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Eugene Khandros

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Articles 34
Citations 818
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Recent Articles
11.
Braun T, Kuoch M, Khandros E, Li H
STAR Protoc . 2022 Jan; 3(1):101070. PMID: 35024628
Early erythroid progenitors are transit-amplifying cells with high proliferative capacity committed to undergoing red cell differentiation. CD71/CD24 progenitors are less mature and have greater proliferative capacity than CD71/CD24. We present...
12.
Cao Z, Budinich K, Huang H, Ren D, Lu B, Zhang Z, et al.
Mol Cell . 2021 Aug; 81(17):3604-3622.e10. PMID: 34358447
The transformed state in acute leukemia requires gene regulatory programs involving transcription factors and chromatin modulators. Here, we uncover an IRF8-MEF2D transcriptional circuit as an acute myeloid leukemia (AML)-biased dependency....
13.
Khandros E, Blobel G
Curr Opin Hematol . 2021 Feb; 28(3):164-170. PMID: 33631783
Purpose Of Review: Small amounts of fetal hemoglobin can be expressed in a subset of adult red blood cells called F-cells. This review examines the potential mechanisms and clinical implications...
14.
Peslak S, Khandros E, Huang P, Lan X, Geronimo C, Grevet J, et al.
Blood Adv . 2020 Sep; 4(18):4560-4572. PMID: 32956454
Increasing fetal hemoglobin (HbF) provides clinical benefit in patients with sickle cell disease (SCD). We recently identified heme-regulated inhibitor (HRI, EIF2AK1), as a novel HbF regulator. Because HRI is an...
15.
Huang P, Peslak S, Lan X, Khandros E, Yano J, Sharma M, et al.
Blood . 2020 Apr; 135(24):2121-2132. PMID: 32299090
Reactivation of fetal hemoglobin remains a critical goal in the treatment of patients with sickle cell disease and β-thalassemia. Previously, we discovered that silencing of the fetal γ-globin gene requires...
16.
Khandros E, Huang P, Peslak S, Sharma M, Abdulmalik O, Giardine B, et al.
Blood . 2020 Apr; 135(22):1957-1968. PMID: 32268371
Reversing the developmental switch from fetal hemoglobin (HbF, α2γ2) to adult hemoglobin (HbA, α2β2) is an important therapeutic approach in sickle cell disease (SCD) and β-thalassemia. In healthy individuals, SCD...
17.
Chonat S, Risinger M, Sakthivel H, Niss O, Rothman J, Hsieh L, et al.
Front Physiol . 2019 Nov; 10:1331. PMID: 31736770
[This corrects the article DOI: 10.3389/fphys.2019.00815.].
18.
Lechauve C, Keith J, Khandros E, Fowler S, Mayberry K, Freiwan A, et al.
Sci Transl Med . 2019 Aug; 11(506). PMID: 31434755
In β-thalassemia, accumulated free α-globin forms intracellular precipitates that impair erythroid cell maturation and viability. Protein quality control systems mitigate β-thalassemia pathophysiology by degrading toxic free α-globin, although the associated...
19.
Chonat S, Risinger M, Sakthivel H, Niss O, Rothman J, Hsieh L, et al.
Front Physiol . 2019 Jul; 10:815. PMID: 31333484
Hereditary spherocytosis (HS) is the most common red blood cell (RBC) membrane disorder causing hereditary hemolytic anemia. Patients with HS have defects in the genes coding for ankyrin (), band...
20.
Lan X, Khandros E, Huang P, Peslak S, Bhardwaj S, Grevet J, et al.
Blood Adv . 2019 May; 3(10):1586-1597. PMID: 31126914
Reactivation of fetal hemoglobin (HbF) production benefits patients with sickle cell disease and β-thalassemia. To identify new HbF regulators that might be amenable to pharmacologic control, we screened a protein...