Molecular and immunologic mechanisms of cancer pathogenesis in solid organ transplant recipients
被引:54
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作者:
Martinez, O. M.
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机构:
Stanford Univ, Sch Med, Dept Surg, Div Transplantat, Stanford, CA 94305 USA
Stanford Univ, Sch Med, Program Immunol, Stanford, CA 94305 USAStanford Univ, Sch Med, Dept Surg, Div Transplantat, Stanford, CA 94305 USA
Martinez, O. M.
[1
,2
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de Gruijl, F. R.
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机构:
Leiden Univ, Med Ctr, Dept Dermatol, NL-2300 RA Leiden, NetherlandsStanford Univ, Sch Med, Dept Surg, Div Transplantat, Stanford, CA 94305 USA
de Gruijl, F. R.
[3
]
机构:
[1] Stanford Univ, Sch Med, Dept Surg, Div Transplantat, Stanford, CA 94305 USA
[2] Stanford Univ, Sch Med, Program Immunol, Stanford, CA 94305 USA
[3] Leiden Univ, Med Ctr, Dept Dermatol, NL-2300 RA Leiden, Netherlands
The increased risk for the development of malignancies in transplant recipients is generally attributed to the debilitated immune system that results from chronic exposure to potent immunosuppressive drugs required to prevent graft rejection. While impaired immunity is clearly a key determinant, there is strong evidence that a constellation of other factors contribute to the pathogenesis of posttransplant cancers. In this article we discuss the underlying molecular and immunologic mechanisms that contribute to the development of de novo malignancies in transplant recipients, with particular focus on the two leading posttransplant neoplasia, skin cancer and Epstein-Barr virus (EBV)-associated posttransplant lymphoproliferative disorder (PTLD).