Kista aterom

Modern tumor classification

schemes name tumors for the
type of normal adult tissue
toward which the tumor appears
to be differentiating. The cell of
origin is often not known.
Sebaceous gland carcinoma
clearly resembles normal
sebaceous glands.[16] One may
reasonably speculate that
sebaceous gland carcinoma
arises from mature sebaceous
glands. Histologic studies have
suggested that periocular
sebaceous gland carcinomas
arise from the sebaceous
glands in this region. The
following 5 types of sebaceous
glands are seen in the
periocular region[6, 7] :

Meibomian glands of
the tarsal plate
Glands of Zeis of the
cilia
Sebaceous glands of
the eyebrows
Glands of the caruncle
Glands of the fine hair
follicles of the eyelid surface
In one histologic series, 51% of
cases reportedly arose from a
specialized sebaceous gland of
the eyelid, the meibomian
gland. Indeed, sebaceous gland
carcinoma is sometimes
referred to as meibomian gland
carcinoma. In the same series,
10% of cases arose from the
glands of Zeis, less than 10% of
cases arose from the caruncle
and the eyebrow each, and
12% were multicentric with no
obvious source of origin.[17]
Isolated case reports describe
sebaceous gland carcinoma
limited to the epithelium, with no
obvious connection to the
underlying sebaceous glands.
[18]
In these rare cases, the

Lipoma

Fibroma

Lipomas differ biochemically

from normal fat by
demonstrating increased levels
of lipoprotein lipase and by the
presence of a larger number of
precursor cells.

The precise mechanism for the

development of dermatofibroma
is unknown. Rather than a
reactive tissue change,
evidence that dermatofibroma
may be a neoplastic process is
demonstrated by its clonal
proliferative growth.[2] Clonality,
by itself, is not necessarily
synonymous with a neoplastic
process; it has been
demonstrated in inflammatory
conditions, including atopic
dermatitis, lichen sclerosis, and
psoriasis.

Approximately 60% of solitary

cutaneous lipomas display
clonal alterations. The most
common alteration involves a
breakpoint on bands 12q13-15.
Karyotype aberrations also
have been noted on arms 6p
and 13q. Multiple lipomas do
not display these alterations.[1]

Results from
immunohistochemical testing
with antibodies to factor XIIIa,
which label dermal dendritic
cells, are frequently positive in
dermatofibroma, while
antibodies to MAC 387, which
label monocyte-derived
macrophages (histiocytes),
show less consistent results.
One study evaluated the
expression in dermatofibroma of
HSP47, a recently used marker
for skin fibroblasts; CD68, a
marker for histiocytes; and
factor XIIIa. Most of the spindleshaped cells in all 28 cases of
dermatofibroma, irrespective of
histologic variant, stained
positively with HSP47,
indicating that skin fibroblasts
are a major constituent of
dermatofibroma. Factor XIIIa
positive dendritic cells also are
present, but the presence of
CD68-positive histiocytes was
inconsistent, especially between
histologic variants.[3]
The cell surface proteoglycan,
syndecan-1,[4] and fibroblast
growth factor receptor 2,
involved in epithelialmesenchymal cross-talk,[5] may

sebaceous gland carcinoma

may fill the conjunctival
epithelium and create the
appearance of squamous cell
carcinoma in situ. Whether
these tumors truly have an
epithelial origin or whether the
dermal connection has been
lost or is simply unappreciated
is unknown.
Approximately 20 case reports
have described the
development of sebaceous
carcinoma in a sebaceous
nevus of Jadassohn.[19, 20, 21, 22,
23]
Sebaceous carcinoma arising
from a nevus sebaceous is
more common in women and
elderly persons, described as a
nodule or ulcerated tumor that
usually demonstrates rapid
growth prior to diagnosis.
[21]
Controversy exists regarding
the prophylactic removal of a
nevus sebaceous, but when
malignant neoplasms are
suspected, removal is
warranted.[24]

play a role in the growth of

dermatofibromas. Transforming
growth factor-beta (TGF-beta)
signaling might be a trigger of
the fibrosis seen in
dermatofibromas.[6] TGF-beta,
along with other fibrinogenic
factors, may be produced by
mast cells, which have been
reported to occur in abnormally
high numbers in
dermatofibromas.[7]