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Sentinel Lymphadenectomy Does Not Increase the Incidence of In-Transit Metastases in Primary Melanoma

From the Roy E. Coats Research Laboratories of the John Wayne Cancer Institute at Saint John’s Health Center, Santa Monica, CA

Address reprint requests to Donald L. Morton, MD, John Wayne Cancer Institute, 2200 Santa Monica Blvd, Santa Monica, CA 90404; e-mail: mortond{at}jwci.org

PURPOSE: Recent reports by European investigators suggest that sentinel lymphadenectomy (SLND), a mainstay of melanoma diagnosis and treatment planning, increases the risk of in-transit metastasis (ITM) and should be abandoned. This study compared the incidence of ITM after wide local excision (WLE), WLE plus SLND (SLND), or WLE plus elective lymphadenectomy (ELND) for primary melanoma.

PATIENTS AND METHODS: Review of our prospective database identified 4,412 patients who underwent WLE (n = 2,771), SLND (n = 1,016), or ELND (n = 625) for stage I/II melanoma (1971 through 2002). The incidence of ITM overall and as a first recurrence was examined before and after computerized prognostic matching of treatment groups. Intergroup statistical comparisons used ² analysis and log-rank test.

RESULTS: The incidence of ITM increased with Breslow depth, Clark level, and T stage. Although overall incidence of ITM was significantly higher (P = .0008) after ELND (6.56%) versus WLE (3.36%) or SLND (3.64%), the ELND group had higher risk primaries. Treatment groups matched by T stage (1,875 patients; 625 per group) or by age, sex, Breslow depth, and primary location (1,680 patients; 560 per group), showed no significant differences in ITM overall or as a first recurrence.

CONCLUSION: There is no relationship between SLND and ITM. Recent reports to the contrary reflect analysis of significantly smaller cohorts not matched for confounding variables such as T stage. The phase III Multicenter Selective Lymphadenectomy Trial will definitively settle the issue; until then, use of SLND, the most accurate staging procedure for early-stage melanoma, should continue.

Supported by grant CA29605 from the National Cancer Institute and by funding from the Amyx Foundation Inc (Boise, ID); Alice Johnson McKinney, the Harold J. McAlister Charitable Foundation (Los Angeles, CA); Nancy and Carroll O’Connor (Los Angeles, CA); the George Hoag Family Foundation (Los Angeles, CA [R. Essner]); and the Saban Family Foundation (Los Angeles, CA [R. Essner]).

Presented at the Annual Meeting of the Society of Surgical Oncology, Atlanta, GA, March 3-6, 2005.

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

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