Management of Kaposi sarcoma after solid organ transplantation: A European retrospective study.

J Am Acad Dermatol

Department of Dermatology, Assistance Publique-Hôpitaux de Paris (AP-HP) Hôpital Saint Louis, Institut National de la Santé et de la Recherche Médicale U976, Université Paris Diderot, Sorbonne Paris Cité, Paris, France.

Published: August 2019

Background: Systemic therapeutic management of post-transplant Kaposi sarcoma (KS) is mainly based on 3 axes: reduction of immunosuppression, conversion to mammalian target of rapamycin (mTOR) inhibitors, chemotherapy, or a combination of these.

Objective: To obtain an overview of clinical strategies about the current treatment of KS.

Methods: We conducted a multicenter retrospective cohort study including 145 solid organ transplant recipients diagnosed with KS between 1985 and 2011 to collect data regarding first-line treatment and response at 6 months.

Results: Overall, 95%, 28%, and 16% of patients had reduction of immunosuppression, conversion to mTOR inhibitor, and chemotherapy, respectively. Patients treated with chemotherapy or mTOR inhibitor conversion were more likely to have visceral KS. At 6 months, 83% of patients had response, including 40% complete responses.

Limitations: The retrospective design of the study.

Conclusion: Currently available therapeutic options seem to be effective to control KS in most patients. Tapering down the immunosuppressive regimen remains the cornerstone of KS management.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.jaad.2019.03.028DOI Listing

Publication Analysis

Top Keywords

kaposi sarcoma
8
solid organ
8
reduction immunosuppression
8
immunosuppression conversion
8
mtor inhibitor
8
management kaposi
4
sarcoma solid
4
organ transplantation
4
transplantation european
4
european retrospective
4

Similar Publications

Epigenetic and epitranscriptomic regulation during oncogenic -herpesvirus infection.

Front Microbiol

January 2025

Departments of Otorhinolaryngology-Head and Neck Surgery and Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States.

Oncogenic gamma herpesviruses, including Epstein-Barr Virus (EBV) and Kaposi's Sarcoma-associated Herpesvirus (KSHV), are opportunistic cancer-causing viruses and induces oncogenesis through complex mechanisms, which involves manipulation of cellular physiology as well as epigenetic and epitranscriptomic reprogramming. In this review, we describe the intricate processes by which these viruses interact with the epigenetic machinery, leading to alterations in DNA methylation, histone modifications, and the involvement of non-coding RNAs. The key viral proteins such as EBNA1 and LMP1 encoded by EBV; LANA and vGPCR encoded by KSHV; play pivotal roles in these modifications by interacting with host factors, and dysregulating signaling pathways.

View Article and Find Full Text PDF

Mouse models of Kaposi sarcoma-associated herpesvirus (KSHV).

Virology

December 2024

Lineberger Comprehensive Cancer Center and Department of Microbiology and Immunology, The University of North Carolina at Chapel Hill, USA. Electronic address:

Infection with Kaposi sarcoma-associated herpesvirus (KSHV) is a prerequisite for the development of several human cancers, including Kaposi sarcoma and primary effusion lymphoma. Efficient long-term infection with KSHV and subsequent virally induced cell transformation is limited to humans, resulting in a lack of small animal models for KSHV-driven malignancies. Various attempts to create a mouse model for KSHV include infection of humanized mice, generating transgenic mice that ectopically express viral proteins, and grafting KSHV-infected tumor, primary, or immortalized cells onto immunodeficient mice.

View Article and Find Full Text PDF

Kaposi's sarcoma-associated herpesvirus (KSHV) is a human gammaherpesvirus associated with Kaposi's sarcoma and B cell malignancies. Like all herpesviruses, KSHV contains conserved envelope glycoproteins (gps) involved in virus binding, entry, assembly, and release from infected cells, which are also targets of the immune response. Due to the lack of a reproducible animal model of KSHV infection, the precise functions of the KSHV gps during infection are not completely known.

View Article and Find Full Text PDF

Modulation of Lymphotoxin β Surface Expression by Kaposi's Sarcoma-Associated Herpesvirus K3 Through Glycosylation Interference.

J Med Virol

January 2025

Department of Infection Biology, Global Center for Pathogen and Human Health Research, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, USA.

Kaposi's sarcoma-associated herpesvirus (KSHV) employs diverse mechanisms to subvert host immune responses, contributing to its infection and pathogenicity. As an immune evasion strategy, KSHV encodes the Membrane-Associated RING-CH (MARCH)-family E3 ligases, K3, and K5, which target and remove several immune regulators from the cell surface. In this study, we investigate the impact of K3 and K5 on lymphotoxin receptor (LTβR) ligands, LTβ and LIGHT, which are type II transmembrane proteins and function as pivotal immune mediators during virus infection.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!