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1.
Oncol Rep ; 49(2)2023 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-36524357

RESUMEN

Following the publication of the above article, the authors have realized that an error was made during the compilation of Fig. 9, as it appears on p. 10; essentially, the ß-actin bands featured in Fig. 9A were inadvertently copied across to Fig. 9B. The revised version of Fig. 9, now showing the correct ß-actin bands for Fig. 9B, is shown on the next page. All the authors approve of the publication of this corrigendum, and the authors are grateful to the Editor of Oncology Reports for granting them the opportunity to publish this. The authors regret their oversight in allowing this error to be included in the published paper, and apologize to the readership for any inconvenience caused. [Oncology Reports 47: 18, 2022; DOI: 10.3892/or.2021.8229].

2.
Front Oncol ; 12: 1021786, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-36505803

RESUMEN

Donor cell-derived leukemia (DCL) is a special type of relapse after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Patients with DCL generally have a poor prognosis due to resistance to conventional chemotherapy. Here, we report a case of donor cell-derived acute lymphoblastic leukemia after umbilical cord blood transplantation. The patient didn't respond to induction chemotherapy. She then received anti-CD19 CAR-T cell therapy and achieved MRD-negative complete remission (CR). However, MRD levels rose from negative to 0.05% at 5 months after CAR-T cell therapy. Higher MRD levels were significantly associated with an increased risk of leukemia recurrence. Afterward, preemptive interferon-α treatment was administrated to prevent disease recurrence. To date, the patient has maintained MRD-negative CR for 41 months. Our results suggested that anti-CD19 CAR-T cells followed by interferon-α therapy are effective in treating donor cell-derived acute lymphoblastic leukemia. This report provides a novel strategy for the treatment of DCL.

3.
Front Oncol ; 12: 879471, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-35494006

RESUMEN

Background: T-cell immunoglobulin and mucin domain-containing molecule 3 (TIM-3) expresses on leukemic stem and progenitor populations of non-M3 acute myeloid leukemia (AML) as well as T lymphocytes. TIM-3 is thought to be involved in the self-renewal of leukemic stem cells and the immune escape of AML cells, however its correlation with AML prognosis is still controversial and worthy of further investigation. Methods: we simultaneously assessed TIM-3 expression levels of leukemic blasts and T lymphocytes in the bone marrow of de novo AML patients using flow cytometry. The correlations of TIM-3 expression between leukemic blasts and T lymphocytes and the correlations of TIM-3 expression with various patient parameters were analyzed. In addition, the Cancer Genome Atlas (TCGA) data of AML patients were acquired and analyzed to verify the results. Results: TIM-3 expression of CD34+ leukemic blasts (R2 = 0.95, p<0.0001) and CD34+CD38- leukemic stem cells (R2 = 0.75, p<0.0001) were significantly and positively correlated with that of the whole population of leukemic blasts. In addition, TIM-3 expression level of leukemic blasts correlated significantly and positively with that of CD8+ (R2 = 0.44, p<0.0001) and CD4+ (R2 = 0.16, p=0.0181) lymphocytes, and higher TIM-3 expression of leukemic blasts was significantly associated with a greater proportion of peripheral CD8+ T lymphocytes (R2 = 0.24, p=0.0092), indicating that TIM-3 on leukemic blasts might alter adaptive immunity of AML patients. Regarding clinical data, the presence of core binding factor (CBF) translocations was significantly correlated with higher TIM-3 expression of leukemic blasts (CBF versus non-CBF, median 22.78% versus 1.28%, p=0.0012), while TIM-3 expression levels of leukemic blasts were not significantly associated with the remission status after induction chemotherapy (p=0.9799), overall survival (p=0.4201) or event-free survival (p=0.9873). Similar to our results, TCGA data showed that patients with CBF translocations had significantly higher mRNA expression level of HAVCR2 (the gene encoding TIM-3) (median, 9.81 versus 8.69, p<0.0001), and as all patients in the cohort were divided into two groups based on the median HAVCR2 expression level, 5-year overall survivals were not significantly different (low versus high, 24.95% versus 24.54%, p=0.6660). Conclusion: TIM-3 expression level on AML blasts correlates with presence of CBF translocations rather than clinical outcomes.

4.
Oncol Rep ; 47(1)2022 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-34792179

RESUMEN

KIF2A has been shown to be involved in the regulation of AML pathology, however, the mechanistic role of KIF2A in AML has not been fully identified. The present study aimed to identify the underlying mechanism of KIF2A regulation of AML cell function and chemosensitivity. A total of 58 patients with AML and 30 healthy subjects were enrolled for clinical analysis. AML cells (KG­1 and Kasumi­1) were transfected with KIF2A or control small interfering (si)RNA. PI3K/AKT pathway activator (740 Y­P) and RhoA overexpression plasmid were added to rescue the effect of KIF2A siRNA. Cell proliferation, apoptosis, chemosensitivity to ADR and AraC, expression levels of mRNA/proteins associated with PI3K/AKT and RhoA/ROCK pathways were measured by Cell Counting Kit­8, flow cytometry, reverse transcription­quantitative PCR and western blotting. KIF2A was overexpressed, and correlated with higher levels of bone marrow blast, poor risk classification, lower treatment response and unfavorable survival profile in patients with AML. KIF2A siRNA inhibited proliferation but enhanced apoptosis and chemosensitivity to ADR and AraC in KG­1 and Kasumi­1 cells, which also inactivated PI3K/AKT and RhoA/ROCK pathways. Subsequent rescue experiments showed that 740 Y­P and RhoA overexpression plasmid promoted cell survival and decreased chemosensitivity, which reversed the effect of KIF2A siRNA in KG­1 and Kasumi­1 cells. KIF2A was correlated with worse clinical features and survival in patients with AML; its knockdown promoted apoptosis and chemosensitivity by inactivating PI3K/AKT and RhoA/ROCK signaling pathways in AML cells. These data suggested KIF2A may be a potential prognostic marker and treatment target for AML management.


Asunto(s)
Cinesinas/metabolismo , Leucemia Mieloide Aguda/metabolismo , Fosfatidilinositol 3-Quinasas/metabolismo , Proteínas Proto-Oncogénicas c-akt/metabolismo , Quinasas Asociadas a rho/metabolismo , Proteína de Unión al GTP rhoA/metabolismo , Adulto , Anciano , Línea Celular Tumoral , Femenino , Humanos , Masculino , Persona de Mediana Edad
5.
Oncol Rep ; 41(1): 415-426, 2019 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-30365089

RESUMEN

The Snail family transcriptional repressor 1 gene (Snail1) was screened in multiple myeloma cells (MMCs) from bortezomib-resistant MM patients and was found to be significantly associated with the development of drug-resistance mechanisms. In the present study, we first confirmed that the protein expression of Snail1 in bortezomib-resistant MMCs was significantly higher than that in MMCs without bortezomib resistance. The mechanistic studies confirmed that the enhancement of Snail1 expression in bortezomib-resistant MMCs directly upregulated transcription of the intracellular MDR1 gene to immediately develop multiple drug resistance mechanisms and inhibited P53 protein expression through the Snail1/hsa-miRNA-22-3p/P53 pathway to inhibit tumor cell apoptosis. By upregulating MDR1 and downregulating P53, Snail1 induced the drug resistance of MMCs to bortezomib, while Snail1 gene silencing effectively improved the drug sensitivity of MMCs to bortezomib chemotherapy. The present study further elucidated the drug resistance mechanisms of MMCs and provides evidence for increased clinical efficacy of bortezomib in MM patients.


Asunto(s)
Bortezomib/uso terapéutico , Resistencia a Antineoplásicos/genética , Mieloma Múltiple/tratamiento farmacológico , Mieloma Múltiple/genética , Factores de Transcripción de la Familia Snail/genética , Adulto , Anciano , Apoptosis/genética , Línea Celular Tumoral , Resistencia a Múltiples Medicamentos/genética , Femenino , Humanos , Masculino , MicroARNs/genética , Persona de Mediana Edad , Transducción de Señal/genética , Activación Transcripcional/genética , Proteína p53 Supresora de Tumor/genética , Regulación hacia Arriba/genética
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