Table 1.

Schematic view of the main drugs and cellular therapies used to prevent and treat relapse after allo-HSCT.

Therapeutic Strategy		Mechanisms of Action	Examples
Drugs	TKI	Intrinsic antitumor activity by inhibition of abnormal tyrosine kinases and other kinases Boost T-cell cytolytic functions Reduction of PD-1 expression by T-cells Reduction of myeloid-derived suppressor cells Induction of IL-15 production	imatinib midostaurin quizartinib gilteritinib crenolanib sorafenib
	HMA	Regulation of cell differentiation and cell growth Up-regulation of HLA and TAA on neoplastic cells, thus improving cellular immune responses against them Reduction of GvHD risk by up-regulation of FoxP3 and subsequent expansion of regulatory T cells	azacytidine decitabine
	HDACi	Down-regulation of genes involved in production of inflammatory cytokines Expansion of regulatory T cells	panobinostat
	ICP inhibitors	Promotion of T cell responses against tumor cells	nivolumab ipilimumab pidilizumab
Cellular Therapies	DLI	Direct antitumor activity derived from infused donor T cells
	DC infusion	Stimulation of antitumor cellular response by enhancing DC ability to process and present TAA to host T cells	Sipuleucel-T
	NK cell based therapies	Stimulation of antitumor cellular responses by direct infusion of either un-manipulated NK cells or IL-2 pre-treated NK cells Promotion of tumoral lysis by antibody-dependent cellular cytotoxicity by administration of antibodies with a double specificity for TAA expressed on neoplastic cells and CD16 expressed on NK cells Use of anti-KIR antibody to disrupt KIR-HLA interaction and improve NK activation Use of bivalent proteins with a double specificity for both NKG2D activating receptor on NK cells and CD138 on myeloma cells	ULBP2-BB4
	CAR-T cell based therapies	Intrinsic antitumoral activity based on ability to recognize specific TAAs and activate T cell cytolytic program against tumor cells

CAR: chimeric antigen receptor, DC: dendritic cells, DLI: donor lymphocyte infusion, HMA: hypomethylating agents, HDACi: inhibitors of histone deacetylase, ICP: immune-checkpoint, NK: natural killer, TAA: tumor associated antigens, TKI: tyrosine kinase inhibitors.