Stock W, et al. A pediatric regimen for older adolescents and young adults with acute lymphoblastic leukemia: results of CALGB 10403. Blood. 2019;133(14):1548–59. Practice changing publication on AYA ALL from an adult cooperative group.
Article CAS PubMed PubMed Central Google Scholar
Schrappe M, et al. Late MRD response determines relapse risk overall and in subsets of childhood T-cell ALL: results of the AIEOP-BFM-ALL 2000 study. Blood. 2011;118(8):2077–84.
Article CAS PubMed Google Scholar
Dunsmore KP, et al. Children's Oncology Group AALL0434: a phase III randomized clinical trial testing nelarabine in newly diagnosed T-cell acute lymphoblastic leukemia. J Clin Oncol. 2020;38(28):3282–93. Practice changing trial for young people with T ALL from the pediatric collaborative group.
Article CAS PubMed PubMed Central Google Scholar
Jing D, et al. Opposing regulation of BIM and BCL2 controls glucocorticoid-induced apoptosis of pediatric acute lymphoblastic leukemia cells. Blood. 2015;125(2):273–83.
Article CAS PubMed Google Scholar
Li Y, et al. IL-7 receptor mutations and steroid resistance in pediatric T cell acute lymphoblastic leukemia: a genome sequencing study. PLOS Med. 2016;13(12):e1002200.
Article PubMed PubMed Central Google Scholar
Barata JT, et al. Activation of PI3K is indispensable for interleukin 7-mediated viability, proliferation, glucose use, and growth of T cell acute lymphoblastic leukemia cells. J Exp Med. 2004;200(5):659–69.
Article CAS PubMed PubMed Central Google Scholar
van der Zwet JCG, et al. MAPK-ERK is a central pathway in T-cell acute lymphoblastic leukemia that drives steroid resistance. Leukemia. 2021;35(12):3394–405.
Dillon M, et al. Progress on Ras/MAPK signaling research and targeting in blood and solid cancers. Cancers (Basel). 2021;13(20).
Ribeiro D, et al. STAT5 is essential for IL-7-mediated viability, growth, and proliferation of T-cell acute lymphoblastic leukemia cells. Blood Adv. 2018;2(17):2199–213.
Article PubMed PubMed Central Google Scholar
de Bock CE, et al. HOXA9 cooperates with activated JAK/STAT signaling to drive leukemia development. Cancer Discov. 2018;8(5):616–31.
Blanco-Aparicio C, Carnero A. Pim kinases in cancer: diagnostic, prognostic and treatment opportunities. Biochem Pharmacol. 2013;85(5):629–43.
Article CAS PubMed Google Scholar
Bachmann M, et al. The oncogenic serine/threonine kinase Pim-1 directly phosphorylates and activates the G2/M specific phosphatase Cdc25C. Int J Biochem Cell Biol. 2006;38(3):430–43.
Article CAS PubMed Google Scholar
Silva A, et al. Overexpression of wild-type IL-7Rα promotes T-cell acute lymphoblastic leukemia/lymphoma. Blood. 2021;138(12):1040–52.
Article CAS PubMed PubMed Central Google Scholar
De Smedt R, et al. Targeting cytokine- and therapy-induced PIM1 activation in preclinical models of T-cell acute lymphoblastic leukemia and lymphoma. Blood. 2020;135(19):1685–95.
Luszczak S, et al. PIM kinase inhibition: co-targeted therapeutic approaches in prostate cancer. Signal Transduct Targeted Ther. 2020;5(1):7.
Mansour MR, et al. High incidence of Notch-1 mutations in adult patients with T-cell acute lymphoblastic leukemia. Leukemia. 2006;20(3):537–9.
Article CAS PubMed Google Scholar
Weng AP, et al. c-Myc is an important direct target of Notch1 in T-cell acute lymphoblastic leukemia/lymphoma. Genes Dev. 2006;20(15):2096–109.
Article CAS PubMed PubMed Central Google Scholar
Moellering RE, et al. Direct inhibition of the NOTCH transcription factor complex. Nature. 2009;462(7270):182–8.
Article CAS PubMed PubMed Central Google Scholar
Real PJ, et al. Gamma-secretase inhibitors reverse glucocorticoid resistance in T cell acute lymphoblastic leukemia. Nat Med. 2009;15(1):50–8.
Article CAS PubMed Google Scholar
Zheng H, et al. KLF4 gene expression is inhibited by the notch signaling pathway that controls goblet cell differentiation in mouse gastrointestinal tract. Am J Physiol Gastrointest Liver Physiol. 2009;296(3):G490–8.
Article CAS PubMed Google Scholar
Zweidler-McKay PA, et al. The safety and activity of BMS-906024, a gamma secretase inhibitor (GSI) with anti-Notch activity, in patients with relapsed T-cell acute lymphoblastic leukemia (T-ALL): initial results of a phase 1 trial. Blood. 2014;124(21):968–8.
Knoechel B, et al. Complete hematologic response of early T-cell progenitor acute lymphoblastic leukemia to the γ-secretase inhibitor BMS-906024: genetic and epigenetic findings in an outlier case. Cold Spring Harb Mol Case Stud. 2015;1(1):a000539.
Article PubMed PubMed Central Google Scholar
Borthakur G, et al. Phase 1 study to evaluate Crenigacestat (LY3039478) in combination with dexamethasone in patients with T-cell acute lymphoblastic leukemia and lymphoma. Cancer. 2021;127(3):372–80.
Article CAS PubMed Google Scholar
O'Neil J, et al. FBW7 mutations in leukemic cells mediate NOTCH pathway activation and resistance to gamma-secretase inhibitors. J Exp Med. 2007;204(8):1813–24.
Article CAS PubMed PubMed Central Google Scholar
Knoechel B, et al. An epigenetic mechanism of resistance to targeted therapy in T cell acute lymphoblastic leukemia. Nat Genet. 2014;46(4):364–70.
Article CAS PubMed PubMed Central Google Scholar
Liu Y, et al. The genomic landscape of pediatric and young adult T-lineage acute lymphoblastic leukemia. Nat Genet. 2017;49(8):1211–8. Article that includes a detailed description of genetic changes seen in T ALL.
Article CAS PubMed PubMed Central Google Scholar
Sicinska E, et al. Requirement for cyclin D3 in lymphocyte development and T cell leukemias. Cancer Cell. 2003;4(6):451–61.
Article CAS PubMed Google Scholar
Choi YJ, et al. The requirement for cyclin D function in tumor maintenance. Cancer Cell. 2012;22(4):438–51.
Article CAS PubMed PubMed Central Google Scholar
Pikman Y, et al. Synergistic drug combinations with a CDK4/6 inhibitor in T-cell acute lymphoblastic leukemia. Clin Cancer Res. 2017;23(4):1012–24.
Article CAS PubMed Google Scholar
Kwiatkowski N, et al. Targeting transcription regulation in cancer with a covalent CDK7 inhibitor. Nature. 2014;511(7511):616–20.
Article CAS PubMed PubMed Central Google Scholar
Mansour MR, et al. Oncogene regulation. An oncogenic super-enhancer formed through somatic mutation of a noncoding intergenic element. Science. 2014;346(6215):1373–7.
Article CAS PubMed PubMed Central Google Scholar
Cidado J, et al. AZD4573 is a highly selective CDK9 inhibitor that suppresses MCL-1 and induces apoptosis in hematologic cancer cells. Clin Cancer Res. 2020;26(4):922–34.
Article CAS PubMed Google Scholar
Olson CM, et al. Pharmacological perturbation of CDK9 using selective CDK9 inhibition or degradation. Nat Chem Biol. 2018;14(2):163–70.
Article CAS PubMed Google Scholar
Chen L, et al. Differential targeting of prosurvival Bcl-2 proteins by their BH3-only ligands allows complementary apoptotic function. Mol Cell. 2005;17(3):393–403.
Article CAS PubMed Google Scholar
Chonghaile TN, et al. Maturation stage of T-cell acute lymphoblastic leukemia determines BCL-2 versus BCL-XL dependence and sensitivity to ABT-199. Cancer Discov. 2014;4(9):1074–87.
Article CAS PubMed PubMed Central Google Scholar
Richard-Carpentier G, et al. Clinical experience with venetoclax combined with chemotherapy for relapsed or refractory T-cell acute lymphoblastic leukemia. Clin Lymphoma Myeloma Leuk. 2020;20(4):212–8.
Jain N, et al. A multicenter phase I study combining venetoclax with mini-hyper-CVD in older adults with untreated and relapsed/refractory acute lymphoblastic leukemia. Blood. 2019;134(Supplement_1):3867–7. An excellent preliminary study in older adults with combination chemotherapy that will likely drive future randomized trials.
Pullarkat VA, et al. Venetoclax and navitoclax in combination with chemotherapy in patients with relapsed or refractory acute lymphoblastic leukemia and lymphoblastic lymphoma. Cancer Discov. 2021;11(6):1440–1453. Early phase study demonstrating effectiveness of BCL-2/BCL-XL combination in relapsed ALL.
Comments (0)