Abstract
Elevated levels of soluble CD30 (sCD30) are linked with various T-cell neoplasms. However, the relationship between sCD30 levels and the development of adult T-cell leukemia (ATL) in human T-cell leukemia virus type 1 (HTLV-1) carriers remains to be clarified. We here investigated whether plasma sCD30 is associated with risk of ATL in a nested case-control study within a cohort of HTLV-1 carriers. We compared sCD30 levels between 11 cases (i.e., HTLV-1 carriers who later progressed to ATL) and 22 age-, sex- and institution-matched control HTLV-1 carriers (i.e., those with no progression). The sCD30 concentration at baseline was significantly higher in cases than in controls (median 65.8, range 27.2-134.5 U/mL vs. median 22.2, range 8.4-63.1 U/mL, P=0.001). In the univariate logistic regression analysis, a higher sCD30 (≥30.2 U/mL) was significantly associated with ATL development (odds ratio 7.88 and the 95% confidence intervals 1.35-45.8, P = 0.02). Among cases, sCD30 concentration tended to increase at the time of diagnosis of aggressive-type ATL, but the concentration was stable in those developing the smoldering-type. This suggests that sCD30 may serve as a predictive marker for the onset of aggressive-type ATL in HTLV-1 carriers.
Highlights
Adult T-cell leukemia (ATL) is a highly aggressive T-cell malignancy that was first proposed as a new disease entity in 1977 (Uchiyama et al, 1977) and that was closely followed by the discovery of the human T-cell leukemia virus type 1 (HTLV-1) as the causative agent (Yoshida et al, 1982)
The results of the present study demonstrated a possible association between the plasma levels of soluble CD30 (sCD30) in HTLV-1 carriers and the development of ATL
The univariate logistic regression analysis indicated that a higher sCD30 concentration (≥30.2 U/mL) in the plasma of asymptomatic HTLV-1 carriers was associated with the development of ATL
Summary
Adult T-cell leukemia (ATL) is a highly aggressive T-cell malignancy that was first proposed as a new disease entity in 1977 (Uchiyama et al, 1977) and that was closely followed by the discovery of the human T-cell leukemia virus type 1 (HTLV-1) as the causative agent (Yoshida et al, 1982). Most HTLV-1-infected people remain asymptomatic, i.e., not diagnosed as having HTLV1-related diseases, such as ATL, HTLV-1-associated myelopathy, and others (Yamaguchi 1994). Approximately 5% of asymptomatic HTLV-1 carriers develop ATL after a long period of latent infection, with the average age of the onset of 67 years (Yamaguchi 1994). For the long-term latency between initial HTLV-1 infection and ATL development, a multistage carcinogenesis theory where five or more genetic changes may be accumulated in HTLV-1-infected cells before the clinical onset of ATL is widely accepted (Okamoto et al, 1989; Franchini, 1995). A large number of reports have been published to date, genetic abnormalities involved in the leukemogenesis of ATL and the molecular mechanisms of malignant transformation of HTLV-1-infected cells remain to be elucidated
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