184
Melanomata in Domesticated Animals
' tolerance of the
tissues
towards the
melanin-forming cells' of melanoma as a point
perhaps in favour of a mesoblastic origin of the
tumour. At the same time it appears certain
that in dealing with melanomata in man, the elabo-
ration of pigment by epiblastic elements must
also be considered [Ewing, 1934].
It is suggested [Ewing, 1934; Maximow and
Bloom, 1935] that the pigment-forming cell arises
very early in the formation of the mesenchyme
and exhibits specific properties, some of which
resemble those of epithelium, and that this would
explain the tendency of some melanomata, the
so-called melanocarcinomata, to manifest an
epitheliomatous histology. Ribbert [1897] and
others are inclined to attribute all naevi and
melanomata to aberrations of the mesoblastic
melanoblast. According to this view, the pig-
ment in the epidermis is derived from the dermal
melanoblast (mesodermal chromatophore) and the
formation of naevi and cutaneous moles would
follow excessive deposition of the pigment in the
skin, leading to proliferation of epidermal cells
with pigment formation [Ewing, 1934]. Summing
up the contention between the epi and mesodermal
origin of the chromatophore, Ewing says 'the
histological data appear to me strongly, but not
decisively, in favour of the epithelial origin,
while the theoretical considerations are all against
the epithelial theory'.
The suggestions of some earlier authors [Demi-
eville, 1880; Ziegler, 1908; Jaeger, 1911] regarding
the endothelial and perithelial origin of naevus
cells has found little support.
Recklinghausen [1882] and subsequently others,
have produced strong evidence to support the
contention that pigmented naevi and neurofib-
romatosis are related conditions. Nerve fibrills
have been detected in groups of naevus cells by
Soldan [1899], and by Masson[1926] who has shown
that naevi and melanomata arise from cells of the
end-apparatus of cutaneous sensory nerves
(Meissner's and Merkel's corpuscles) and that the
two should be considered as disorders of the
nervous system. The cells actually proliferate in
the neoplastic process, but their origin is not
definitely known. Masson's findings are expressed
in the following quotation from Ewing [1934].
'In the derma, the naevus cells come from the
cells of Meissner's corpuscles, in the epidermis,
they come from the cells of Merkel-Ranvier, and
from the chromatophores, in both situations.
Masson does not attempt to decide whether the
cells involved are mesodermal, glial, or epidermal
Whereas in the opinion of certain authors, the
evidence favours the epithelial origin of the
melanoblast [MacCallum, 1932], others, not with-
out reservation, consider this cell to be of meso-
blastic origin [Beattie and Dickson, 1926]. But
the view, in keeping with our present knowledge,
should be the one expressed by Ewing [1934]
Pigmented cells from melanotic sarcoma have
been shown to reveal in tissue cultures [Grand,
Chambers and Cameron, 1935] characters con-
sistent with a mesenchymal origin. But this
by no means precludes the possibility, not
yet exhaustively investigated, that cells taken
from melanotic carcinoma will reveal epithelial
characters in tissue cultures. It may be stated
here that Caylor and Schlotthauer [1926] were
unsuccessful in their attempt to transplant
porcine melanotic epitheliomata.
The position with regard to equine melanoma-
tosis is far from satisfactory. The work of van
Dorssen [1903] on the histology of equine skin
shows that, in coloured horses of all ages, the epi-
dermis is pigmented and the cutis devoid of
pigment-cells, but that in aged grey horses, the
opposite is the case. Unfortunately, information
on the situation of pigment in the skin of grey
foals is not available for comparison. Van Dors-
sen suggested that the pigment is conveyed to
the epidermis by dermal (i.e. mesoblastic) melano-
blasts and that in aged grey horses the demand for
pigment is so much diminished that it accumulates
in the cutis and, following the upset in pigment-
metabolism, the growth of melanomata results
(as mentioned earlier). On the contrary Schwalbe
[1893] found nothing to indicate the transport
of pigment from cutis to epidermis. Virchow-
views the frequency of the tumour in grey horses
as an evidence of congenital dyscrasia, although
why this should be so particularly in the grey
horse is not explained.
Whatever the origin of the melanoblast, the
question still remains. What is it that transforms
it into a neoplastic cell? The history of contu-
sion in one of our equine melanomata (1116/1927)
and the discovery of filariasis in a bovine tumour
(958/1926) may, however, have interest in view of
the statement of Kettle [1925] that in three of
his cases in man a history of previous injury by
a rusty nail was associated with the development
of melanoma on the foot, in the absence of a
pre-existing mole. Yet, one finds it difficult to
explain the notorious susceptibility of aged grey
horses to melanomatosis on the theory of chronic
'local' irritation, of toxaemia* or of microparasitic
invasion, for these factors must operate equally in
*Since writing, a paper has appeared by Hadwen [1937]
wherein he mentions that he has succeeded in producing
growth of black hair around needle-punctures in rabbits
inoculated with diptheria toxin. He suggests that
injuries such as saddle-galls and insect-bites may induce
a de or hyper-pigmentation of the skin.