Mycosis fungoides and Sezary syndrome are not associated with HTLV‐I infection: an international study

Bazarbachi, Ali; Soriano, Vincent; Pawson, Rachel; Vallejo, Alejandro; Moudgil, Tarsem; Matutes, E.; Périès, J.; Molina, Arturo; Schulz, Thomas F.; Catovsky, Daniel; Gill, Pooria

doi:10.1046/j.1365-2141.1997.3213138.x

Cited by 58 publications

(37 citation statements)

References 21 publications

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“…Increased levels of wild-type p53 with a longer half-life have been demonstrated by immunoprecipitation in IL-2-independent cell lines with no evidence for gene mutation (Reid et al, 1993;Gartenhaus & Wang, 1995). However, in our experience, T-PLL and Sezary syndrome are not associated with HTLV-1 infections (Bazarbachi et al, 1997;Pawson et al, 1997). In some cases of non-Hodgkin lymphoma, p53 overexpression has been observed without detectable p53 gene mutation, and the transactivating function of the protein is retained, resulting in increased p21 expression (Mansukhani et al, 1997).…”

Section: Discussionmentioning

confidence: 87%

p53 allele deletion and protein accumulation occurs in the absence of p53 gene mutation in T‐prolymphocytic leukaemia and Sezary syndrome

et al. 2000

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Summary. In a series of 24 patients with chronic T-lymphoid disorders [13 T-prolymphocytic leukaemia (T-PLL) and 11Sezary syndrome] we have studied (i) chromosome 17p abnormalities and p53 allele deletion by fluorescence in situ hybridization; (ii) mutation in the exons of the p53 gene by direct DNA sequencing; and (iii) p53 protein expression by immunocytochemistry and, in some cases, also by flow cytometry with DO-1, a monoclonal antibody to the p53 protein. The study revealed p53 deletion and accumulation of p53 protein in the absence of mutation in the exons that included the hot-spots and differs from that described in B-prolymphocytic leukaemia. Seven T-PLL and five Sezary syndrome patients had p53 overexpression, and five T-PLL and nine Sezary syndrome patients showed p53 deletion. Although the majority of cases with p53 accumulation had p53 deletion, the proportion of cells with the deletion did not correlate with the proportion of cells positive for p53 expression. Two cases of T-PLL showed strong p53 expression in the absence of p53 deletion, and one case of Sezary syndrome with p53 deletion in 97% of cells did not express p53. These findings suggest that a non-mutational mechanism exists for the accumulation of p53 protein in these T-cell disorders. The oncogenic effect of the accumulating wild-type protein has been reported in other malignancies. Whether haploidy resulting from p53 deletion contributes to this mechanism has yet to be determined. Alternatively, the frequent loss of the p53 gene could be associated with the deletion of an adjacent gene, which could be involved in the pathogenesis of these diseases.

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Section: Discussionmentioning

confidence: 87%

p53 allele deletion and protein accumulation occurs in the absence of p53 gene mutation in T‐prolymphocytic leukaemia and Sezary syndrome

et al. 2000

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“…Because of the striking similarities of CTCL spectratypes and HIV-1 spectratypes, we favor the first possibility. Previous reports implicating the lymphotropic retrovirus HTLV-1 (human T-cell lymphotrophic virus type 1) in CTCL have so far remained conflicting, 41,42 but involvement of a virus related to HTLV-1 remains a possibility. The precise nature of such a putative agent is the subject of intensive study.…”

Section: Discussionmentioning

confidence: 99%

Profound loss of T-cell receptor repertoire complexity in cutaneous T-cell lymphoma

Yawalkar

Ferenczi

Jones

et al. 2003

Blood

152

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Cutaneous T-cell lymphoma (CTCL) is a malignancy of skin-homing T cells. A major feature of CTCL is profound immunosuppression, such that patients with advanced mycosis fungoides or Sé zary syndrome have been compared with patients with advanced HIV disease and are susceptible to opportunistic infection. The etiology of this immunosuppression is unclear. We analyzed peripheral blood T cells of patients with CTCL with stage I to IV disease, using a sensitive betavariable complementarity-determining region 3 spectratyping approach. Our data revealed a profound disruption of the complexity of the T-cell repertoire, which was universally observed in patients with advanced disease (stages III and IV), and present in up to 50% of patients with early-stage disease (stages I and II). In most patients, multiple monoclonal and oligoclonal complementarity-determining region 3 (CDR3) spectratype patterns in many different beta-variable families were seen. Equally striking was a reduction of normal T cells (as judged by absolute CD4 counts) across multiple beta-variable families. In general, CTCL spectratypes were reminiscent of advanced HIV spectratypes published elsewhere. Taken together, these data are most consistent with a global assault on the T-cell repertoire in patients with CTCL, a process that can be observed even in early-stage disease. (Blood. 2003;102:4059-4066)

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“…Zucker-Franklin et al (31) reported the release of retroviral particles from cultured lymphocytes of 18 MF patients. However, to date, there is no convincing evidence for an involvement of either human T-cell Lymphotropic Virus Type-I nor human Herpesvirus 8 in the pathogenesis of MF (32,33). Patients with HL show defects in cellmediated immunity that can precede the development of the disease (34).…”

Section: Discussionmentioning

confidence: 99%

Epstein-Barr Virus–Negative Hodgkin's Lymphoma After Mycosis Fungoides: Molecular Evidence for Distinct Clonal Origin

et al. 2001

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Mycosis fungoides and Sezary syndrome are not associated with HTLV‐I infection: an international study

Cited by 58 publications

References 21 publications

p53 allele deletion and protein accumulation occurs in the absence of p53 gene mutation in T‐prolymphocytic leukaemia and Sezary syndrome

p53 allele deletion and protein accumulation occurs in the absence of p53 gene mutation in T‐prolymphocytic leukaemia and Sezary syndrome

Profound loss of T-cell receptor repertoire complexity in cutaneous T-cell lymphoma

Epstein-Barr Virus–Negative Hodgkin's Lymphoma After Mycosis Fungoides: Molecular Evidence for Distinct Clonal Origin

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