c<i>-myc</i> Is Not Useful as Prognostic Immunohistochemical Marker in Cutaneous Melanoma

Abstract

Background: Several studies indicate that immunohistochemical detection of the c-myc oncogene might serve as an additional prognostic marker in malignant melanoma. Objective: To study c-myc expression in paraffin-embedded cutaneous melanoma and to correlate to metastatic potential and onset of metastases. Methods: Cytoplasmic c-myc protein expression was visualized using the APAPP method, and reactivity (percent total tumor cells stained) was assessed in 62 formalin-fixed paraffin-embedded primary cutaneous melanomas (21 not metastasizing, mean Breslow 3.0 ± 2.9 mm, 41 metastasizing, mean Breslow 3.1 ± 3.0 mm) and 24 metastases of the same patients. Results: There was no significant difference of c-myc reactivity in cutaneous melanoma who did not metastasize (n = 21, c-myc reactivity 32.7 ± 19.3%, follow-up 10.6 ± 1.8 years) and primaries who metastasized (n = 41, c-myc reactivity 27.7 ± 22.4%, p = 0.29). This finding was independent of the thickness of the primary and was found within thin cutaneous melanoma with a Breslow <0.75 mm (range 0.24–0.65 mm, n = 20, c-myc reactivity 29.1 ± 15.7%, p = 0.32) or within thick cutaneous melanoma with a Breslow >1.5 mm (range 1.6–11 mm, n = 41, c-myc reactivity 29.6 ± 23.8%, p = 0.46). No correlation of c-myc expression between thin cutaneous melanoma, thick cutaneous melanoma (p = 0.83) or metastasizing primaries and their metastases (n = 24, c-myc reactivity 29.3 ± 22%) was found (p = 0.64). The time period until development of first metastasis did not correlate with the percentage of cells expressing c-myc in the primary (p = 0.56). Conclusion: c-myc expression is independent of metastatic potential and onset of metastases and, therefore, does not serve as a prognostic immunohistochemical marker in primary cutaneous melanoma.

Expression of c-myc and bcl-2 in Primary and Advanced Cutaneous Melanoma

“…[20] Previous immunohistochemical and flowcytometric studies demonstrated an enhanced c-myc [21,22] and bcl-2 expression [23] in MMET. In accordance with the results of Böni et al, [24] no association between tumor thickness and c-myc expression at both the RNA and protein level could be found (data not shown). However, a positive correlation of an enhanced bcl-2 expression and tumor thickness could be found in NMM, concordant to previous results [18] and in SSM, but not in ALM and LMM.…”

The cytoplasmic Purkinje onconeural antigen cdr2 down-regulates c-Myc function: implications for neuronal and tumor cell survival

“…c-Myc has been detected previously in the cytoplasm of cell lines (Craig et al 1993) and tumor samples (Lipponen 1995;Pietilainen et al 1995;Boni et al 1998). In neurons, the detection of c-Myc in Purkinje cell cytoplasm parallels the observation that N-Myc, which is expressed in the nuclei of cerebellar Purkinje neurons during development, but localizes to Purkinje cell cytoplasm in adults (Wakamatsu et al 1993).…”

Oncogenes in melanoma

“…However, none of the 12 nevi revealed these changes (Kraehn et al, 2001). As critical as the activities of MYC alleles might be, their role in melanoma is uncertain at this point, as other studies have drawn conflicting conclusions (Boni et al, 1998;Chana et al, 2001). …”