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Continuation:
The lesion in question is so bland and so at peace with its surroundings that it would be tempting to classify the lesion as organoid. In the mid “60’s,” I
actually classified somewhat similar lesions as organoid melanomas. My “organoid” melanomas would be comparable to some of the lesions currently being classified as “nevoid” melanomas.
It is tempting to compare some of the patterns in the problem case to those of a common nevus. In this approach, the lesion is lentiginous, junctional, and dermal
(i.e., it is compound). One feature strongly against the notion that this is a peculiar congenital nevus is the observation that on the original biopsy the nests of cells at all levels of the dermal component are
rounded in outline; this quality is not a feature of common congenital nevi. The next consideration is an evaluation of cytologic atypia. This is a task requiring the evocation of relevant virtual images. Relevant
images must be a part of our stores to allow for meaningful evaluations of degrees of atypia. Some of you have been told, and then some of you accepted, that such stores were beyond human resources. As a consequence
for you, degrees of atypia (and dysplasia) unfortunately are not pertinent to the classification of melanocytic neoplasms and unusual patterns; dermal components are likely to be dismissed as either representative
of a variant nevus or a common melanoma; the distinctions are likely to be as arbitrary as the flip of a coin.
Take the nesting patterns in the dermis and the degree of (monotonous) cytologic atypia, and try to fit them in our parcels of virtual images having utility in
the interpretation of COMMON NEVI and COMMON MELANOMAS. They don’t fit and alternatives are required. Add to all this the inability of the host to react to the abnormal cells in abnormal patterns in the dermis. The
absence of host immune response (another collective term for both lymphoid infiltrates and patterns of fibrosis) is another puzzling aspect of the consultation case, and perhaps one which would again lead the unwary
to the notion that the lesion is a nevus instead of a melanoma. Where are the lymphoid infiltrates and the lamellar fibrosis of an evolving melanoma? Even the lentiginous and junctional components are not associated
with the common markers of an evolving melanocytic premalignant dysplasia.
Do the patterns fit the mold (the parcel of virtual images) of a variant of lentigo maligna melanoma? The following are common features of lesions in the category of lentigo maligna and lentigo maligna melanoma:
1.) an epidermis with a straight interface and mild acanthosis or even atrophy, 2.) a prominence of lentiginous patterns and a preponderance of spindle cells in junctional components, 3.) involvement of hair
follicles by the lentiginous and junctional components, 4.) inflammation that often is mild, 5.) vertical growth in fascicular patterns (often in patterns of “variant” or “migrant” vertical growth - see Whithers,
above or to left and above in the MASTER BORDER), 6.) rather bland, monotonous nuclear characteristics, often
out of keeping with what might be expected at a particular level of invasion, and 7.) evidence of actinic damage. All these features are manifested in the consultation case, if both the original specimen and the
recurrent lesion are evaluated. Why the problems? The lentiginous and junctional component is spotty and the lentiginous component is not particularly dense. The nesting patterns in the dermis and the bland,
monotonous cytologic features are deviant qualities. On the original biopsy, the nests are rounded rather than fascicular and the small tumor cells are more likely to be characterized as epithelioid rather than
spindle shaped. In what manner can we accommodate the distinctions? The lesion is a minimally deviant (nevoid) variant but most of you have accepted that there is no utility in such an approach!
There are remarkable cytologic variations and even variations in patterns of cellular aggregation when the patterns on the original biopsy specimen are compared
to those of the recurrent lesion. Should we then assume that the two are unrelated other than in anatomic relationships? A more productive approach would be to attribute the distinctions to neoplastic progressions.
In support of this interpretation are the comparable stromal responses on both specimens. In addition, higher grades of nuclear atypia are represented on the 2000 material than on the 1993 material (Fig. P15-48, and Figs. P15-54 & 55). The last two photographs at the end of the page, PHOTOS3, provide a nice demonstration of the sequential changes in cytologic features that are evident when the 1993 material is compared with the 2000
material. The patterns of growth are less organized on the recent material. On the recent material, there are extensions into the subcutaneous fat and there are micronodular components which are associated with
lymphoid infiltrates.
Another disturbing aspect of the more recent material is an association between nests of tumor cells and small peripheral nerves (Fig. P15-53). Some of the patterns qualify as limited neurotropic spread. Neurotropism is another expression of variations in vertical growth patterns and should
be accepted as something more than a chance encounter between nerves and an infiltrating tumor. It is an inherent property that greatly modifies the behavior of the respective melanoma and, if a well developed
feature, greatly compromises the likelihood of successful control. It is a variation much more closely associated with spindle cells and fascicular patterns in vertical growth than with the common patterns of the
common melanoma (superficial spreading melanoma), It is closely associated with melanomas in the clinical and histologic setting of lentigo maligna melanoma. The most disturbing aspect of the recent material is the
presence of a partly “encapsulated” nodule in the subcutaneous fat (Fig. P15-51). The nodule is composed of melanogenic atypical cells and is associated
with dense peripheral infiltrates of lymphocytes. I have seen this pattern as the initial manifestation of neurotropic spread in minimal deviation (as defined above), pigmented spindle cell melanomas. There is
no clear evidence of extension of the tumor along a nerve away from the nodule on the available sections. There is extension of the tumor beyond the “capsule” into the lymphoid infiltrates and the fat in one limited
area at the periphery of the nodule. The surgical margins are free but the patient shoud be considered at risk and carefully followed for evidence of local recurrence and neurotropic spread into neighboring tissues.
In view of the long interval between the original biopsy and the “recurrence,” the patient should also be examined for occult metastases. The patient remains at risk for metastasis.
The lesion of the original biopsy specimen is a NEVOID MINIMAL DEVIATION LENTIGO MALIGNA MELANOMA. Its
distinguishing characteristics include: 1.) the lentiginous and junctional patterns of lentigo maligna, 2.) a migrant vertical growth pattern, 3.) bland cytologic features that are associated with nevoid nesting
patterns (i.e., rounded nests of uniform, moderately atypical, small, epithelioid cells), 4.) low mitotic rate, and 5.) lack of stromal response and absence of inflammatory infiltrates. The recurrence is
additionally distinguished by: 1.) evidence of neoplastic progression (i.e., greater atypia and even a change in phenotype, expressed in spindle cell and fascicular patterns), 2.) some evidence of minimal
neurotropic spread, 3.) irregular patterns of growth to level V, and 4.) markers for host immune reponse.
Richard J. Reed, M.D.
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