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Factors Predictive of Tumor-Positive Nonsentinel Lymph Nodes After Tumor-Positive Sentinel Lymph Node Dissection for Melanoma

From the John Wayne Cancer Institute, Santa Monica, CA

Address reprint requests to Richard Essner, MD, John Wayne Cancer Institute, 2200 Santa Monica Blvd, Santa Monica, CA 90404; e-mail: essnerr{at}jwci.org

PURPOSE: Approximately 20% of sentinel node (SN) positive melanoma patients have additional non-SN (NSN) metastasis. The rationale for this study was to identify the factors associated with additional nodal disease, as a method to determine which patients may most benefit from completion lymph node dissection (CLND).

PATIENTS AND METHODS: During 1990 to 2002, 1,599 patients have undergone SN biopsy at our institute. 19.5% underwent CLND for tumor-positive SN. One hundred ninety-one of these patients had clinicopathologic information available for review. Univariate analyses used ² test, Wilcoxson rank sum test, and ² test for trend. Multivariate analyses used logistic regression and Wald test.

RESULTS: Forty-six (24%) patients had tumor-positive NSN. Univariate analyses showed that primary thickness (Breslow and Clark), primary site, SN tumor size, and number of tumor-positive SNs were significantly associated with tumor-positive NSN. Multivariate analysis (167 patients), confirmed that Breslow and SN tumor size were independently predictive. Sex, histology, ulceration, mitotic index, and SN basin location were not predictive. Risk stratification by the number of prognostic factors present (Breslow 3 mm and SN tumor size 2 mm) showed that probability of finding tumor-positive NSN was 12.3% in the low-risk group (0 factors), 30.9% in the intermediate-risk group (1 factor), and 41.9% in the high-risk group (2 factors).

CONCLUSION: Thicker primary and larger SN tumor size are factors that correlate best with tumor-positive NSN. Although none of these factors are absolutely predictive of residual nodal disease, these factors must be strongly considered if the SN contains metastasis, as they provide enhanced risk assessment for NSN tumor-positivity.

This work was supported in part by the National Institutes of Health, Bethesda, MD (grant No. CA29605), Saban Family Foundation (Los Angeles, CA), George Hoag Family Foundation (Los Angeles, CA), Harold J. McAlister Charitable Foundation (Los Angeles, CA), and funding from Nancy and Carroll O'Connor (Los Angeles, CA).

This work has been presented at the 39th Annual Meeting of the American Society of Clinical Oncology, Chicago, IL, May 31-June 3, 2003, and received the Merit Award.

Authors' disclosures of potential conflicts of interest are found at the end of this article.

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