Objective: Between 2% and 9% of cardiac transplant recipients develop posttransplant lymphoproliferative disease, which includes lymphomas. These are usually aggressive Epstein-Barr virus-associated B-cell proliferations similar to those seen in other immunodeficiency states. A retrospective pathologic study of the tumor tissue from 21 cardiac transplant recipients with posttransplant lymphoproliferative disease was undertaken.
Design: Tumor histology, immunohistochemistry, immunophenotyping, and DNA analysis for clonal gene rearrangement and the presence of Epstein-Barr virus DNA were performed.
Patients: The mean patient age was 53.4 +/- 10.2 years (range 33-67 years); 33% of the patients were alive at the time of study.
Results: Histologically, the samples comprised one Burkitt's lymphoma, three diffuse mixed lymphomas, eight diffuse large-cell lymphomas, and nine immunoblastic lymphomas. Thirteen (93%) of 14 samples were infiltrated by small reactive T cells; five of the lymphomas qualified as T-cell rich. Of 14 cases studied, 12 had clonal immunoglobulin gene rearrangements, 1 had oligoclonal bands, and 1 exhibited only a germline pattern. The B cells were CD10+, CD19+, and CD20+, and the reactive T cells were CD2+, CD3+, CD5+, CD7+, CD8+, and CD57+ by immunophenotyping.
Conclusions: In this patient series, morphologically aggressive lymphomas and disseminated disease occurred early as well as late after transplantation. Most of the tumors showed a reactive T-cell component, which may represent a host attempt at controlling the B-cell proliferation.
Download full-text PDF |
Source |
---|
PLoS Pathog
January 2025
Department of Cancer and Genomic Sciences, College of Medicine and Health, University of Birmingham, Birmingham, United Kingdom.
Upon infection, human papillomavirus (HPV) manipulates host cell gene expression to create an environment that is supportive of a productive and persistent infection. The virus-induced changes to the host cell's transcriptome are thought to contribute to carcinogenesis. Here, we show by RNA-sequencing that oncogenic HPV18 episome replication in primary human foreskin keratinocytes (HFKs) drives host transcriptional changes that are consistent between multiple HFK donors.
View Article and Find Full Text PDFFront Immunol
January 2025
Center for Bioscience Research and Education, Utsunomiya University, Utsunomiya, Japan.
The cellular and molecular mechanisms underlying lymphocyte development are diverse among teleost species. Although recent scRNA-seq analyses of zebrafish hematopoietic cells have advanced our understanding of teleost hematopoiesis, comparative studies using another genetic model, medaka, which is evolutionarily distant among teleosts, is useful for understanding commonality and species-specificity in teleosts. In order to gain insight into how different molecular and cellular mechanisms of lymphocyte development in medaka and zebrafish, we established a () mutant medaka, which exhibited defects in V(D)J rearrangement of lymphocyte antigen receptor genes, accordingly lacking mature B and T cells.
View Article and Find Full Text PDFDouble-strand breaks represent the most dangerous form of DNA damage, and in resting cells, these breaks are sealed via the non-homologous end joining (NHEJ) factor Ligase IV (LIG4). Excessive NHEJ may be genotoxic, necessitating multiple mechanisms to control NHEJ activity. However, a clear mechanism of transcriptional control for them has not yet been identified.
View Article and Find Full Text PDFBiochem Pharmacol
January 2025
Department of Hematology of First Affiliated Hospital, and Department of Public Health, Zhejiang University School of Medicine, Hangzhou, China; Cancer Center, Zhejiang University, Hangzhou, China. Electronic address:
Acute myeloid leukemia (AML) is a highly heterogeneous and aggressive blood cancer. Genetic abnormalities, such as the t(8;21) rearrangement, play a significant role in AML onset. This rearrangement leads to the formation of the RUNX1/RUNX1T1 fusion protein, disrupting gene regulation and genomic stability, ultimately causing full-blown leukemia.
View Article and Find Full Text PDFGenes (Basel)
December 2024
Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA.
Background: Acute promyelocytic leukemia (APL) is characterized by abnormal promyelocytes and t(15;17)(q24;q21) . Rarely, patients may have cryptic or variant rearrangements. All-trans retinoic acid (ATRA)/arsenic trioxide (ATO) is largely curative provided that the diagnosis is established early.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!