JC Virus Infection in Colorectal Neoplasia That Develops after Liver Transplantation

Autor: Edward B. DeVol, C. Richard Boland, Elizabeth B. Haagsma, Robert C. Verdonk, Lucia Fini, Wytske Boersma-van Ek, Luigi Ricciardiello, Gerard Dijkstra, S Williams, Rong Huang, Ajay Goel, Jan J. Koornstra, Steven de Jong, Michael Selgrad, R Meyer, M. Blom
Přispěvatelé: Selgrad M., Koornstra J.J., Fini L., Blom M., Huang R., Devol E.B., Boersma-van Ek.W., Dijkstra G., Verdonk R.C., de Jong S., Goel A., Williams S.L., Meyer R.L., Haagsma E.B., Ricciardiello L., Boland C.R., Guided Treatment in Optimal Selected Cancer Patients (GUTS), Groningen Institute for Gastro Intestinal Genetics and Immunology (3GI), Targeted Gynaecologic Oncology (TARGON), Translational Immunology Groningen (TRIGR), Groningen Institute for Organ Transplantation (GIOT)
Jazyk: angličtina
Rok vydání: 2008
Předmět:
Male
POLYPS
Cancer Research
Pathology
Colorectal cancer
medicine.medical_treatment
viruses
JC virus
PROTEIN
medicine.disease_cause
Polymerase Chain Reaction
Adenomatous Polyps
Antigens
Viral
Tumor
POPULATION
Aged
80 and over
RISK
education.field_of_study
COLON-CANCER
virus diseases
Immunosuppression
Middle Aged
PRIMARY SCLEROSING CHOLANGITIS
Prognosis
JC Virus
Oncology
ULCERATIVE-COLITIS
Adenocarcinoma
Female
Colorectal Neoplasms
Adenoma
Adult
medicine.medical_specialty
Adolescent
Population
HUMAN POLYOMAVIRUS
Article
Young Adult
medicine
Humans
education
Aged
Immunosuppression Therapy
Polyomavirus Infections
T-ANTIGEN
business.industry
Cancer
medicine.disease
Liver Transplantation
Transplantation
Tumor Virus Infections
RECIPIENTS
Case-Control Studies
DNA
Viral
Cancer research
Virus Activation
business
Zdroj: Clinical Cancer Research, 14(20), 6717-6721. AMER ASSOC CANCER RESEARCH
ISSN: 1078-0432
Popis: Purpose: Liver transplant recepients (LTRs) have an increased risk of colorectal neoplasia. The mechanism responsible for this is unknown. JCV encodes for TAg and has been implicated in colorectal carcinogenesis. We hypothesized that the use of immunosuppression in LTRs facilitates activation of JCV and is responsible for the increased risk of neoplasia. Experimental Design: JCV TAg DNA and protein expression were determined in normal colonic epithelium (n = 15) and adenomatous polyps (n = 26) from LTRs and compared with tissue samples from control patients (normal colon, n = 21; adenomas, n = 40). Apoptosis and proliferation were determined by M30 and Ki-67 immunoreactivity, respectively. Results: JCV TAg DNA was found in 10 of 15 (67%) of normal colonic mucosa from LTRs compared with 5 of 21 (24%) of control normal mucosa (P = 0.025). JCV TAg DNA was detected in 16 of 26 (62%) of the adenomas from LTRs and in 20 of 40 (50%) of control adenomas. JCV TAg protein was expressed in 13 of 26 (50%) adenomas from LTRs versus 2 of 40 (5%) of adenomas from controls (P < 0.001). In adenomas from LTRs, the mean proliferative activity was higher compared with controls (60.3 ± 3.2% versus 42.7 ± 2.8%, P < 0.001), whereas mean apoptotic indices were lower in LTRs (0.29 ± 0.08% versus 0.39 ± 0.06%, P = 0.05). Conclusions: The presence of JCV in the colorectal mucosa and adenomas from LTRs, in concert with the use of immunosuppressive agents, suggests that JCV may undergo reactivation, and the subsequent TAg protein expression might explain the increased risk of colorectal neoplasia in LTRs.
Databáze: OpenAIRE
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