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Fig. P1-1: The lesion is polypoid at the
surface of the skin. There are regional variations in patterns. From right to left in the polypoid portion, there is a reduction in the degree of basophilia. This in large
part reflects a cytologic variation in which the cells on the left side of the polypoid portion have more cytoplasm and nuclei are more widely spaced. In the cellular, more basophilic portion on the right, the
cells resemble common nevus cells. In the component on the left, the cells show mild to moderate cytologic atypia. The oval, dark blue area to the left
and above the center of the field is a small cluster of lymphocytes within a nest of atypical spindle cells.
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This melanocytic neoplasm focally deviates from patterns seen in common nevi. The lesion is fairly solid and expansile (nodular) to the left of the center of the field. On the other hand, to the right of the center
of the field, the patterns offer support for the interpretation that the nodular component has had its origin in a common nevus. The pattern to the left raises the question of whether the nodular component is
vertical growth. It satisfies morphologic criteria for the recognition of vertical growth, as defined in the concept of minimal deviation melanoma.
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Fig. P1-2: This section is near the margin
of the lesion. Rete ridges are cut in cross section just to the left of the center of the field. In the polypoid portion to the right, fascicles of distinctive cells are irregularly
spaced in a widened papillary dermis. In the center of the field at the interface between the papillary dermis and the reticular dermis, a nevus cell component is represented.
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In this second field, the nevus-like patterns, to the left and below, are interrupted in the superficial portion of the polypoid component, to the right of the center of the field. Again, the patterns in the
superficial polypoid component deviate somewhat from the collection of virtual images which we use to characterize a common nevus. The lesion, even at this magnification, is remarkable for its lack of
inflammation.
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Fig. P1-3: In the center of the field and to
the left, the epidermis shows regular elongation of rete ridges. In this component near the center of the field, there is lentiginous melanocytic dysplasia of indeterminate type: the cytologic atypia
is not associated with markers for host immune response. Small nests of atypical spindle cells are loosely spaced in the underlying dermis.To the right, the
patterns resemble those of a common nevus but there is cytologic atypia in the nests near the dermal-epidermal interface and, again, there are no significant markers for host immune response.
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Although the patterns to the right are nevus-like, the psoriasiform patterns to the left are not a regular feature of common nevi. In the psoriasiform component, plump melanocytes are arranged in lentiginous patterns
but are not associated with markers for host immune response. On the basis of atypia in the lentiginous component, the lesion might be characterized as a melanocytic dysplasia but, in the absence of markers for host
immune response, the lesion is not acceptable as a marker for the dysplastic nevus syndrome. Lentiginous and junctional dysplasias which lack markers for host immune response might be best characterized as
dysplasias of indeterminate type. The small fascicles of spindle cells in the dermis beneath the psoriasiform component might tempt some observers to classify the lesion as a Spitz variant.
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There are regional variations in patterns. In the column outlined by green arrows, there is continuity with the epidermis and, with this marker, the column might be characterized as the progeny of a neoplastic
population which is evolving at the dermal-epidermal interface. The population above the red arrows has the features of a common nevus (the lesion has apparently had its origin in a preexisting nevus). On the other
hand, the sheet of nevus-like cells to the right of the blue arrows might be cited as a new clone manifested in the cytologic features of a common nevus; this population could thus be characterized as a dysplasia
lacking a primary configuration (i.e., lacking continuity with the epidermis). It would qualify as a marker for a low grade dermal dysplasia.
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Fig. P1-5: A classic nevus cell component is represented. In the nest outlined by blue arrows, there is cytologic disparity; cytologic atypia is moderate. This nest is in continuity with a junctional nest
as seen in fig. 4. To the left of the green arrows, the lesion is more densely cellular although the cells individually somewhat resemble common nevus cells.
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The pattern to the right of the green arrows provides a clear marker for a remnant of a common nevocytic nevus. The more classic, common nevus cell component is complicated by a column of cells of different cytologic
nature (blue arrows). The column might be interpreted as a manifestation of intralesional transformation.
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Fig.P1-7: The zone of nevus-like
cells in sheets is represented to the left of the green arrows. A small portion of the classic nevus cell component is represented in the lower right corner of the field (red arrows). Yellow arrows outline a
column of disparate “nevus” cells in continuity with the epidermis.
Blue arrows outline a nest of disparate (atypical) “nevus” cells. This nest of cells in not in continuity with the epidermis (i.e., dermal intralesional transformation).
Although there are cytologic variations in patterns, the atypia is mild to moderate and markers for host immune response are scantily represented;
atypia is seen in the column outlined by yellow arrows, the micronodule outlined by blue arrows, and in the sheet of nevus-like cells to the left of the green arrows..
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The column outlined by yellow arrows is composed of atypical cells and is in continuity with the epidermis. These features identify the column as the site of neoplastic progressions, and additionally identify the
junctional component as the source of the neoplastic cells; this is progression at the dermal-epidermal interface in accretive patterns. In this type of neoplastic progression, the epidermal component is the
generative nidus and cells in this location generally are more advanced neoplastically than any cells in the underlying dermis (for as long as vertical growth has not ensued). The population outlined by blue arrows
is isolated in the dermal population and might be cited as evidence of progression in the dermal component, independent of the phenomena at the dermal-epidermal interface (see Whithers1, 2, & 3). Green arrows delimit a portion of an expansile (nodular) component but atypia is too mild to characterize this component as convincing vertical growth..
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The population of deviant cells of junctional origin is outlined by yellow arrows. The deviant cells have hyperchromatic nuclei, and slightly more cytoplasm. They are less intimately attached to their neighbors.
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Fig. P1-9a (see extreme left corner of P1-6): Plump junctional and dermal nests of nevus-like cells are represented to the left of the center of the field. The papillary dermis is widened but
essentially free of markers for host immune response (i.e., lamellar fibrosis and infiltrates of lymphocytes).
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Fig. P1-9c (see extreme right corner of P1-6; region of green arrows): common nevus cells in common patterns are represented in the papillary dermis and at the interface between the papillary dermis
and the reticular dermis.
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PICTORIAL 1 - 2 - 3
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