There are no specific abnormalities commonly associated with mycosis fungoides. Using cDNA microarray analysis, a signature of 27 genes, including oncogenes and other genes involved in the control of apoptosis, has been recently identified in cases of early- and late-stage mycosis fungoides . Oncogenes such as p16 and p53 do not show alterations in early lesions, but are often mutated in late (tumour) phases
of the disease. Amplification and overexpression of JUNB has been found in one study .
Rearrangement of the T-cell receptor (TCR) gene is commonly found in plaques and tumours, but is present in only approximately 50% of early (patch) lesions [55,56]. Development of 'patient-specific' DNA probes can identify the neoplastic clone in lesions that are not specific histopatho-logically [57-59].
The presence of a monoclonal population of T lymphocytes has been detected in the peripheral blood in patients
with early-stage mycosis fungoides [28-30]. In many of these patients, the clone was different from that detected within the skin, but in some cases the same clone was present both in the peripheral blood and in the cutaneous lesions of mycosis fungoides, even after successful treatment and complete clinical remission [28,30,31]. The exact diagnostic and prognostic value of molecular genetic analysis of the TCR gene rearrangement within the peripheral blood in patients with early mycosis fungoides is still unclear .
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