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In Chapter 3 ((pictorial 7),), we are now 7 years away from the time of the initial biopsy procedure and the subsequent surgical excision of the skin lesion. The patient presented with
an enlarged lymph node which was excised. The lesion measured, on the slide, 3 x 1.5 cm. It was a multi-nodular tumor. In one area at the periphery, the architecture of a preexisting lymph node was preserved (C7P4-1). The tumor was a metastasis to a regional lymph node.
The tumor is composed of ‘large,’ spindle and round (‘epithelioid’) cells in the pattern of solid sheets (C7P4-2). Focally, in areas of
degeneration, the cells are loosely spaced in a clear, delicate, fibrous matrix. The cells have round or oval nuclei and show variations in nuclear size. Nuclear chromatin patterns are open and nucleoli are
prominent. Mitoses are fairly regular in distribution. In areas of degeneration, there are scattered melanophages among the loosely spaced tumor cells. Some of the tumor cells are melanogenic (C7P4-3). The tumor cells are immunoreactive for S-100 protein and HMB45 (C7P4-4&5). The patterns and the immunoreactions are in keeping with metastatic melanoma.
DISCUSSION and CONCLUSIONS
The patterns of the lesions in the skin and the lymph node, and the sequence of events are in keeping with a diagnosis of minimal deviation melanoma. We can take
the interpretation to another level and characterize the skin lesion as a MDM of halo nevus-like type in a primary configuration. The primary lesion also qualifies as showing: 1.) patterns of variant vertical
growth, 2.) halo nevus-like phenomena, and 3.) a vertical dimension of less than 1.0 mm. The lesion additionally qualifies as borderline (it measures less than 1 mm in vertical dimensions) melanocytic
neoplasia of indeterminate malignant potential.
With this characterization, the overall clinical course provides evidence that the lesion had already metastasized to a regional node at the time of the initial
biopsy of the skin lesion; the metastasis was occult and remained so for years. Although the original lesion had been interpreted as a minimal deviation melanoma, the vertical dimensions of the lesion did not
warrant a recommendation for a regional lymph node dissection. Currently, such a lesion might be cited as justification for a sentinel lymph node biopsy. Dr. Bill Weems and Dr. Ron Barr can attest to the value
of sentinel lymph node biopsies in providing useful diagnostic information for the management of some examples of minimal deviation melanoma.
In my experience, metastases from thin (borderline) MDM of halo nevus-like type are extremely uncommon. In this category, I would be more concerned about a
lesion in a primary configuration than about a lesion of dermal type. In the former variant, the lesion seems to evolve primarily from a population of cells at the dermal-epidermal interface and nests of cells
are delivered in sequence to a widened, inflamed papillary dermis; the kinetics of neoplasia are similar to those of the sequenced phenomena in the evolution of common premalignant dysplasias to common melanomas;
the same criteria for diagnosis and prognosis can be utilized. In the alternate form of MDM of halo nevus-like type, the neoplastic progressions seem to evolve mostly in a population of dermal melanocytes or
nevus cells rather than in primary configurations at the dermal-epidermal interface. Plump, epithelioid cells are a characteristic of the progressions in the dermal component. Often, mitoses are infrequent.
Commonly, a remnant of a common nevus is preserved in the dermis adjacent to the dermal nodule. In the nodule, the nests of cells may be closely, or loosely, clustered. Lymphoid infiltrates in halo nevus-like
patterns may be relatively confined to the periphery of such a lesion, intermingled among nests of tumor cells and remnant nevus cells. They may be multifocal among the nests of neoplastic cells
forming the nodule.
The neoplastic cells in the dermis of a MDM of halo nevus-like type in a primary configuration, often are small, uniform cells and often are round cells (as they
are in this case). They may be round or spindle shaped. In contrast, the cells in the dermal nodule of a MDM of halo nevus-like type lacking a primary configuration (i.e., dermal variant) often are plump,
round cells, and often the chromatin patterns of the nuclei of these cells are dense.
The lentiginous and junctional component extends in the epidermis beyond the dermal component on one of the sections. On the basis of this pattern of lateral
extensions, the lesion qualifies as a MDM arising in an atypical halo nevus (as defined in the concept of MDM). As previously mentioned, the upward migration of cells and nests of cells in the epidermis is a
feature commonly emphasized in the diagnosis of melanoma in situ. It is also an important feature in the definition of the common final pathway as emphasized in the concept of MDM. If, in turn, the observer then
classifies our problem lesion as a variant of superficial spreading melanoma, he will have ignored a large parcels of virtual images having relevance to the category of halo nevus-like phenomena. Admittedly, tumor
infiltrating lymphocytes, as emphasized in prognostic evaluations, result in patterns that from another perspective could be accommodated in the concept of halo nevus-like phenomena.
The cytologic and histologic patterns in the nodal metastasis differ markedly from the patterns of the primary lesion. The differences, when the two lesions are
compared, include deviations in the patterns produced by aggregates of cells and even in the features of individual cells. The thin, loosely spaced nests of the primary lesion contrast with the solid sheets of cells
in the metastasis. The uniform, small cells of the primary lesion contrast with the large cells and focal cellular pleomorphism of the metastasis. These variations, which might at first glance be dismissed as
evidence that the two components are not sequentially related, can be accommodated in the concept of progressive neoplastic transformations (i.e., dedifferentiation). They are relevant to the very features which are
emphasized in the definition of both the common final pathway, and superficial spreading melanoma (as opposed to the patterns in earlier stages of neoplastic progressions as exemplified in lesions of minimal
deviation melanoma). Quite simply, over a period of nine years, the cells of the metastases have progressed considerably from the stage of neoplasia in the primary lesion; the two populations are genetically related
but neoplastically distant, one to the other.
I would not waste time contesting with those observers who would simply dismiss the primary lesion as nothing more than superficial spreading melanoma. Perhaps,
the observers, who might classify the lesion as ‘nevoid’ melanoma without additional qualifications, would approach such a contest with smugness and confidence; I would suggest that such an assignment is merely a
peak into a neoplastic process in which many clues will always remain puzzles for those find comfort in an unqualified diagnosis of ‘nevoid’ melanoma. The latter category is the trash of complacent pathologists who
are only superficially concerned with the secrets of complex histologic patterns.
The long interval between diagnosis of the primary lesion and the excision of the metastasis is not uncommon in the category of MDM. It may speak for the relative
indolence of a tumor in vertical growth in minimal deviation patterns in a primary lesion. Just as minimal deviation primary lesions may lose their histologic distinctiveness, if left to evolve to higher stages of
neoplasia in the primary site, minimally deviant cells, having been transported to metastatic sites, have the potential to progress to higher grades of neoplasia. There are no features in the metastasis which could
be cited as a definite link to an earlier lesion of halo nevus-like type. The metastasis has in essence entered the common final pathway in which a variety of malignant neoplasms of diverse lineage come to resemble
one another.
What is embodied in the concept is dismissed by some with the observation that what I do is philosophy, not pathology. It could be argued that I created the tools
for the interpretation of halo nevus-like variants, and have used the creations to assign foolish significance to insignificant patterns. From the same perspective, melanoma in situ is a comparable delusion,
differing only in its simplicity and lack of challenge. The diagnosis, ‘melanoma in situ,’ presented no challenge for its chief proponent; it antedated his
discovery of it and a simple acceptance was all that was required. There is no challenge for an observer, who, in using this tool, is merely endorsing a stipulation and in the process mistaking a creation for a
biologic truth; there are no challenges, which in the pursuit thereof, might betray the secrets of the respective neoplastic process (these secrets are relatively secure, if ‘melanoma in situ’ is selected as a
satiation for the lure which might otherwise lead to an unmasking of the secrets of the morphology of neoplasia). Perhaps, the concept of MDM is out of order in time and place. Hopefully, it will be viewed
differently when egoistic pressures become a less important consideration.
On review, there is a certain bitterness in my approach. I regret it but will leave it a marker of my feelings at the time I wrote this.
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