melanoma resembling Spitz nevus part2

CASE OF THE WHENEVER #24, PART TWO OR WHY I DO NOT DO TELEPATHOLOGY

This case is presented for two reasons. 1.) I was inspired by the teaching value of a case having ambiguous morphologic features presented by Reed and Mihm. 2.) I am occasionally asked to establish a telepathology practice; this case illustrates reasons why I do not do this.

The sequence of examination of various fields on a slide is determined by subconscious algorithms that start with the recognition of images that have proven diagnostic value to an individual pathologist. The submitting pathologist in a telepathology situation is, by definition, having difficulty with the case and may not select these key images. There has been progress in methods for depicting difficult cases (see Kutzner et al and/or Balis) but such methods either are not generally available or are very time consuming.

All of the images in Part Two are taken from the same slide (except Fig. 11b) that was used for Part One. The selection of fields in Part One was based on the premise that the submitting pathologist thought this might be a benign lesion, specifically a spindle cell nevus (Spitz). The selection of fields in Part Two was dictated by the initial impression that this is a malignant melanoma, which is how I signed it out. Fascinating conjecture regarding the probably biology of this lesion will not be delved into.

SOME ACCEPTABLE DIAGNOSES

Nevoid melanoma. Inasmuch as this melanoma is symmetrical in profile and it has a component of closely spaced, small clusters of minimally atypical cells (in addition to frank melanoma), it could be argued that this is a nevoid melanoma. The use of that term should be done with the realization that some fully malignant melanomas, some minimal deviation melanomas, and some borderline lesions might fit into that category. Therefore the term has descriptive value but not prognostic value.

Superficial spreading melanoma. Areas having the features of the radial growth component of a superficial spreading melanoma combined with a vertical growth component typically of the type found in common superficial spreading melanomas would justify this diagnosis. By placing this melanoma into a category that is familiar to oncologists, one avoids telephone inquiries as to the meaning of other terms. This diagnosis might be appended with qualifiers such as 'having some of the features of a spindle cell nevus' or 'arising in a background of compound melanocytic dysplasia' or 'arising in a background of minimal deviation melanoma'..

Fig. 8: This is just a larger picture that is in better focus than that seen in Fig. 1 Part1. Unfortunately, the quality of images submitted for telepathologic diagnosis may be of inferior quality.
Although the overall profile is symmetrical, there are clusters of varying size composed of cells of varying cytology. Therefore, there is internal asymmetry with abnormal cell constituents being found side to side. I stress 'abnormal cell constituents' since many normal compound and intradermal nevi are asymmetrical from top to bottom (so-called maturation), and some nevi contain morphologically dissimilar cells on either side of each other. The juxtaposition of clusters of abnormal cells is disturbing, even at this magnification..
The cluster that is just to the left of center has expansile properties, and this finding should alert one to the probability that this is some type of malignant melanoma.

Fig. 9: The expansile nature of the cluster is manifested by the curved modification of the adjacent rete ridge. Note the 'nests within nests' pattern. This pattern is seen more often in melanomas than in nevi. There also is atypical intraepidermal melanocytic hyperplasia (dysplasia).

Fig. 10: High power view of above. This pattern is typical for vertical growth in a melanoma. The cells to the left of the epithelioid cells are also abnormal but not frankly malignant cytologically.

Fig. 11a: High power view from an area close to the expansile cluster. Pagetoid melanocytes and clusters of large, atypical, epithelioid melanocytes qualify this as the fully developed radial growth component of an ordinary superficial spreading melanoma.

Fig. 11b: Composite medium power view taken from another slide of the same lesion. Radial growth component of superficial spreading melanoma.

Fig. 12 (Fig. 7, Part 1 revisited:)
A false impression of 'maturation' can be created by the fact that pre-existing nevus cells can be displaced downward by the melanoma. Another mechanism is the stratification created by sequential invasion of phenotypically different dysplastic or melanoma cell populations. The large, atypical, epithelioid melanoma cell population seen in the top of the picture usually arrives after pagetoid spread develops in the overlying epidermis. I target the deepest cells that are not unequivocal normal nevus cells for the Breslow's measurement.

Fig. 13: This particular melanoma is polymorphic in that there are minimal deviant cell populations in closely spaced, small clusters (variant vertical growth pattern). This can be confused with combined nevus patterns. Pushing borders in apposition with abnormal cell populations favor melanoma.

Click on PART 3 for some general remarks.
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	Fig. 9: The expansile nature of the cluster is manifested by the curved modification of the adjacent rete ridge. Note the 'nests within nests' pattern. This pattern is seen more often in melanomas than in nevi. There also is atypical intraepidermal melanocytic hyperplasia (dysplasia).
	Fig. 10: High power view of above. This pattern is typical for vertical growth in a melanoma. The cells to the left of the epithelioid cells are also abnormal but not frankly malignant cytologically.
	Fig. 11a: High power view from an area close to the expansile cluster. Pagetoid melanocytes and clusters of large, atypical, epithelioid melanocytes qualify this as the fully developed radial growth component of an ordinary superficial spreading melanoma.
	Fig. 11b: Composite medium power view taken from another slide of the same lesion. Radial growth component of superficial spreading melanoma.
	Fig. 12 (Fig. 7, Part 1 revisited:) A false impression of 'maturation' can be created by the fact that pre-existing nevus cells can be displaced downward by the melanoma. Another mechanism is the stratification created by sequential invasion of phenotypically different dysplastic or melanoma cell populations. The large, atypical, epithelioid melanoma cell population seen in the top of the picture usually arrives after pagetoid spread develops in the overlying epidermis. I target the deepest cells that are not unequivocal normal nevus cells for the Breslow's measurement.
	Fig. 13: This particular melanoma is polymorphic in that there are minimal deviant cell populations in closely spaced, small clusters (variant vertical growth pattern). This can be confused with combined nevus patterns. Pushing borders in apposition with abnormal cell populations favor melanoma.