Fertility restoration in patients that survived a hematological cancer during childhood is a core part of their care pathway. Nonetheless, there might be a risk of contamination of the gonads by cancer cells, especially in patients presenting with leukemia and lymphoma. When only a few cancer cells have reached the gonad, they may not be detected by routine histological examination, and therefore more sensitive techniques are required before being confident of the safety of transplanting cryostored testicular and ovarian tissues or cells back to the patient after recovery. Furthermore, if neoplastic cells are identified in the gonadal tissue, methods to eliminate such cells are urgently awaited as the presence of only a few cancer cells may induce disease relapse in these patients. In this review, contamination rates of human gonadal tissue in the case of leukemia or lymphoma as well as decontamination methods applied to both adult and prepubertal testicular and ovarian tissues are presented. Prepubertal gonads will be the main focus as we aim to show how far we have come in establishing safe approaches to fertility restoration. Advances have been made using animal tissue that is usually artificially contaminated by the addition of cancer cell lines to the gonadal cells or tissue, but these techniques need to be improved and still await development in the case of in vivo cancer cell invasion of tissue.

Summary Biliary tract complications (BTCs) still burden liver transplantation (LT). The wide reporting variability highlights the absence of systematic screening. From 2000 to 2009, simultaneous liver biopsy and direct biliary visualization were prospectively performed in 242 recipients at 3 and 6 months (n = 212, 87.6%) or earlier when indicated (n = 30, 12.4%). Median follow‐up was 148 (107–182) months. Seven patients (2.9%) experienced postprocedural morbidity. BTCs were initially diagnosed in 76 (31.4%) patients; 32 (42.1%) had neither clinical nor biological abnormalities. Acute cellular rejection (ACR) was present in 27 (11.2%) patients and in 6 (22.2%) BTC patients. Nine (3.7%) patients with normal initial cholangiography developed BTCs after 60 (30–135) months post‐LT. BTCs directly lead to 7 (2.9%) re‐transplantations and 14 (5.8%) deaths resulting in 18 (7.4%) allograft losses. Bile duct proliferation at 12‐month biopsy proved an independent risk factor for graft loss (P = 0.005). Systematic biliary tract and allograft evaluation allows the incidence and extent of biliary lesions to be documented more precisely and to avoid erroneous treatment of ACR. The combination ‘abnormal biliary tract‐canalicular proliferation’ is an indicator of worse graft outcome. BTCs are responsible for important delayed allograft and patient losses. These results underline the importance of life‐long follow‐up and appropriate timing for re‐transplantation.