chronic parenchymatous and cholestatic (auto- immune) liver diseases (75%), benign and malignant hepatobiliary tumours (10 to 20%), acute liver failure (10%), and inherited liver-based metabolic diseases (5%).(Table 64.2). Recent signs of progress in hepatology, oncology, molecular biol­ogy, and societal behaviour drastically changed these indica­tions’ respective weights [11]. The original concept of LT as the treatment of unresectable liver cancers was abandoned because of the very early and high recurrence rates and the growing mortality on the waiting list of patients presenting end-stage failure due to benign, chronic liver diseases. In 1996, the Milan Criteria (MC) became the “gold standard” to allocate allografts to HCC patients because markedly improving ve-year disease-free survival rates reaching 85% [12]. These criteria reduced these tumour patients’ access to the waiting list from 50% to 10%. Recent studies, many based on LDLT experiences, revealed that up to 60% of HCC patients are unjustiedly excluded from a potential curative LT when adhering to these restrictive MC [13]. Unexpected good results in some recipients outlying the MC started a movement to again broaden the inclusion criteria for LT in both Western and Eastern hemispheres without severely compromising oncologic outcome [14–16]. These exten­sions were merely driven by the application of sound onco­logic principles combining “dynamic” tumour morphology (number and diameter with the evaluation of radiological response or downstaging to locoregional therapies based on m-RECIST criteria) [17] and biology (evolution of alpha­fetoprotein, descarboxy-prothrombin, neutrophil- or platelet­to- lymphocyte ratios) [18]. The use of reduced IS load, steroid-free and m-Tor inhibitor-based IS, will play an important role in the ongoingre-development of oncologic transplantation [19, 20]. The fact that unresectable hilar and intrahepatic cholangiocellular cancer (CCC) are nowadays also considered for LT if strict criteria and neoadjuvant radio-chemotherapy (Mayo Clinic protocol) are applied in line with this evolution [21]. Conversely, LT for mixed HCC­CCC,intrahepatic CCC or sarcomatoid HCC remains very questionnableseen their high recurrence rate.

leads to haemolytic graft versus host syndrome. This anti­genic stimulus should be reduced by switching the blood product use to the blood group of the graft. ABO-incompatible LT evidently can only be done after specic recipient prepa­ration, including plasmapheresis to reduce the natural antibody titer and B-cell therapy using anti-CD20 antibodies to neutralize antibody formation [64].