p53 and bcl‐2 expression do not correlate with prognosis in primary cutaneous large T‐cell lymphomas

Abstract

Overexpression of p53 protein in cutaneous T‐cell lymphoma (CTCL) has been reported in primary cutaneous large T‐cell lymphomas (PCLTCL) and has been associated with tumor progression and transformation in mycosis fungoides. However, the prognostic significance of p53 expression has not been studied thus far. In the present study we investigated the expression of p53 as well as bcl‐2 protein in 27 PCLTCL, including 19 CD30‐positive and 8 CD30‐negative lymphomas, retrieved from the registry of the Dutch Cutaneous Lymphoma Working Group. The results were correlated with follow‐up data and proliferative activity, as assessed by the percentage of MIB‐1 positive tumor cells. Overexpression of p53 protein, defined as nuclear staining of more than 5% of the tumor cells, was found in 10 of 27 cases (37%), including 6 of 19 (32%) CD30+lymphomas and 4 of 8 (50%) CD30–PCLTCL. bcl‐2 protein was expressed in 6 of 19 (32%) CD30+lymphomas and in only 1 of 8 (12%) CD30–PCLTCL. However, no significant correlation between p53 or bcl‐2 expression and prognosis was found, neither in the whole group, nor within the CD30+ or CD30– group. In addition, no relationship between p53 expression and proliferative activity was found. The results confirm that p53 expression is more common in PCLTCL than in mycosis fungoides and Sézary syndrome. However, neither p53 nor bcl‐2 expression correlated with survival or proliferative activity.

Genomic Aberrations and Survival in Cutaneous T Cell Lymphomas

“…Well-known tumor suppressor genes such as tumor protein 53 (P53; 17p13.1) and CT-10 regulator of kinase (CRK; 17p13.1) are encoded in this region. Similar to our chromosomal findings, a study of P53 expression in CTCL did not find a correlation with prognosis (van Haselen et al, 1997).…”

Expression of p53 and retinoblastoma gene in high‐grade nodal peripheral T‐cell lymphomas: immunohistochemical and molecular findings suggesting different pathogenetic pathways and possible clinical implications

“…41 Our findings showed that p53 was detected by immunohistochemistry in 9/45 cases (20 per cent), while molecular analysis did not show the presence of mutations in exons 4-8 in any of these cases. These results are not substantially different from those of Matsushima et al on HTLV-1-negative post-thymic T-cell lymphomas 37 or those of de Misa et al, 38 Marks et al, 39 and Van Haselen et al 40 on cutaneous T-cell lymphomas, indicating altogether that p53 is detectable by immunohistochemistry in 20-50 per cent of PTCL cases. Since p53 expression is rarely due to mutation, this presumably reflects an abnormality of the functional pathway of p53, resulting in the accumulation (or stabilization) of a wild-type protein, which then becomes detectable by immunohistochemical analysis.…”

“…[38][39][40] Conversely, p53 mutations seem to be more frequent in HTLV-1-positive adult T-cell leukaemia/lymphoma. 41 Our findings showed that p53 was detected by immunohistochemistry in 9/45 cases (20 per cent), while molecular analysis did not show the presence of mutations in exons 4-8 in any of these cases.…”

Consequences of p16 tumor suppressor gene inactivation in mycosis fungoides and Sézary syndrome and role of the bmi-1 and ras oncogenes in disease progression

“…The classical cell cycle-control gene p53 has been reported to be overexpressed in late stages of CTCL, that is, during large-cell transition [4][5][6][7]. However, the importance of this finding for the prognosis is controversial [8].…”