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The first 2 authors contributed equally to this work.
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Cancer Genetics
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Nuclear PTEN expression and clinicopathologic features in a population-based series of primary cutaneous melanoma
Article first published online: 26 FEB 2002
DOI: 10.1002/ijc.10294
Copyright © 2002 Wiley-Liss, Inc.
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How to Cite
Whiteman, D. C., Zhou, X.-P., Cummings, M. C., Pavey, S., Hayward, N. K. and Eng, C. (2002), Nuclear PTEN expression and clinicopathologic features in a population-based series of primary cutaneous melanoma. International Journal of Cancer, 99: 63–67. doi: 10.1002/ijc.10294
Publication History
- Issue published online: 27 MAR 2002
- Article first published online: 26 FEB 2002
- Manuscript Accepted: 14 DEC 2001
- Manuscript Revised: 29 NOV 2001
- Manuscript Received: 22 OCT 2001
Funded by
- Queensland Cancer Fund
- National Health and Medical Research Council of Australia
- American Cancer Society. Grant Number: RPG98-211-01
- National Cancer Institute. Grant Number: P30CA16058
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Keywords:
- PTEN;
- p53;
- 10q;
- skin;
- melanoma
Abstract
Germline mutations of the PTEN tumor-suppressor gene, on 10q23, cause Cowden syndrome, an inherited hamartoma syndrome with a high risk of breast, thyroid and endometrial carcinomas and, some suggest, melanoma. To date, most studies which strongly implicate PTEN in the etiology of sporadic melanomas have depended on cell lines, short-term tumor cultures and noncultured metastatic melanomas. The only study which reports PTEN protein expression in melanoma focuses on cytoplasmic expression, mainly in metastatic samples. To determine how PTEN contributes to the etiology or the progression of primary cutaneous melanoma, we examined cytoplasmic and nuclear PTEN expression against clinical and pathologic features in a population-based sample of 150 individuals with incident primary cutaneous melanoma. Among 92 evaluable samples, 30 had no or decreased cytoplasmic PTEN protein expression and the remaining 62 had normal PTEN expression. In contrast, 84 tumors had no or decreased nuclear expression and 8 had normal nuclear PTEN expression. None of the clinical features studied, such as Clark's level and Breslow thickness or sun exposure, were associated with cytoplasmic PTEN expressional levels. An association with loss of nuclear PTEN expression was indicated for anatomical site (p = 0.06) and mitotic index (p = 0.02). There was also an association for melanomas to either not express nuclear PTEN or to express p53 alone, rather than both simultaneously (p = 0.02). In contrast with metastatic melanoma, where we have shown previously that almost two-thirds of tumors have some PTEN inactivation, only one-third of primary melanomas had PTEN silencing. This suggests that PTEN inactivation is a late event likely related to melanoma progression rather than initiation. Taken together with our previous observations in thyroid and islet cell tumors, our data suggest that nuclear–cytoplasmic partitioning of PTEN might also play a role in melanoma progression. © 2002 Wiley-Liss, Inc.