Epstein-Barr Virus–Associated Smooth Muscle Tumor

Dekate, Jyoti; Chetty, Runjan

doi:10.5858/arpa.2015-0120-rs

Cited by 50 publications

(79 citation statements)

References 25 publications

(33 reference statements)

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“…EBV‐SMT have two defining morphologic criteria, namely, variable proportions of admixed intratumoral small lymphocytes and the presence of primitive‐looking round cell areas that may transition gradually or abruptly from areas of well‐differentiated spindled smooth muscle cellular proliferation. However, given the considerable histopathologic variability of EBV‐SMT, detection of EBV in tumor cells (most commonly by nuclear staining for EBER) is often the key for definitive diagnosis . We recently encountered two EBV‐SMT cases post lung transplantation and their presentations and clinical courses are summarized in this report.…”

Section: Introductionmentioning

confidence: 98%

“…However, given the considerable histopathologic variability of EBV-SMT, detection of EBV in tumor cells (most commonly by nuclear staining for EBER) is often the key for definitive diagnosis. 2 We recently encountered two EBV-SMT cases post lung transplantation and their presentations and clinical courses are summarized in this report. In addition, we reviewed the literature describing EBV-SMT and compared its features with those of PTLD.…”

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confidence: 99%

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Epstein‐Barr virus‐associated smooth muscle tumors after lung transplantation

Hirama

Tikkanen

Pal

et al. 2019

Transplant Infectious Dis

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Background Recipients of solid organ transplants are prone to various complications that are seldom encountered in immunocompetent individuals. Post‐transplant lymphoproliferative disorder (PTLD) is the best known and commonest Epstein‐Barr Virus (EBV)‐associated malignancy post solid organ transplant. EBV‐associated smooth muscle tumors (EBV‐SMT) including leiomyomas and leiomyosarcomas are rare and much less studied than PTLD. We recently encountered two cases of EBV‐SMT post lung transplantation and here we summarize their clinical features and course together with a literature review. Method Clinical data and treatment details of two patients who developed EBV‐SMT were reviewed and retrieved up to December 31, 2017. English literature was searched through the PubMed database from 1965 to 2017 for studies of the association between lung transplant and EBV‐SMT. Results The incidence of PTLD is higher among lung transplant recipients compared to kidney transplant recipients, an observation that has been attributed to stronger immune suppression in the lung patients. EBV‐SMT showed a higher incidence among kidney recipients than among lung recipients, suggesting that the degree of immunosuppression may be a less important factor in the development of EBV‐SMT. EBV‐SMT has most often been seen among lung transplant recipients with EBV mismatch. Conclusions Because EBV‐SMT is a rare tumor, its incidence, risk factors, and optimal management have not been well‐defined and further study is needed.

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Section: Introductionmentioning

confidence: 98%

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confidence: 99%

Epstein‐Barr virus‐associated smooth muscle tumors after lung transplantation

Hirama

Tikkanen

Pal

et al. 2019

Transplant Infectious Dis

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“…Twenty-five years later, their association with EBV was described by Lee et al (8). Although EBV-SMTs can be seen in different clinical settings in immunosuppressed patient, the majority of patients affected by EBV-SMT are (60%) posttransplant (9) and in HIV patients (10). Few cases associated with congenital immunodeficiency are also reported.…”

Section: Discussionmentioning

confidence: 99%

EBV-associated hepatic smooth muscle tumor of uncertain biologic behavior after heart transplantation in a pediatric patient: case report

Liu

Chintalapati

Dietz

et al. 2017

J. Gastrointest. Oncol.

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Epstein-Barr virus-associated smooth muscle tumor (EBV-SMT) is a rare neoplasm recognized in immunocompromised patients. There are less than 30 cases of EBV-SMT reported in pediatric population following solid organ transplantation. Herein, we report a case of an 8-year-old female who was incidentally noted to have multiple lesions in the liver 8 years after heart transplantation. The tumor was composed of a cellular proliferation of spindle-shaped cells with low mitotic activity. The diagnosis of EBV-SMT was confirmed by in situ hybridization for EBV-encoded small RNA (EBER) transcripts. Multiple additional lesions were detected by whole body positron emission tomography-computed tomography (PET-CT) scan 4 months after the initial finding of the hepatic lesions. Immunosuppression was switched to a mechanistic target of rapamycin (mTOR) inhibitor. We conclude that EBV-SMT should be included in the differential diagnoses in post-transplantation patients and further investigations should be performed to evaluate additional lesions. transplantation. Serial testing for EBV DNA by quantitative polymerase chain reaction (PCR) was performed on peripheral blood starting 3 years after the heart transplant (she presented with cough and fever), which showed amplification with up to 131,600 copies/mL. Her EBV viral load has been consistent since then. She developed acute abdominal pain and an appendiceal perforation was diagnosed 8 years post-transplant. Two liver masses were incidentally identified in the left and right hepatic lobes by abdominal computed tomography (CT) scan. Both appeared hypoechoic and individually measured up to 2.5 cm. Whole body positron emission tomography (PET)-CT scan was performed thereafter with no evidence of lymphadenopathy or other lesions. The mass in the right lobe was excised and found to be well circumscribed, white, and firm on gross examination. The mass in the left lobe was not removed due to its deep location. KeywordsHistologically, the hepatic lesion was well demarcated from the adjacent liver parenchyma, and exhibited interlacing fascicles of spindle cells with eosinophilic cytoplasm and elongated, blunt-ended nuclei with stippled chromatin (Figure 1). Rare (less than 5%) primitive round cell component was identified. There was no evidence of necrosis or hemorrhage. Few small blood vessels were interspersed within the fascicles of spindle cells. Mitotic activity was less than 1 per 10 high power fields (HPF). Occasional lymphoid cells were seen at the junction between the tumor and adjacent liver parenchyma (Figure 2). Immunohistochemical (IHC) stains were performed to categorize the lesion. Smooth muscle actin ( Figure 3A) and HHF 35 ( Figure 3B) were positive, and desmin showed focal and weak equivocal staining consistent with smooth muscle origin. Ki67 showed only 1-2% of proliferative activity. EBV in situ hybridization was positive with a diffuse staining pattern (Figure 4), diagnostic of EBV infection. All these features were consistent with a diagnosis of EBV-SMT.W...

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“…This cycle results in a lifelong persistence, which can lead to the development of malignancies originated by B-lymphocytes as in Burkitt and Hodgkin lymphomas or epithelial cells such as nasopharyngeal carcinoma and certain gastric carcinomas (Longnecker et al, 2013). In addition, smooth muscle cells support infection and replication of EBV, which in some cases result in the development of EBV positive smooth muscle tumors, the second most prevalent malignancy of children with AIDS (Dekate andChetty, 2016, Jenson et al, 1997). EBV can also rarely infect other cell types such as T cells and NK cells in immunosuppressed patients resulting in T/NK-cell lymphoproliferative disorders (Akashi and Mizuno, 2000, Coleman et al, 2015, Isobe et al, 2004, Park and Ko, 2014.…”

Section: Route Of Infection and Host Cell Tropismmentioning

confidence: 99%

Gammaherpesvirus entry and fusion: A tale how two human pathogenic viruses enter their host cells

Möhl

Chen

Longnecker

2019

Advances in Virus Research

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The prototypical human γ-herpesviruses Epstein-Barr virus (EBV) and Kaposi Sarcomaassociated herpesvirus (KSHV) are involved in the development of malignancies. Like all herpesviruses, they share the establishment of latency, the typical architecture, and the conserved fusion machinery to initiate infection. The fusion machinery reflects virus-specific adaptations due to the requirements of the respective herpesvirus. For example, EBV evolved a tropism switch involving either the B-or epithelial cell-tropism complexes to activate fusion driven by gB. Most of the EBV entry proteins and their cellular receptors have been crystallized providing molecular details of the initial steps of infection. For KSHV, a variety of entry and binding receptors has also been reported but the mechanism how receptor binding activates gB-driven fusion is not as well understood as that for EBV. However, the downstream signaling pathways that promote the early steps of KSHV entry are well described. This review summarizes the current knowledge of the key players involved in EBV and KSHV entry and the cell-type specific mechanisms that allow infection of a wide variety of cell types.

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Epstein-Barr Virus–Associated Smooth Muscle Tumor

Cited by 50 publications

References 25 publications

Epstein‐Barr virus‐associated smooth muscle tumors after lung transplantation

Epstein‐Barr virus‐associated smooth muscle tumors after lung transplantation

EBV-associated hepatic smooth muscle tumor of uncertain biologic behavior after heart transplantation in a pediatric patient: case report

Gammaherpesvirus entry and fusion: A tale how two human pathogenic viruses enter their host cells

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