Table 4.

Summarized data of acute myeloid leukemia (AML) and chronic myelogenous leukemia (CML): disease characteristics and treatment modalities

Disease characteristics	AML	CML	References
Nature of disease	Originates from leukemia stem cells; marked by increased myeloid cells in bone marrow	Slow-progressing expansion of pluripotent bone marrow stem cells	[57]; [84]
Prevalence	Most common acute leukemia in adults; 70% of acute leukemias	Accounts for 15–20% of adult leukemia cases	[58]; [84]
Clinical features	Hematopoietic insufficiency with/without leukocytosis	Leucocytosis, basophilia, splenomegaly	[57]; [8]
Risk factors	Genomic heterogeneity, selective treatment pressure	Smoking, radiation, pesticides, obesity, solvents	[59]; [85]
Age of onset	Higher prevalence in patients ≤ 60 years	Median age 53 years, affects all age groups	[62]; [84]
Cytogenetic markers	t(8;21) translocation, FLT3 mutations	Philadelphia chromosome from BCR–ABL gene fusion	[60, 62, 86]
Initial treatment approaches	Induction chemotherapy, “3 + 7” regimen, allo-HSCT	IFN-α, BCR–ABL TKIs (e.g., imatinib)	[64, 65, 87, 88]
Challenges and resistance	Disease relapse, drug resistance	Resistance via BCR–ABL kinase domain mutations	[65, 89]
Advanced treatment options	Exploration of novel, less toxic strategies	Ponatinib for T315I mutation; exploration of new therapies	[65, 90, 93]
Role of HHT	Effective in enhancing apoptosis, reducing proliferation	Alternative therapy for BCR–ABL TKI-resistant cases	[67, 68, 91]

AML: Acute Myeloid Leukemia; BCR–ABL: Breakpoint Cluster Region–Abelson; CML: Chronic Myelogenous Leukemia; FLT3: Fms-related tyrosine kinase 3; HHT: Homoharringtonine; IFN-α: Interferon Alpha; TKI: Tyrosine Kinase Inhibitor