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The term leukaemia is derived from the Greek words leukos, meaning white, and haima, meaning blood. It is currently used to classify a broad spectrum of haematopoietic malignancies according to morphology, immunophenotype, cytogenetic and molecular abnormalities, and clinical features—literally referring to the excess of white blood cells seen in patients with these diseases[1]. Clinically, these diseases fall into four broad categories: myeloid or lymphoid lineage, and acute or chronic, which help to dictate treatment. The latter refers to the rapidity of clinical onset and disease progression. Although many specific diagnoses exist, the most commonly studied leukemias are acute myeloid leukaemia (AML), acute lymphoblastic leukaemia/lymphoma (ALL), chronic lymphocytic leukaemia/small lymphocytic lymphoma (CLL/SLL) and chronic myeloid leukaemia (CML)[2].

Acute myeloid leukaemia (AML) is the most aggressive adult leukaemia, characterised by clonal differentiation arrest of progenitor or precursor haematopoietic cells. Chromosomal aberrations, gene mutations and epigenetic alterations drive AML pathogenesis while concurrently providing vulnerabilities to specifically target leukemic cells. Other molecules aberrantly active or over-expressed in leukaemic stem cells may also be leveraged for therapeutic benefit (Figure 1)[3].

Acute lymphoblastic leukaemia (ALL) is a severe blood cancer arising from B-cell (B-ALL) or T-cell (T-ALL) lymphoid precursors. It represents a heterogeneous malignancy with diverse clinical and molecular features. Wnt signalling is crucial for lymphocyte-progenitor survival and proliferation; abnormal regulation of this pathway may contribute to lymphoid leukaemia. Aberrant activation of β-catenin, a key Wnt component, is implicated in various haematological malignancies (Figure 2)[4-7].

Chronic myeloid leukaemia (CML) is characterised by clonal proliferation of myeloid-lineage cells in the bone marrow. It arises from the t(9;22)(q34;q11) reciprocal translocation forming the Philadelphia chromosome. This fuses the BCR gene with ABL1, generating the constitutively active BCR::ABL1 tyrosine kinase that promotes proliferation and inhibits apoptosis (Figure 3)[8,9].

Chronic lymphocytic leukaemia (CLL) is a B-cell malignancy whose progression depends on the lymph-node and bone-marrow microenvironment. CLL cells interact with extracellular-matrix fibres and with specialised hematopoietic or mesenchymal-derived cells (BM MSCs, FDCs, NLCs, T cells, ECs). These micro-environmental components establish uni- or bi-directional interactions promoting CLL migration, immune suppression and accessory-cell recruitment that sustain survival and proliferation (Figure 4)[11].

Freya Freya is a technical support expert of enkilife, familiar with immunology and cell biology, and is committed to providing customers with high-quality product portfolio and technical support to help customers efficiently complete research.

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