Acute myeloid leukemia (AML) is a hematological cancer comprising of cancer stem cells (CSCs) that are responsible for the disease progression, drug resistance and post treatment relapses. Advances in genomic technologies have identified AML as a genetically heterogenous disease with dysregulated gene expression networks. Furthermore, observation of intracellular signaling in individual CSCs by mass cytometry has demonstrated the dysregulation of the mitogen associated protein kinase (MAPK) pathways. It has been envisaged that the future treatment for AML would entail upon formulating individualized treatment plans leading to decreased drug related toxicities for patients. However the emerging role of signaling pathways as dynamic molecular switches influencing the cell cycle process, thereby leading to varying stages of cell differentiation, is making community rethink about the current strategies used for the treatment of AML. This commentary will focus on discovering novel biomarkers and identifying new therapeutic targets, to analyze and treat AML, on a platform enabled by systems biology approach.
Keyphrases
- acute myeloid leukemia
- gene expression
- cell cycle
- allogeneic hematopoietic stem cell transplantation
- signaling pathway
- healthcare
- protein kinase
- cancer stem cells
- squamous cell carcinoma
- end stage renal disease
- cell proliferation
- mental health
- ejection fraction
- acute lymphoblastic leukemia
- young adults
- emergency department
- newly diagnosed
- pi k akt
- inflammatory response
- peritoneal dialysis
- toll like receptor
- health insurance
- patient reported outcomes
- lymph node metastasis
- current status
- genome wide
- papillary thyroid