Table 2. The drug sensitizing effects of EPA and DHA in combination with conventional chemotherapeutic drugs used for the treatment of haematological malignancies.

DHA	EPA	Type of malignancy/model	Chemotherapy drug	Effect and suggested mechanism	Reference
*	*	Multiple myeloma cell lines	Bortezomib (Valcane)	NM	[20]
*		arsenic trioxide–resistant leukemic HL-60 cells (as well as solid tumor cell lines)	As2O3 [A ROS inducing chemotherapy agent]	↑Bax expression ↑Caspase 3 activation ↑ROS production and lipid peroxidation [Selective effect]	[13, 14]
*		HTLV-I–immortalized and –transformed T cells (a model of ATL)	As2O3	↑Cell death, ↓Proliferation, ↑ROS production ↓ mitochondrial membrane potential Down regulation of AP-1 and AKT expression [Selective; only marginal effect on healthy PBMCS]	[24]
*		BDF1 mice bearing L1210 leukemic cells	AraC	↑Survival time in ↓Drug-toxicity induced death	[51]
	*	HL-60 myeloid leukemia cell line	TPA	↑ROS production and NBT reduction ↑Differentiation of myeloid leukemia cells	[25]
*		Bcr-Abl expressing HL-60 cells	Imatinib	↓Viability, ↑Apoptosis, ↓Membrane integrity, ↑DNA fragmentation	[65]
*	*	B-CLL-derived cell lines EHEB and MEC-2 B-PLL-derived cell line JVM-2	Doxorubicin	↓Viability, ↑Apoptosis ↑ROS production ↑Lipid peroxidation	[85]
			Fludarabine
			Vincristine
*		T27A (murine leukemia cell line)	methotrexate	Growth inhibition via synergistic effect

As₂O₃, Arsenic trioxide; ATL, Acute T-cell Leukemia; AraC, Arabinosylcytosine; TPA, 12-O-tetradecanoylphorbol-13-acetate; NM, not mentioned