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Correction

Correction: Dhillon et al. Molecular Insights and Therapeutic Advances in Low-Risk Myelodysplastic Neoplasms: A Clinical Review. Cancers 2025, 17, 3610

by
Vikram Dhillon
1,
Jaroslaw Maciejewski
2 and
Suresh Kumar Balasubramanian
1,2,*
1
Department of Oncology, Karmanos Cancer Institute, Wayne State University, Detroit, MI 48201, USA
2
Department of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA
*
Author to whom correspondence should be addressed.
Cancers 2026, 18(1), 172; https://doi.org/10.3390/cancers18010172
Submission received: 9 December 2025 / Accepted: 15 December 2025 / Published: 4 January 2026

Error in Figure 1 Legend

In the original publication [1], there was an error in the legend for Figure 1 as published. An incorrect version of the Figure 1 legend was inadvertently included in the revised manuscript. The correct legend appears below.
  • Figure 1. Diagnostic algorithm for pre-MDS conditions. This flowchart illustrates the diagnostic pathway for distinguishing between clonal and non-clonal cytopenias and dysplasia that can precede or may progress to MDS. The algorithm differentiates four key entities based on the presence or absence of cytopenias, dysplastic features, and clonal mutations: ICUS (Idiopathic Cytopenias of Uncertain Significance)—cytopenia without clonal mutations or dysplasia; CCUS (Clonal Cytopenias of Uncertain Significance)—cytopenia with clonal mutations but without dysplasia; CHIP (Clonal Hematopoiesis of Indeterminate Potential)—clonal mutations without cytopenia or dysplasia; and IDUS (Idiopathic Dysplasia of Unknown Significance)—morphologic dysplasia without cytopenia or clonal mutations. # High risk mutations include ASXL1, CBL, DNMT3A, ETV6, EZH2, IDH2, KRAS, NPM1, NRAS, RUNX1, SF3B1, SRSF2, and U2AF1.

Error in Figure 1

In the original publication, there was an error in Figure 1 as published. An incorrect version of Figure 1 was inadvertently included in the revised manuscript. The corrected Figure 1 appears below.

Error in Figure 3 Legend

In the original publication, there was an error in the legend for Figure 3 as published. An incorrect version of the Figure 3 legend was inadvertently included in the revised manuscript. The correct legend appears below.
  • Figure 3. Our treatment approach to low-risk myelodysplastic syndrome (LR-MDS). This flowchart outlines the therapeutic approach to low-risk MDS based on clinical presentation and laboratory parameters. The algorithm stratifies patients into four categories: Moderate and asymptomatic cytopenias (observation only), symptomatic anemia, symptomatic neutropenia, and symptomatic thrombocytopenia. Green boxes with solid backgrounds indicate FDA-approved therapies; green boxes with italicized text denote clinically used but not formally approved treatments. Blue boxes represent clinical decision points. Abbreviations: ATG, antithymocyte globulin; del(5q), deletion of chromosome 5q; chr, chromosome; EPO, erythropoietin; G-CSF, granulocyte colony-stimulating factor; Hb, hemoglobin; MDS, myelodysplastic syndrome; RBC, red blood cell; RS, ring sideroblasts; SF3B1, splicing factor 3B subunit 1 gene; TPO-RAs, thrombopoietin receptor agonists; and U/L, units per liter.

Error in Figure 3

In the original publication, there was an error in Figure 3 as published. An incorrect version of Figure 3 was inadvertently included in the revised manuscript. The corrected Figure 3 appears below.

Error in Table 1

In the original publication, there was an error in Table 1 as published. Under Imetelstat efficacy outcomes, the RBC-TI percentage was incorrectly listed as 40% when it should be 39.8%. The corrected Table 1 appears below.

Text Correction

There was an error in the original publication. Under Section 3.6. Telomerase inhibitor: Imetelstat, the RBC-TI percentage was incorrectly listed as 40% when it should be 39.8%. A correction has been made to Section 3.6, second paragraph:
Follow-up phase-II studies demonstrated durable transfusion independence in 42% of LR-MDS patients ineligible for ESA therapy [48]. The Phase-III IMerge trial (NCT02598661) enrolled 178 patients randomized to imetelstat or placebo [49]. In the treatment arm, about 40% achieved RBC-transfusion independence with durable responses lasting 52 weeks. Molecular profiling revealed SF3B1 as the most frequently mutated gene (75.8%), with SF3B1-mutant patients demonstrating superior transfusion independence rates with Imetelstat versus placebo (48.8% vs. 16.3% at 8 weeks) [49]. Responses varied across SF3B1 hotspots, with T663P and A744P mutations achieving 100% response rates, while the most common K700E hotspot achieved 43.9% response. Other frequently mutated genes also responded: TET2-mutant patients achieved 50% transfusion independence versus 21.4% with placebo, and ASXL1-mutant patients achieved 27.8% response versus 0% with placebo [49]. Notably, higher mutational burden (>2 mutations) was associated with enhanced response rates (45.5% versus 6.7% with placebo), and even patients harboring traditionally poor-prognosis mutations (TP53, ETV6, RUNX1, ASXL1, or EZH2) achieved 31.8% transfusion independence with Imetelstat versus 0% with placebo [50]. Neutropenia was the most serious adverse event (91% treatment arm vs. 47% placebo), though it is manageable with dose delays and reductions, and based on this trial, Imetelstat has received FDA approval for LR-MDS in heavily TD patients.
The authors state that the scientific conclusions are unaffected. This correction was approved by the Academic Editor. The original publication has also been updated.

Reference

  1. Dhillon, V.; Maciejewski, J.; Balasubramanian, S.K. Molecular Insights and Therapeutic Advances in Low-Risk Myelodysplastic Neoplasms: A Clinical Review. Cancers 2025, 17, 3610. [Google Scholar] [CrossRef]
Figure 1. Diagnostic algorithm for pre-MDS conditions. This flowchart illustrates the diagnostic pathway for distinguishing between clonal and non-clonal cytopenias and dysplasia that can precede or may progress to MDS. The algorithm differentiates four key entities based on the presence or absence of cytopenias, dysplastic features, and clonal mutations: ICUS (Idiopathic Cytopenias of Uncertain Significance)—cytopenia without clonal mutations or dysplasia; CCUS (Clonal Cytopenias of Uncertain Significance)—cytopenia with clonal mutations but without dysplasia; CHIP (Clonal Hematopoiesis of Indeterminate Potential)—clonal mutations without cytopenia or dysplasia; and IDUS (Idiopathic Dysplasia of Unknown Significance)—morphologic dysplasia without cytopenia or clonal mutations. # High risk mutations include ASXL1, CBL, DNMT3A, ETV6, EZH2, IDH2, KRAS, NPM1, NRAS, RUNX1, SF3B1, SRSF2, and U2AF1.
Figure 1. Diagnostic algorithm for pre-MDS conditions. This flowchart illustrates the diagnostic pathway for distinguishing between clonal and non-clonal cytopenias and dysplasia that can precede or may progress to MDS. The algorithm differentiates four key entities based on the presence or absence of cytopenias, dysplastic features, and clonal mutations: ICUS (Idiopathic Cytopenias of Uncertain Significance)—cytopenia without clonal mutations or dysplasia; CCUS (Clonal Cytopenias of Uncertain Significance)—cytopenia with clonal mutations but without dysplasia; CHIP (Clonal Hematopoiesis of Indeterminate Potential)—clonal mutations without cytopenia or dysplasia; and IDUS (Idiopathic Dysplasia of Unknown Significance)—morphologic dysplasia without cytopenia or clonal mutations. # High risk mutations include ASXL1, CBL, DNMT3A, ETV6, EZH2, IDH2, KRAS, NPM1, NRAS, RUNX1, SF3B1, SRSF2, and U2AF1.
Cancers 18 00172 g001
Figure 3. Our treatment approach to low-risk myelodysplastic syndrome (LR-MDS). This flowchart outlines the therapeutic approach to low-risk MDS based on clinical presentation and laboratory parameters. The algorithm stratifies patients into four categories: Moderate and asymptomatic cytopenias (observation only), symptomatic anemia, symptomatic neutropenia, and symptomatic thrombocytopenia. Green boxes with solid backgrounds indicate FDA-approved therapies; green boxes with italicized text denote clinically used but not formally approved treatments. Blue boxes represent clinical decision points. Abbreviations: ATG, antithymocyte globulin; del(5q), deletion of chromosome 5q; chr, chromosome; EPO, erythropoietin; G-CSF, granulocyte colony-stimulating factor; Hb, hemoglobin; MDS, myelodysplastic syndrome; RBC, red blood cell; RS, ring sideroblasts; SF3B1, splicing factor 3B subunit 1 gene; TPO-RAs, thrombopoietin receptor agonists; and U/L, units per liter.
Figure 3. Our treatment approach to low-risk myelodysplastic syndrome (LR-MDS). This flowchart outlines the therapeutic approach to low-risk MDS based on clinical presentation and laboratory parameters. The algorithm stratifies patients into four categories: Moderate and asymptomatic cytopenias (observation only), symptomatic anemia, symptomatic neutropenia, and symptomatic thrombocytopenia. Green boxes with solid backgrounds indicate FDA-approved therapies; green boxes with italicized text denote clinically used but not formally approved treatments. Blue boxes represent clinical decision points. Abbreviations: ATG, antithymocyte globulin; del(5q), deletion of chromosome 5q; chr, chromosome; EPO, erythropoietin; G-CSF, granulocyte colony-stimulating factor; Hb, hemoglobin; MDS, myelodysplastic syndrome; RBC, red blood cell; RS, ring sideroblasts; SF3B1, splicing factor 3B subunit 1 gene; TPO-RAs, thrombopoietin receptor agonists; and U/L, units per liter.
Cancers 18 00172 g003
Table 1. Currently approved for low-risk MDS.
Table 1. Currently approved for low-risk MDS.
AgentClass/TargetIncluded PatientsNEfficacy OutcomesTrial (Phase)
Erythropoietin alpha,
Darbepoetin alpha
ESALR-MDS patients with anemia, low transfusion burden 1130ER: 45.9% vs. 4.4% (placebo)EPOANE3021
(Phase III) 2
LenalidomideIMiDsTD LR-MDS with del (5Q)205RBC-TI: 42.6 to 56.1%
vs. 5.9% (placebo)
MDS-004
(Phase III) 3
DeferasiroxICTTD LR-MDS with iron overload225EFS on ICT: 3.9 years vs. 3 (placebo)TELESTO
(Phase II) 4
Etrombopag,
Romiplostim
TPOLR-MDS with severe thrombocytopenia169PLT-R: 47% vs. 11% (placebo)EQOL-MDS
(Phase II) 5
LuspaterceptErythroid
maturation
agents
TD LR-MDS,
ESA-refractory 6
354; 229RBC-TI: 58.5% vs. 31.2% (placebo);
38% vs. 13% (placebo)
MEDALIST
(Phase III) 6,
COMMANDS
(Phase III) 7
Azacitidine,
Decitabine,
Guadecitabine
HMAsTD LR-MDS,
ESA-unresponsive
113RBC-TI: 41% decitabine
vs. 15% azacitadine
NCT01720225
(Phase II) 8
ImetelstatTelomerase
inhibitor
TD LR-MDS,
ESA-refractory
178RBC-TI: 39.8% vs. 15%
(placebo)
IMerge
(Phase III) 9
1 Inclusion: Hb ≤ 10.0 g/dL, ≤4 RBC units/8 weeks, serum EPO < 500 mU/mL.
2 ESAs have been studied in multiple trials over decades (ECOG E1996 Trial, ARCADE Trial); no single definitive phase III trial established efficacy, though EPOANE3021 (NCT01381809) is one recent example showing ER of 45.9% vs. 4.4% at 24 weeks (N = 130).
3 Inclusion: TD patients with del(5Q). Primary endpoint: RBC-TI ≥ 26 weeks. MDS-003 (phase II, N = 148) was the initial registration trial. NCT00179621.
4 Inclusion: TD patients with serum ferritin > 2247 pmol/L (>1000 ng/mL) and prior receipt of 15–75 pRBCs. Primary endpoint: EFS from randomization to first nonfatal event (cardiac, hepatic, death, or AML transformation). Median EFS 1440 vs. 1091 days (p = 0.015). NCT00940602.
5 Inclusion: Platelet count < 30 × 103/mm3 with high bleeding risk. Primary endpoint: PLT response for ≥25 weeks. NCT02912208.
6 COMMANDS (NCT03682536, N = 354): ESA-naive TD patients with or without ring sideroblasts; <5% blasts, sEPO < 500 U/L. Primary endpoint: RBC-TI ≥ 12 weeks with Hb increase ≥ 1.5 g/dL within the first 24 weeks. Compared luspatercept vs. epoetin alfa (first-line, head-to-head comparison). First drug to demonstrate superiority over ESAs in first-line treatment of LR-MDS.
7 MEDALIST (NCT02631070, N = 229): Registration trial in ESA-refractory or failed patients with ring sideroblasts (≥15% RS or ≥5% with SF3B1 mutation); <5% blasts, sEPO ≤ 500 U/L. Primary endpoint: RBC-TI ≥ 8 weeks during weeks 1–24. Compared luspatercept vs. placebo. Led to initial FDA approval (2020) for ESA-refractory, RS+ disease.
8 Inclusion: TD patients unresponsive to ESAs with refractory anemia and ringed sideroblasts. Primary endpoint: ORR at 8 weeks.
9 Inclusion: TD patients relapsed, refractory, or ineligible for ESAs; non-del(5q); no prior lenalidomide or HMA. Primary endpoint: RBC-TI ≥ 8 weeks. Secondary endpoints included RBC-TI ≥ 24 weeks (28% vs. 3%). NCT02598661.
Abbreviations: ER = erythroid response; ESA = erythropoiesis stimulating agent; RBC-TI = red blood cell transfusion independence; IMiDs = immunomodulatory drugs; EFS = event-free survival; ICT = iron chelation therapy; TPO = thrombopoietin; PLT-R = platelet response; HMAs = hypomethylating agents; ORR = overall response rate.
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MDPI and ACS Style

Dhillon, V.; Maciejewski, J.; Balasubramanian, S.K. Correction: Dhillon et al. Molecular Insights and Therapeutic Advances in Low-Risk Myelodysplastic Neoplasms: A Clinical Review. Cancers 2025, 17, 3610. Cancers 2026, 18, 172. https://doi.org/10.3390/cancers18010172

AMA Style

Dhillon V, Maciejewski J, Balasubramanian SK. Correction: Dhillon et al. Molecular Insights and Therapeutic Advances in Low-Risk Myelodysplastic Neoplasms: A Clinical Review. Cancers 2025, 17, 3610. Cancers. 2026; 18(1):172. https://doi.org/10.3390/cancers18010172

Chicago/Turabian Style

Dhillon, Vikram, Jaroslaw Maciejewski, and Suresh Kumar Balasubramanian. 2026. "Correction: Dhillon et al. Molecular Insights and Therapeutic Advances in Low-Risk Myelodysplastic Neoplasms: A Clinical Review. Cancers 2025, 17, 3610" Cancers 18, no. 1: 172. https://doi.org/10.3390/cancers18010172

APA Style

Dhillon, V., Maciejewski, J., & Balasubramanian, S. K. (2026). Correction: Dhillon et al. Molecular Insights and Therapeutic Advances in Low-Risk Myelodysplastic Neoplasms: A Clinical Review. Cancers 2025, 17, 3610. Cancers, 18(1), 172. https://doi.org/10.3390/cancers18010172

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