The cBio Cancer Genomics Portal (http://cbioportal.org) is an open-access resource for interactive exploration of multidimensional cancer genomics data sets, currently providing access to data from more than 5,000 tumor samples from 20 cancer studies. The cBio Cancer Genomics Portal significantly lowers the barriers between complex genomic data and cancer researchers who want rapid, intuitive, and high-quality access to molecular profiles and clinical attributes from large-scale cancer genomics projects and empowers researchers to translate these rich data sets into biologic insights and clinical applications.

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The cBio Cancer Genomics Portal: An Open Platform for Exploring Multidimensional Cancer Genomics Data

The cBioPortal for Cancer Genomics (http://cbioportal.org) provides a Web resource for exploring, visualizing, and analyzing multidimensional cancer genomics data. The portal reduces molecular profiling data from cancer tissues and cell lines into readily understandable genetic, epigenetic, gene expression, and proteomic events. The query interface combined with customized data storage enables researchers to interactively explore genetic alterations across samples, genes, and pathways and, when available in the underlying data, to link these to clinical outcomes. The portal provides graphical summaries of gene-level data from multiple platforms, network visualization and analysis, survival analysis, patient-centric queries, and software programmatic access. The intuitive Web interface of the portal makes complex cancer genomics profiles accessible to researchers and clinicians without requiring bioinformatics expertise, thus facilitating biological discoveries. Here, we provide a practical guide to the analysis and visualization features of the cBioPortal for Cancer Genomics.

Integrative analysis of complex cancer genomics and clinical profiles using the cBioPortal

All cancers are caused by somatic mutations; however, understanding of the biological processes generating these mutations is limited. The catalogue of somatic mutations from a cancer genome bears the signatures of the mutational processes that have been operative. Here we analysed 4,938,362 mutations from 7,042 cancers and extracted more than 20 distinct mutational signatures. Some are present in many cancer types, notably a signature attributed to the APOBEC family of cytidine deaminases, whereas others are confined to a single cancer class. Certain signatures are associated with age of the patient at cancer diagnosis, known mutagenic exposures or defects in DNA maintenance, but many are of cryptic origin. In addition to these genome-wide mutational signatures, hypermutation localized to small genomic regions, 'kataegis', is found in many cancer types. The results reveal the diversity of mutational processes underlying the development of cancer, with potential implications for understanding of cancer aetiology, prevention and therapy.

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Signatures of mutational processes in human cancer

EASL-EORTC clinical practice guidelines : management of hepatocellular carcinoma

Since the publication of the American Association for the Study of Liver Diseases (AASLD) practice guidelines on the management of hepatocellular carcinoma (HCC) in 2005, new information has emerged that requires that the guidelines be updated. The full version of the new guidelines is available on the AASLD Web site at http://www.aasld.org/practiceguidelines/ Documents/Bookmarked%20Practice%20Guidelines/ HCCUpdate2010.pdf. Here, we briefly describe only new or changed recommendations.

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AASLD PRACTICE GUIDELINE Management of Hepatocellular Carcinoma: An Update

Graft-versus-host disease (GVHD) is the most common and well-known cause of morbidity and mortality following allogeneic bone marrow transplantation. Sporadic cases have been reported after cadaveric donor liver transplantation with usually fatal outcomes, however, the actual incidence and the characteristics of GVHD after living donor liver transplantation (LDLT) remain unknown. We herein report a person who developed fatal GVHD following LDLT and discuss the applicability of an HLA-homozygous donor to an HLA-haploidentical recipient. A 48-year-old male underwent LDLT for unresectable hepatocellular carcinoma with alcoholic liver cirrhosis. The donor was his 20-year-old son whose pretransplant HLA typing was homozygous at all loci. GVHD occurred 35 days after LDLT and was characterized by fever, diarrhea, maculopapular rash, and leukopenia, which led to the development of fatal pneumonia. We identified 4 cases of GVHD after LDLT in Japan and 1 in the United States, all associated with the use of an HLAhomozygous donor. The use of an HLA homozygous donor which results in a complete 1-way donor-recipient HLA match carries an extremely high risk of developing GVHD after LDLT. Therefore, it is possible that LDLT should be ruled out for such donors. A pretransplant work-up of the HLA type in both the donors and recipients is therefore imperative before determining the indications for LDLT. [Abstract reproduced by permission of Liver Transpl 2004; 10: 460–4]

https://www.journal-of-hepatology.eu/article/S0168-8278(04)00311-3/pdf

Graft-versus-host disease following living donor liver transplantation: high risk when the donor is HLA-homozygous

Immunosuppressed organ transplant recipients have an increased risk of developing cancer such as Kaposi’s sarcoma and posttransplant lymphoproliferative disorders (PTLDs) [1–3]. After organ transplantation, about 40% of patients with PTLDs survive, either because of spontaneous resolution after the cessation of immunosuppressive therapy, or possibly because of the efficacy of antiviral drugs, monoclonal antibodies and chemoradiotherapy [4]. Determination of the best treatment is difficult because of the limited number of published series, and because of the morphologic spectrum of the lymphoproliferative disorders which appears to range from a benign reactive lymphoid process to a malignant lymphoma. We reexamined our experience of 28 transplant recipients with a PTLD observed at our institution in an attempt to determine the response to therapy in 25 treated patients with reduction of immunosuppressants, monoclonal antibodies, surgery and/or chemotherapy after a median of follow-up of 60 months (range 4–84 months).

Didier Samuel

Papers

Graft-versus-host disease following living donor liver transplantation: high risk when the donor is HLA-homozygous

Therapeutic issues in lymphoproliferative disorders: Treatment and outcome of 28 cases observed in a single center

Management of Hepatitis B Virus Infection Post Transplantation

Foie artificiel. Concept et développements actuels

Predictive factors of antibody response after anti-SARS-CoV-2 vaccine in liver transplant recipients