Acute lymphoblastic leukemia (ALL) is mainly classified into acute T lymphoblastic leukemia (T-ALL) and acute B lymphoblastic leukemia (B-ALL) according to the source of its lymphocytes. Among them, the incidence of adult T-ALL accounts for about 25% of adult ALL, but the degree of malignancy is high, the treatment rate and prognosis are poor. At this stage, there are few targeted drugs for T-ALL, and the commonly used broad-spectrum chemotherapeutic drugs have poor efficacy and many adverse drug reactions (ADR). Understanding the pathogenesis of T-ALL and looking for the pathogenesis for interventional treatment is very important for further developing new T-ALL targeting drugs and improving existing drugs. Dysregulated signaling pathways are the main etiological factors of T-ALL those play crucial roles in promoting tumor initiation, progression, drug design and therapy responses. This is primarily due to the fact that signaling pathways are indispensable for many cellular biological processes, including the tumor growth, migration, invasion, metastasis and others. As a result, small molecule inhibitors targeting the major kinase components of the signaling pathway have received a lot of attention and have been developed and evaluated in preclinical models and clinical trials. Already marketed drugs are also being developed as combination therapies to further improve efficacy and overcome tumor cell resistance. In this review, we aimed to introduce the latest and most classical signaling pathways in the aetiology of T-ALL, and shed light on potential targeting agents for T-ALL therapy.
Keyphrases
- signaling pathway
- drug induced
- adverse drug
- liver failure
- cancer therapy
- acute lymphoblastic leukemia
- small molecule
- clinical trial
- acute myeloid leukemia
- pi k akt
- bone marrow
- respiratory failure
- emergency department
- induced apoptosis
- randomized controlled trial
- drug delivery
- stem cells
- intensive care unit
- oxidative stress
- risk assessment
- cell proliferation
- risk factors
- open label
- tyrosine kinase
- smoking cessation