Viral genotypes and p53 expression in epstein-barr virus-associated primary malignant lymphomas of the intestines

Kim, Young Sik; Kim, Jung Bun; Kang, Yong Koo; Nam, Eun Sook; Park, Seol Hee; Kim, Insun

doi:10.1016/s0046-8177(99)90030-8

Cited by 4 publications

(1 citation statement)

References 39 publications

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“…The role of p53 in the oncogenesis of EITCL is not known. Varied reports have documented EBV positivity (by PCR and FISH with EBER-1 analysis) in association with EITCL including cases of EBV-related EITCL PTLD suggesting a possible etiologic role of EBV in the pathogenesis of EITCL (281)(282)(283)(284)(285)(286)(287)(288)(289). Furthermore, analysis comparing the prevalence of EBV in Mexican versus European EITCL cases demonstrated that there are significant epidemiologic differences in EBV association (100% versus 10%, respectively) (288, 289).…”

Section: Enteropathy-type Intestinal T-cell Lymphoma (Eitcl)mentioning

confidence: 99%

Molecular etiology of mature T-cell non-hodgkins lymphomas

Evens

Gartenhaus²

2003

Front Biosci

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T-cell non-Hodgkin's lymphomas (NHL) represent approximately 10-15% of all lymphomas diagnosed in Western countries. Significant progress has been made over the last 2 decades in defining non-random chromosomal abnormalities. Cytogenetic and molecular analyses have enhanced diagnostic capabilities as well as improved classification and prognostication for T-cell NHL. Gamma-delta T-cell receptor (TCR) clonality now represents the more common TCR rearrangement in subcutaneous panniculitis-like T-cell lymphoma (SCPTCL), hepatosplenic T-cell lymphoma (HSTCL), extranodal NK/T-cell lymphoma, nasal type and enteropathy-type intestinal T-cell lymphoma (EITCL). Non-random, recurrent chromosome abnormalities such as isochrome 7 with HSTCL, complex karyotypes with peripheral T-cell lymphoma, not otherwise characterized (PTCL-NOC), trisomies 3 and 5 with angioimmunoblastic lymphoma (AIL) and t(2;5) with systemic anaplastic T-cell lymphoma have been recognized. Furthermore, identification of relevant protooncogenes and tumor suppressor genes involved in the pathogenesis of T-cell NHL such as the NPM/ALK fusion protein, p53, cyclin dependent kinase inhibitors (p15, p16, p21) and EBV as well as their interplay with the various regulatory pathways of cell cycle progression and apoptosis represent potential candidates for molecular-based therapy. This review presents a detailed analysis of the molecular and genetic perturbations present in mature T-cell lymphomas including discussion of how tumor-specific alterations impact on clinical outcome. Future studies in T-cell NHL are likely to provide additional disease-specific chromosomal translocations and molecular alterations with important translational implications.

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