Treatment of Acute Myeloid Leukemia in Adolescent and Young Adult Patients

Seval, Güldane Cengiz; Özcan, Muhıt

doi:10.3390/jcm4030441

Cited by 16 publications

(22 citation statements)

References 69 publications

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“…1 It is characterized by the rapid growth of abnormal cells in the bone marrow and blood, interfering with normal blood cells. 2,3 AML a highly heterogeneous disease, symptoms of which include easy bruising and bleeding, shortness of breath and easy feeling tired. 4 As an acute leukaemia, AML always progresses speedily and patients usually die within weeks or months if left untreated.…”

Section: Introductionmentioning

confidence: 99%

LncRNA LINC00899 promotes progression of acute myeloid leukaemia by modulating miR‐744‐3p/YY1 signalling

Dong

Guan

2020

Cell Biochemistry & Function

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Long non‐coding RNA (lncRNA) LINC00899 is one kind cytoplasmic lncRNA, however, there is rarely little information about its function in physiological process. Here, we demonstrated that lncRNA LINC00899 was upregulated in acute myeloid leukaemia (AML) cells and was quite correlated with poor prognosis of AML patients. High expression of LINC00899 in AML cells could promote cell proliferation and inhibit cell apoptosis, and facilitate the progression of AML consequently both in vitro and in vivo. Besides, LINC00899 acted as a molecular sponge of miR‐744‐3p. Furthermore, we characterized YY1 as the direct target of miR‐744‐3p, and LINC00899/miR‐744‐3p interaction modulated YY1 expression in AML cells. Finally, we verified LINC00899 modulated AML cell proliferation and apoptosis via regulating YY1. Our study revealed novel mechanism about how did lncRNA LINC00899 execute function in AML and thus provided potential therapeutic interventions for AML.Significance of the study LncRNA LINC00899 is upregulated in AML cells and is correlated with poor prognosis of AML patients. LncRNA LINC00899 mediates cell proliferation and apoptosis of acute myeloid leukaemia cells. Knockdown of LINC00899 inhibited the growth of xenograft glioma tumour in vivo. LINC00899 acts as a molecular sponge of miR‐744‐3p. YY1 is the downstream target of LINC00899/miR‐744‐3p signalling.

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Section: Introductionmentioning

confidence: 99%

LncRNA LINC00899 promotes progression of acute myeloid leukaemia by modulating miR‐744‐3p/YY1 signalling

Dong

Guan

2020

Cell Biochemistry & Function

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“…Despite the availability of multiple novel agents, prognosis of patients with relapsed AML remains poor [119,125]. The personalized approach is promising but will bring about new challenges for treating physicians [125].…”

Section: Treatment Of Relapsed / Refractory Amlmentioning

confidence: 99%

“…Although increasing age is associated with poorer survival, higher comorbidities and poor performance status have more negative impact than age per se [145]. The increasing number and experience with alternative donors will facilitate allogeneic HSCT and make it a more achievable therapeutic option for elderly AML patients [119,145]. Also, the advent of RIC regimens made allogeneic HSCT an available treatment option with curative intent for older AML patients [114,146].…”

Section: Allogeneic Hsct For Amlmentioning

confidence: 99%

“…RICallogeneic HSCT has resulted in better survival among older patients with AML than autologous HSCT or conventional chemotherapy [146]. Despite the acceptable outcomes of alternative donors and the reports of equivalent outcomes of MRD and MUD allografts, grafts obtained from HLA-identical siblings continue to be associated with the most favorable outcomes after allogeneic HSCT [119,146].…”

Section: Allogeneic Hsct For Amlmentioning

confidence: 99%

“…[119,123],(2) chemotherapy and donor lymphocyte infusion (DLI)[123,124],(3) myeloablative allogeneic HSCT, RIC-allogeneic HSCT and second allogeneic HSCT[119,122,123],(4)novel and targeted therapies including: (a) immunomodulatory agents such as lenalidomide, (b) aminopeptidase inhibitors such as tosedostat, (c) purine analogs such as clofarabine, (d) mTOR inhibitors such as sirolimus and everolimus, (e) hypomethylating agents such as azacytidine and decitabine, (f) histone deacetylase (HDAC) inhibitors such as vorinostat, (g) farnesyl transferase inhibitors such as tipifarnib, (h) FLT3 inhibitors such as quizartinib, sorafenib and lestaurtinib, (i) CXCR4 antagonists such as plerixafor, (j) combination of azacytidine and sorafenib, and (k) monoclonal antibodies such as GO, lintuzumab, avastin and bevacizumab[122,123,125,126], (5) appropriate clinical trials, and (6) palliative care and supportive measures[122].…”

mentioning

confidence: 99%

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Update on Non-M3 Acute Myeloid Leukemia — Etiology, Classification, Risk Stratification, Emergencies, Complications, Disease in Special Circumstances and Current and Future Therapeutics

Al-Anazi¹

2015

Leukemias - Updates and New Insights

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Acute myeloid leukemia (AML) is a heterogeneous condition characterized by clonal proliferation of myeloid precursors and accumulation of leukemic blasts in the bone marrow (BM), ultimately resulting in failure of the BM. It accounts for approximately 80% of cases of acute leukemia in adults. AML has several life-threatening complications. After establishing the diagnosis of AML, classifying the disease into the appropriate subtype, stratifying the risk group and determining fitness of the patient for chemotherapy, induction treatment is usually commenced. For elderly individuals and those unfit for chemotherapy, several alternative therapeutic options are available. After achieving complete remission of the disease, the patient will either receive consolidation therapy or will be subjected to hematopoietic stem cell transplantation (HSCT). Autologous and allogeneic forms of HSCT have their own indications, inclusion as well as exclusion criteria. The recent advancements in the diagnostics and therapeutics have facilitated the introduction of personalized therapy in patients with AML. There are several targeted therapies for AML and their clinical use is increasing with time. Evaluation of minimal residual disease and determination of drug resistance are vital tools to improve the outcome of AML therapy.

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Risk factors for length of stay and charge per day differ between older and younger hospitalized patients withAML

et al. 2018

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Acute myeloid leukemia (AML) is associated with frequent hospitalizations. We evaluated factors associated with length of stay (LOS) and charge per day (CPD) for admissions in older (≥60 years) and younger patients (<60 years). We identified patients with ICD‐9‐CM codes for AML or myeloid sarcoma in the 2012 HCUP‐NIS. In separate models based on age, we examined patient (sex, race, income, insurance payer, chronic conditions, chemotherapy administration, death) and hospital (type, geography) characteristics. Multivariable negative binomial regression estimated factor effects on LOS and CPD using rate ratios, with HCUP‐NIS weights. In 43,820 discharges, LOS was longer in patients <60 than ≥60 (6.8 vs. 5.4 days). For patients <60, longer LOS was seen with more chronic conditions (RR = 1.10), Black race (RR = 1.16), chemotherapy (RR = 2.27), and geography; shorter LOS was associated with older age (RR = 0.93), Medicare (RR = 0.83), and hospital type. For patients ≥60, longer LOS associated with chronic conditions (RR = 1.07) and Asian race (RR = 1.33). Shorter LOS associated with older age (RR = 0.86), higher income (RR = 0.93), and hospital type. For patients <60, higher CPD associated with chronic conditions (RR = 1.05), death (RR = 1.93), and geography; lower CPD associated with increasing age (RR = 0.96), Medicaid (RR = 0.93), and rural hospitals (RR = 0.65). For patients ≥60, higher CPD associated with Medicare (RR = 1.05), more chronic conditions (RR = 1.02), younger age (RR = 1.1), west geography (RR = 1.37), death (RR = 1.45), and Hispanic race (RR = 1.15). We identify predictors for increased healthcare utilization in hospitalized patients with AML, which differ within age groups. Future efforts are needed to link utilization outcomes with clinical treatments and response.

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Treatment of Acute Myeloid Leukemia in Adolescent and Young Adult Patients

Cited by 16 publications

References 69 publications

LncRNA LINC00899 promotes progression of acute myeloid leukaemia by modulating miR‐744‐3p/YY1 signalling

LncRNA LINC00899 promotes progression of acute myeloid leukaemia by modulating miR‐744‐3p/YY1 signalling

Update on Non-M3 Acute Myeloid Leukemia — Etiology, Classification, Risk Stratification, Emergencies, Complications, Disease in Special Circumstances and Current and Future Therapeutics

Risk factors for length of stay and charge per day differ between older and younger hospitalized patients withAML

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