long GV, Dummer R, Hamid O, et al. Epacadostat plus pembrolizumab versus placebo plus pembrolizumab in patients with unresectable or metastatic melanoma (ECHO-301/KEYNOTE-252): a phase 3, randomised, double-blind study. Lancet Oncol. 2019;20(8):1083–1097.
- Van den Eynde BJ, van Baren N, Baurain J-F. Is there a clinical future for IDO1 inhibitors after the failure of epacadostat in melanoma? Annu Rev Cancer Biol. 2020;4(1):241–256.
- Emadi A, Duong VH, Pantin J, et al. Indoximod combined with standard induction chemotherapy is well tolerated and induces a high rate of complete remission with MRD-negativity in patients with newly diagnosed AML: results from a phase 1 trial. Blood. 2018;132(Suppl. 1):332.
- Zeidan AM, Knaus HA, Robinson TM, et al. A multi-center phase I trial of ipilimumab in patients with myelodysplastic syndromes following hypomethylating agent failure. Clin Cancer Res. 2018;24(15):3519–3527.
- Morita K, Kantarjian HM, Montalban Bravo G, et al. A phase II study of double immune checkpoint inhibitor blockade with nivolumab and ipilimumab with or without azacitidine in patients with myelodysplastic syndrome (MDS). Blood. 2020;136(Suppl. 1):7–9.