{"title":"Viral associations with hematologic cancers.","authors":"Mark Stasiewicz, Tomasz M Karpiński","doi":"10.1016/j.jfma.2025.07.001","DOIUrl":null,"url":null,"abstract":"<p><p>Hematologic malignancies (HMs) continue to present a burden upon healthcare systems worldwide, with over one million incident cases reported in 2020 alone. It has been known for decades that infectious agents serve as the etiologic agents for a number of neoplastic disorders and outright cancers. Viruses are the predominant infectious contributor to oncogenesis among HMs. The PubMed database was utilized to outline the present state of understanding as it relates to viral associations with HMs. Viruses with the most evidence supporting their association with the development of HMs include Epstein-Barr virus, human immunodeficiency virus, human T-lymphotropic virus, hepatitis C virus and Kaposi sarcoma herpesvirus. Reactivation of latent hepatitis B virus is associated with treatment regimens commonly used in the management of HMs. Furthermore, brief summaries of the oncogenic mechanisms underlying the aforementioned associations and an overview of current management principles are presented. Such information may serve to guide clinicians in establishing the etiology of their patients' malignancy and help establish best practices to prevent the spread and reactivation of viruses associated with the development and treatment of HMs.</p>","PeriodicalId":17305,"journal":{"name":"Journal of the Formosan Medical Association","volume":" ","pages":""},"PeriodicalIF":2.6000,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of the Formosan Medical Association","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.jfma.2025.07.001","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
引用次数: 0
Abstract
Hematologic malignancies (HMs) continue to present a burden upon healthcare systems worldwide, with over one million incident cases reported in 2020 alone. It has been known for decades that infectious agents serve as the etiologic agents for a number of neoplastic disorders and outright cancers. Viruses are the predominant infectious contributor to oncogenesis among HMs. The PubMed database was utilized to outline the present state of understanding as it relates to viral associations with HMs. Viruses with the most evidence supporting their association with the development of HMs include Epstein-Barr virus, human immunodeficiency virus, human T-lymphotropic virus, hepatitis C virus and Kaposi sarcoma herpesvirus. Reactivation of latent hepatitis B virus is associated with treatment regimens commonly used in the management of HMs. Furthermore, brief summaries of the oncogenic mechanisms underlying the aforementioned associations and an overview of current management principles are presented. Such information may serve to guide clinicians in establishing the etiology of their patients' malignancy and help establish best practices to prevent the spread and reactivation of viruses associated with the development and treatment of HMs.
期刊介绍:
Journal of the Formosan Medical Association (JFMA), published continuously since 1902, is an open access international general medical journal of the Formosan Medical Association based in Taipei, Taiwan. It is indexed in Current Contents/ Clinical Medicine, Medline, ciSearch, CAB Abstracts, Embase, SIIC Data Bases, Research Alert, BIOSIS, Biological Abstracts, Scopus and ScienceDirect.
As a general medical journal, research related to clinical practice and research in all fields of medicine and related disciplines are considered for publication. Article types considered include perspectives, reviews, original papers, case reports, brief communications, correspondence and letters to the editor.