Sabato 27 ottobre 2012 - Pacini Editore

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Sertoli-Leydig cell tumors, teratomas, carcinoid tumor, small
cell carcinoma, large cell neuroendocrine carcinoma (LCNC).
The latter has been previously described twenty-nine times in
the literature and usually associated with another type of surface
epithelial tumor, usually a mucinous histotype. Only few cases of
pure LCNC of the ovary have been reported to date. Herein, we
describe the first case of simultaneous occurrence of primitive
pure large cell neuroendocrine carcinoma of the ovary with a well
differentiated neuroendocrine tumor of the appendix.
Materials and methods. A 58 year-old female with no significant
past medical history presented with abdominal discomfort,
nausea and general fatigue. Abdominal ultrasonography (US)
and whole body computed tomography (CT) showed a 3-cm solid
tumor in the right ovary. The pre-operative diagnosis was that of
ovarian cancer, thus the patient underwent total hysterectomy,
bilateral salpingo-oophorectomy, omentectomy and appendicectomy.
After fixation in 10% formaldehyde, sections were taken
from the tumour for histological examination and the following
antibodies were checked: cytokeratin 7 and 20, WT1, Vimentin,
estrogen and progesterone receptors, chromogranin, synaptophysin,
CD56 both on ovary and appendix samples.
Results. The left ovary measured 3 cm in largest diameter. The
serosa was intact and the tube normal. The cut surface was solid
grey-white with a whitish nodule of 2 cm. The right ovary was
enlarged by a 2,5 cm-solid whitish-yellow mass infiltrating
the ovarian capsule. The tube showed multiple nodules on the
external surface. The uterus was deformed by numerous leiomyomas
and the appendix was normal. Cytological examination
of peritoneal fluid showed no malignant cells. Microscopically
the tumor showed a solid growth pattern and was composed of
medium to large cells forming sharply demarcated sheets and
cords with abundant eosinophilic and granular cytoplasm. The
nuclei showed condensation of nuclear material (salt and pepper
chromatin) and large prominent nucleoli were present. Foci
of necrosis were observed. Mitoses were frequent (40 mitotic
figures per 10 high power field-HPF). Tumor extension to the
serosa surface and tube infiltration was observed as well as vascular
invasion. The neuroendocrine differentiation was confirmed
by immunohistochemistry showing positivity for chromogranin,
synaptophysin and CD56. Proliferative index (Mib-1) was approximately
40%. The final diagnosis was pT2aNxMx (TNM7)
primitive large cell neuroendocrine carcinoma of the ovary. The
appendix showed a well differentiated neuroendocrine tumor
GEnITALE MASCHILE E FEMMInILE
Differential roles of SnAI2/SLUG transcription
factor in the epithelial and stromal compartments
of the human prostate cancer
C. Sorrentino, S. Di Meo, M.G. Tupone, T. D’Antuono, P. Musiani,
E. Di Carlo
Section of Anatomic Pathology and Molecular Medicine, Department of
Medicine and Sciences of Aging, “G. d’Annunzio” University of Chieti-
Pescara, Chieti, Italy; Ce.S.I. Aging Research Center, “G. d’Annunzio”
University Foundation, Chieti, Italy
Introduction. SNAI2/SLUG is a zinc-finger transcription factor
that acts as a master regulator of cell migration 1 , by trigger-
CONGRESSO aNNualE di aNatOmia patOlOGiCa SiapEC – iap • fiRENzE, 25-27 OttOBRE 2012
Venerdì, 26 ottobre 2012
Sala Botticelli ore 17,00 – 17,36
(NET) (7 mm in maximum diameter) with a typical organoid
arrangement of neoplastic cells in nests and trabeculae. Cells
were small, round and monomorphic with monotonous nuclei,
inconspicuous nucleoli and characteristic stippled chromatin. The
tumor infiltrated the sub-serosa. Proliferative index (Mib-1) was
less than 1%. Neither mitotic figures nor necrosis was appreciated.
The diagnosis was that of pT2 G1 well-differentiated NET
(TNM7-ENETS).
Discussion. Ovarian LCNC is a rare entity, defined as “a malignant
tumor composed of large cells that show neuroendocrine
differentiation”. Although mostly in stage I at diagnosis, patients
usually follow an aggressive poor outcome. The etiology
of LCNC of the ovary remains unclear. Since most cases are
admixed with another surface epithelial tumour, it is likely that
LCNC arises from the concurrent epithelial tumor. This hypothesis
is supported by the presence of scattered neuroendocrine
cells reported in the epithelial tumours associated with LCNC as
well as in ovarian tumors not associated with LCNC. The description
of 4 cases of pure LCNC suggests the possibility that LCNC
may arise directly from the ovarian tissue. This hypothesis is
supported by the fact that isolated neuroendocrine cells have been
identified in normal ovary. Neuroendocrine carcinomas result
from multidirectional differentiation of a multipotent epithelial
stem cell. The occurrence of pure primary ovarian LCNC with
well differentiated neuroendocrine tumor of the appendix rather
than being casual may suggest a progression of hyperplastic neuroendocrine
lesions. It may be speculated that due to a genetic
imbalance, our patient developed proliferative endocrine cell
lesions which led to a LCNC in the ovary and to a well differentiated
neuroendocrine tumor in the appendix.
references
Chênevert J, Bessette P, Plante M, et al. Mixed ovarian large cell
neuroendocrine carcinoma, mucinous adenocarcinoma, and teratoma:
a report of two cases and review of the literature. Pathol Res
Pract 2009;205:657-61.
Draganova-Tacheva RA, Khurana JS, Huang Y, et al. Large cell neuroendocrine
carcinoma of the ovary associated with serous carcinoma
with mucin production: a case report and literature review. Int J Clin
Exp Pathol 2009;2:304-9.
Lindboe CF. Large cell neuroendocrine carcinoma of the ovary. AP-
MIS 2007;115:169-76.
Veras E, Deavers MT, Silva EG, et al. Ovarian nonsmall cell neuroendocrine
carcinoma: a clinicopathologic and immunohistochemical study
of 11 cases. Am J Surg Pathol 2007;31:774-82.
ing epithelial-mesenchymal transition (EMT) during embryonic
development and tumor metastatization, and also regulates cellcycle
progression and survival 2 . In this study, we investigated its
role in prostate cancer (PCa) development and progression, under
normal and androgen deprivation therapy (ADT) conditions.
Materials and methods. We used laser capture microdissection
followed by real-time RT-PCR to determine SLUG gene expression
levels in normal and cancerous prostatic epithelium and stroma,
differentiating neoplastic foci with low (well differentiated)
versus high (poorly differentiated) Gleason grade (≤ 3 versus >)
3 . Epithelial and stromal cells were isolated from cancerous and
normal (selected from the prostatic lobe opposite to the PCa or
normal prostatic tissue far from it) prostate specimens from 55
untreated and 35 ADT-treated patients who underwent radical
prostatectomy for PCa, and normal prostate specimens from 12