highly radio-sensitive malignancies. to limit radiation exposure, murine antibodies were chosen, as their high immunogenicity promotes rapid tumor clearance. tositumomab is an example used for non-hodgkin's lymphoma. antibody-directed enzyme prodrug therapy antibody-directed enzyme prodrug therapy (adept) involves the application of cancer-associated monoclonal antibodies that are linked to a drug-activating enzyme. systemic administration of a non-toxic agent results in the antibody's conversion to a toxic drug, resulting in a cytotoxic effect that can be targeted at malignant cells. the clinical success of adept treatments is limited. antibody-drug conjugates antibody-drug conjugates (adcs) are antibodies linked to one or more drug molecules. typically when the adc meets the target cell (e.g. a cancerous cell) the drug is released to kill it. many adcs are in clinical development. as of 2016 a few have been approved. immunoliposome therapy immunoliposomes are antibody-conjugated liposomes. liposomes can carry drugs or therapeutic nucleotides and when conjugated with monoclonal antibodies, may be directed against malignant cells. immunoliposomes have been successfully used in vivo to convey tumour-suppressing genes into tumours, using an antibody fragment against the human transferrin receptor. tissue-specific gene delivery using immunoliposomes has been achieved in brain and breast cancer tissue. checkpoint therapy checkpoint therapy uses antibodies and other techniques to circumvent the defenses that tumors use to suppress the immune system. each defense is known as a checkpoint. compound therapies combine antibodies to suppress multiple defensive layers. known checkpoints include ctla-4 targeted by ipilimumab, pd-1 targeted by nivolumab and pembrolizumab and the tumor microenvironment. the tumor microenvironment (tme) features prevents the recruitment of t cells to the tumor. ways include chemokine ccl2 nitration, which traps t cells in the stroma. tumor vasculature helps tumors preferentially recruit other immune cells over t cells, in part through endothelial cell (ec)–specific expression of fasl, etbr, and b7h3. myelomonocytic and tumor cells can up-regulate expression of pd-l1, partly driven by hypoxic conditions and cytokine production, such as ifnβ. aberrant metabolite production in the tme, such as the pathway regulation by ido, can affect t cell functions directly and indirectly via cells such as treg cells. cd8 cells can be suppressed by b cells regulation of tam phenotypes. cancer-associated fibroblasts (cafs) have multiple tme functions, in part through extracellular matrix (ecm)–mediated t cell trapping and cxcl12-regulated t cell exclusion. fda-approved therapeutic antibodies for a more comprehensive list, see list of therapeutic monoclonal antibodies.