scholarly journals Adhesion Deregulation in Acute Myeloid Leukaemia

Cells ◽  
2019 ◽  
Vol 8 (1) ◽  
pp. 66 ◽  
Author(s):  
Alicja Gruszka ◽  
Debora Valli ◽  
Cecilia Restelli ◽  
Myriam Alcalay
Keyword(s):  
Cell Adhesion ◽  
Acute Myeloid Leukaemia ◽  
Myeloid Leukaemia ◽  
Epithelial To Mesenchymal Transition ◽  
Chemotherapeutic Agents ◽  
Prognostic Impact ◽  
Mesenchymal Transition ◽  
Haematopoietic Cells ◽  
Variable Extent ◽  
Acute Myeloid

Cell adhesion is a process through which cells interact with and attach to neighboring cells or matrix using specialized surface cell adhesion molecules (AMs). Adhesion plays an important role in normal haematopoiesis and in acute myeloid leukaemia (AML). AML blasts express many of the AMs identified on normal haematopoietic precursors. Differential expression of AMs between normal haematopoietic cells and leukaemic blasts has been documented to a variable extent, likely reflecting the heterogeneity of the disease. AMs govern a variety of processes within the bone marrow (BM), such as migration, homing, and quiescence. AML blasts home to the BM, as the AM-mediated interaction with the niche protects them from chemotherapeutic agents. On the contrary, they detach from the niches and move from the BM into the peripheral blood to colonize other sites, i.e., the spleen and liver, possibly in a process that is reminiscent of epithelial-to-mesenchymal-transition in metastatic solid cancers. The expression of AMs has a prognostic impact and there are ongoing efforts to therapeutically target adhesion in the fight against leukaemia.

scholarly journals Normal myeloid progenitor cell subset-associated gene signatures for acute myeloid leukaemia subtyping with prognostic impact

PLoS ONE ◽  
2020 ◽  
Vol 15 (4) ◽  
pp. e0229593 ◽  
Author(s):  
Anna A. Schönherz ◽  
Julie Støve Bødker ◽  
Alexander Schmitz ◽  
Rasmus Froberg Brøndum ◽  
Lasse Hjort Jakobsen ◽  
...  
Keyword(s):  
Acute Myeloid Leukaemia ◽  
Myeloid Leukaemia ◽  
Progenitor Cell ◽  
Cell Subset ◽  
Prognostic Impact ◽  
Gene Signatures ◽  
Myeloid Progenitor ◽  
Myeloid Progenitor Cell ◽  
Acute Myeloid

scholarly journals Complex and monosomal karyotype are distinct cytogenetic entities with an adverse prognostic impact in paediatric acute myeloid leukaemia. A NOPHO-DBH-AML study

2018 ◽  
Vol 183 (4) ◽  
pp. 618-628
Author(s):  
Ninna Bager ◽  
Kristian L. Juul-Dam ◽  
Julie D. Sandahl ◽  
Jonas Abrahamsson ◽  
Berna Beverloo ◽  
...  
Keyword(s):  
Acute Myeloid Leukaemia ◽  
Myeloid Leukaemia ◽  
Prognostic Impact ◽  
Monosomal Karyotype ◽  
Acute Myeloid

scholarly journals The Clinical Features and Prognosis of NPM1/FLT3-ITD/DNMT3A Triple-mutated Acute Myeloid Leukaemia

2021 ◽  
Author(s):  
Xingchun Luo ◽  
Bei Liu ◽  
Haiping Liang ◽  
Long Zhao ◽  
Yuancheng Guo ◽  
...  
Keyword(s):  
Acute Myeloid Leukaemia ◽  
Myeloid Leukaemia ◽  
Bioinformatics Analysis ◽  
De Novo ◽  
Prognostic Significance ◽  
Gene Expression Omnibus ◽  
Prognostic Impact ◽  
Newly Diagnosed ◽  
De Novo Aml ◽  
Acute Myeloid

Abstract Purpose: Previous studies have shown that patients with NPM1+/FLT3-ITD+ acute myeloid leukaemia (AML) have a poor prognosis, especially those with a high FLT3-ITD allelic ratio. However, no studies have confirmed a clear prognostic impact of DNMT3A on NPM1+/FLT3-ITD+ AML patients. Methods: Our study included a total of 165 patients with newly diagnosed non-acute promyelocytic leukaemia (non-APL) AML at The First Hospital of Lanzhou University between January 2018 and June 2021. Further bioinformatics analysis was performed using the Gene Expression Omnibus (GEO) database. Results: We retrospectively studied 165 patients newly diagnosed non-APL AML and identified 11 (6.7%) patients with NPM1/FLT3-ITD/DNMT3A triple mutations. The patients with triple-mutated AML had advanced age, higher white blood cell (WBC) counts, de novo AML, normal karyotypes, and poor survival, and all were in the M4/M5 French-American-British (FAB) category. Notably, half of the patients with triple-mutated AML had mature monocyte characteristics that were difficult to distinguish from chronic myelomonocytic leukaemia (CMML). We validated the prognosis of patients with triple-mutated AML by further bioinformatics analysis and found that the GNG4 gene, one of the hub genes, was related to triple-mutated AML patients' survival. Conclusion: Our data demonstrate that DNMT3A gene mutation has adverse prognostic significance in NPM1+FLT3-ITD+comutation AML patients.

scholarly journals The prognostic impact of CD7 expression of leukaemic blasts in de novo intermediate cytogenetic risk acute myeloid leukaemia

Pathology ◽  
2016 ◽  
Vol 48 ◽  
pp. S99
Author(s):  
Murali Kesavan ◽  
Hun Chuah ◽  
S.Aqif Mukhtar ◽  
Ashier Leigh Parsons ◽  
Kerryn Stoner ◽  
...  
Keyword(s):  
Acute Myeloid Leukaemia ◽  
Myeloid Leukaemia ◽  
De Novo ◽  
Prognostic Impact ◽  
Acute Myeloid

scholarly journals The eukaryotic Initiating Factor 4E protein is overexpressed, but its level has no prognostic impact in acute myeloid leukaemia

2011 ◽  
Vol 156 (4) ◽  
pp. 547-550 ◽  
Author(s):  
Alexa S. Green ◽  
Sophie Grabar ◽  
Micheline Tulliez ◽  
Sophie Park ◽  
Chadi Al-Nawakil ◽  
...  
Keyword(s):  
Acute Myeloid Leukaemia ◽  
Myeloid Leukaemia ◽  
Prognostic Impact ◽  
Acute Myeloid

scholarly journals Targeting the FLT3 Mutation in Acute Myeloid Leukaemia

2017 ◽  
Vol 13 (02) ◽  
pp. 139 ◽  
Author(s):  
Sabine Kayser ◽  
Richard F Schlenk ◽  
◽  
◽  
Keyword(s):  
Acute Myeloid Leukaemia ◽  
Tyrosine Kinase ◽  
Myeloid Leukaemia ◽  
Kinase Inhibitors ◽  
Point Mutations ◽  
Kinase Domain ◽  
Tyrosine Kinase Domain ◽  
Prognostic Impact ◽  
Newly Diagnosed ◽  
Acute Myeloid

Acute myeloid leukaemia (AML) exhibiting an internal tandem duplication of the FLT3 gene (FLT3-ITD) is an aggressive haematologic malignancy with a poor prognosis due to a high relapse rate and very limited options after relapse with conventional salvage regimens, whereas the prognostic impact of point mutations in the tyrosine kinase domain of the FLT3 gene (FLT3-TKD) are less clear. A number of tyrosine kinase inhibitors (TKIs) have been developed that inhibit the constitutively activated kinase activity caused by the FLT3 mutation, thus interrupting signalling pathways. Early clinical trials of these agents as monotherapy failed to elicit enduring complete responses, leading to clinical testing of FLT3 TKI in combination with conventional chemotherapy. Midostaurin has demonstrated improved survival in combination with standard intensive chemotherapy as compared to standard chemotherapy alone in younger adult patients with newly diagnosed FLT3-mutated AML and is the first and currently the only approved FLT3 TKI. Newer, more selective compounds, such as gilteritinib and crenolanib, have also demonstrated significant potency and specificity. Several combination trials are ongoing or planned in both relapsed and newly diagnosed AML patients with activating FLT3 mutations.

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