Studies which have found that histologic features of metastatic melanoma in sentinel lymph nodes (SNs) were predictive of survival have differed considerably in their design and results. We investigated in detail the influence of SN tumor characteristics and clinical and primary tumor parameters on clinical outcomes in a large cohort of patients treated in a single center.
In SN-positive melanoma patients, the association of clinical, primary tumor, and SN tumor features [maximum size (MaxSize), % cross-sectional area of SN occupied by tumor (%CS), tumor-penetrative depth (TPD), intranodal location of tumor, extranodal spread (ENS), and perinodal lymphatic invasion (PLI)] with disease-free (DFS), distant metastasis-free (DMFS), and melanoma-specific (MSS) survival was analyzed.
In 409 SN-positive patients, independent predictors of poorer DFS were primary tumor features [anatomic site: head/neck (HR = 3.65, 95% CI 1.65–8.08) and limbs (HR = 2.46, 95% CI 1.21–4.98) compared with trunk; ulceration (HR = 1.70, 95% CI 1.15–2.51); satellites (HR = 2.85, 95% CI 1.49–5.44)], SN tumor features [MaxSize (HR = 1.53, 95% CI 1.04–2.26); ENS in SN (HR = 2.05, 95% CI 1.06–4.00); PLI (HR = 1.85, 95% CI 1.11–3.07)], and positive CLND (HR = 1.92, 95% CI 1.26–2.91). Factors independently predictive of poorer MSS were age ≥50 years (HR 1.64, 95% CI 1.01–2.67), primary tumor features [ulceration (HR = 2.55, 95% CI 1.44–4.52); satellites (HR = 3.95, 95% CI 1.83–8.49)], and ENS in SN (HR = 2.34, 95% CI 1.06–5.13).
The use of clinical, primary tumor, and SN tumor characteristics shown to be independent predictors of clinical outcomes in melanoma patients will assist in accurate prediction of prognosis and optimize clinical management.
In 409 sentinel node (SN)-positive melanoma patients, independent predictors of poorer disease-free survival were primary tumor features (anatomic site: head/neck and limbs compared to trunk; ulceration; satellites), SN tumor features (maximum size, extranodal spread, perinodal lymphatic invasion) and positive non-SNs.
*Tissue Pathology and Diagnostic Oncology, Royal Prince Alfred Hospital, Sydney, NSW, Australia
†Melanoma Institute Australia, Sydney, NSW, Australia; and
‡Discipline of Pathology, Sydney Medical School, The University of Sydney, Sydney, NSW, Australia; and
§Discipline of Surgery, Sydney Medical School, The University of Sydney, Sydney, NSW, Australia
Reprints: Dr. Rajmohan Murali, Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, Box 20, New York, NY 10065, USA. Email: MuraliR@mskcc.org
Sources of support: Professor Scolyer is a Cancer Institute New South Wales Clinical Research Fellow.