The aggressiveness of mucosal melanoma may be explained by its late presentation and delayed diagnosis, the vascularity of the mucous membranes, which promotes hematogenous metastases, or by cellular and molecular differences that have been shown to exist between cutaneous and mucosal melanoma[ 2 5, ].
Single locus or multilocus molecular data and/or morphological differences have been used previously to identify cryptic species diversity in southeast Asian [ 10, 48, 49] and African [ 50, 51] hipposiderids.
Thorough characterization of these conditions using proteomic profiling methods has increased our knowledge of these molecular differences and has helped to unravel the complexity and heterogeneity of this debilitating condition.
These differences have stimulated the search for molecular markers of strain phenotypes and host tropisms.
53 Reasons for such differences have been suggested to be genetic, pathologic, molecular, and/or socioeconomic.
These findings lead to the conclusion that the differences in TN-IBC and TN-non-IBC are from a very subtle molecular difference or have nothing to do with the tumor itself.
Product differences have faded.
The molecular basis for these differences has not been addressed yet.
For example, the molecular basis of caste differences has been investigated in bees [ 30- 35], ants [ 36, 37], wasps [ 38], and termites [ 13, 39- 41].
In addition, if in vivo changes during infection were responsible for the clinical and environmental isolate molecular differences we would have expected the clinical isolates to differ from each other, and this is not the case (Figure 5B).
