Fig 1.
Location of primary tumors on the body of melanoma patients and their route of progression.
Red font represents poor prognosis (“non-survivors”), green font represents good prognosis (“survivors”).
Table 1.
Clinical information of patient characteristics.
Breslow thickness and Clarks refer to primary melanoma feature.
Fig 2.
(A) Overall survival of the prognostic groups, “survivors” (group 1) and “non-survivors” (group 2). (B) All ten cases were subjected to rigorous review both on histological and clinical grounds. (C) Those were omitted (lighter grey text), where the tumor content of the examined tissue was low (<10%) or the clinical follow-up data resulted in non-disease-specific outcome measures (one patient in group 2 died without evidence of malignancy). Abbreviations: l: left; r: right; LN met: lymph node metastasis; CNS: central nervous system; tx: therapy. Numbers in brackets mean lymph nodes containing metastatic melanomas / all lymph nodes dissected from either the groin or the axilla: nmetastatic/nall.
Table 2.
Histopathological properties of the melanoma metastases evaluated in this study.
The ten tumors are grouped according to clinicopathological classification.
Fig 3.
(A) Volcano plot showing differences in approximate protein abundance between survivors and non-survivors. T-test p-value and mean fold difference shown (protein abundance evaluated as sum of PSMs). (B) As in (A), but only significant proteins shown (p<0.05). (C) Biological relationship network (IPA) for proteins differentiating between survivors and non-survivors (shown in B), and having literature links to melanoma or metastasis. Only significant proteins shown (T-test p-value below 0.01), excluding proteins having no IPA relationships within the presented set.
Fig 4.
Identified melanoma markers and pathobiological processes in tissue samples of melanoma lymph node metastases.
The graphics displays key upstream regulators found according to analysis based on DAVID and IPA evaluation. The graph displays major regulated canonical pathways and subnetworks resulting in cellular functions and molecular fingerprints providing survival advantage for malignant cells with promotion to further progression and metastasis.