96. Jahrestagung der Deutschen Gesellschaft für Pathologie e. V ...

Abstracts
mia and lenticular ectopia. Additional features concerned hydrocephaly,
a characteristic round face with cleft lip and palate, hypertelorism and
prominent front, short stature, brachydactyly, and also cardiac, renal,
genital and cerebral malformations including occipital meningocele. Peters’
plus syndrome was confirmed by sequence analysis of the B3GALTL
gene revealing homozygosity for the common 660+1G>A donor splice
site mutation in intron 8 in all four cases and heterozygosity for this mutation
in the Caucasian, non-consanguineous parents.
Conclusions. The four affected fetuses show a characteristic facial aspect
that in association with the accompanying malformations should enable
the diagnosis of a Peters’ plus syndrome. Peters’ anomaly of the eyes,
representing an evolutive feature, is already evident at 18 weeks of gestation.
However, manifestation of the disorder is variable. Occipital meningocele
is a novel finding in Peters’ plus syndrome.
SO-057
Massive ovarian edema (MOE)
V . Sailer1 , S . Huss1 , F . Fronhoffs1 , E . Wardelmann1 , A .M . Müller2 1University Clinic of Bonn, Institute of Paidopathology and Institute of Pathology,
Bonn, 2University Bonn, Department of Pediatric Pathology, Bonn
Aims. Massive ovarian edema (MOE) is a very rare benign tumor-like
condition found in young women resulting from accumulation of fluid
mostly due to partial or intermittent torsion of the ovary or secondary to
a pre-existing ovarian lesion.
Methods. We report a case of a 13-year-old girl that presented with an
ovarian mass measuring 16 cm in diameter. Ultrasound and CT-scan
revealed a multilobulated cystic mass. CA-12-5 levels were increased.
Concerns regarding underlying malignancy lead to unilateral salpingooophorectomy.
Results. Pathological evaluation revealed a MOE and multiple thromboses
of ovarian veins.
Conclusions. Differentiation MOE from malignant tumor is crucial to
prevent unnecessary surgery potentially resulting in hormonal dysfunction
and infertility. Conservative treatment is possible and may be more
appropriate in cases when histology on frozen section supports a benign
lesion.
SO-058
Infantile myofibroma of the thyroid gland
A . Agaimy1 , D . Schmidt 2 , P . Klein3 , R . Carbon4 , W . Holter5 1Friedrich-Alexander University of Erlangen, Institute of Pathology, Erlangen,
2Friedrich-Alexander University of Erlangen, Department of Nuclear Medicine,
Erlangen, 3Friedrich-Alexander University of Erlangen, Department of
Surgery, Erlangen, 4Friedrich-Alexander University of Erlangen, Department
of Surgery, Erlangen, 5Friedrich-Alexander University of Erlangen, University
Children‘s Hospital, Erlangen, Erlangen
Aims. Spindle cell lesions of the thyroid gland are rare and may thus be
diagnostically challenging. They encompass a heterogeneous group of
reactive mesenchymal lesions, and a variety of benign and malignant
neoplasms of epithelial and mesenchymal origin.
Methods. A 5-year-old girl presented with a rapidly growing firm nodular
cervical mass localized to the right thyroid lobe associated with bilateral
lymphadenopathy. Because of symptoms and concern about malignancy,
an open surgical biopsy was performed followed by resection
of the right lobe and biopsy of the cervical nodes. The patient is alive with
no evidence of recurrence 18 months after surgery.
Results. The specimen contained a 3.8 cm firm tan circumscribed nodular
mass surrounded by a thin rim of thyroid tissue. Histological examination
displayed a moderately cellular lesion composed of alternating
fascicles of eosinophilic myoid spindled cells and primitive looking
small rounded cells with hemangiopericytoma-like vascular pattern and
a prominent myointimal proliferation at the periphery of the lesion. The
78 | Der Pathologe · Supplement 1 · 2012
myoid cells expressed strongly alpha-smooth muscle actin but were negative
for desmin, h-caldesmon, epithelial membrane antigen, pankeratin,
CK7, thyroglobulin, TTF-1, protein S100, TLE1, ALK-1, beta-catenin,
CD31, CD34 and CD99. The lymph nodes showed reactive florid hyperplasia
without evidence of tumor.
Conclusions. To our knowledge, this case represents the first report of
solitary myofibroma presenting as a thyroid mass. Awareness of this differential
diagnosis is necessary to avoid misinterpretation as a sarcoma
with the sequelae of unnecessary over-treatment.
AG Urologische Pathologie I
SO-061
Mechanisms of VEGF-C and Neuropilin-2 induced therapy resistance
in prostate cancer
M . Muders1 , S . Haberlau 1 , M . Stanton 2 , H . Zhang3 , S . Dutta2 , M . Krause4 ,
K . Datta2 , G .B . Baretton1 1University Hospital Carl Gustav Carus at the University of Dresden, Institute
of Pathology, Dresden, 2University of Nebraska Medical Center, Omaha, NE,
United States, 3Mayo Clinic, Department of Urology, Rochester, MN, United
States, 4University Hospital Carl Gustav Carus at the University of Dresden,
Department of Radiation Oncology, Dresden
Aims. Resistance to treatment is a major contributor to prostate cancer
mortality in advanced stages. Therefore, in order to develop new treatment
modalities and improve the efficacy of current ones, it is important
to understand the molecular mechanisms that promote resistance to
therapy in prostate cancer cells.
Methods. To investigate the signaling pathways involved in induction
of therapy resistance by VEGF-C and Neuropilin-2 we knocked down
VEGF-C or Neuropilin 2 by RNA interference in standard prostate cancer
cells lines and treated these cell lines with ionizing irradiation or Docetaxel.
During or after treatment autophagic pathways were evaluated
by studying autophagic flux.
Results. VEGF-C and Neuropilin-2 are important molecules of radiation
and chemotherapy resistance in prostate cancer. Furthermore, we
have found that the VEGF-C/NRP-2 axis is involved in the activation
of autophagy, which maintains cancer cell survival following treatment.
Blocking autophagy also limits the ability of Neuropilin2 and VEGF-C
to induce therapy resistance in prostate cancer cell lines.
Conclusions. Together, these data suggest a link between the VEGF-C/
NRP-2 axis in prostate cancer cell survival in the presence of therapy-induced
stress by activating autophagy. Effective targeting of this pathway
may lead to the development of new cancer therapies.
SO-062
The ETS family of transcription factors and prostate cancer: The
role of the family prototype ETS-1
Z . Shaikhibrahim1 , N . Wernert1 1University Hospital Bonn, Institute of Pathology, Bonn
Aims. The ETS family of transcription factors plays important roles in
both normal and neoplastic cells for various biological processes. In
prostate cancer (PCa), recurrent gene fusions occurring between the
androgen-regulated prostate-specific serine protease TMPRSS2 gene,
and several ETS family members, most commonly ERG, are frequently
reported. ETS-1, the prototype of the family is reported to be overexpressed
in latent and clinically manifest PCas. The ETS-1 gene encodes three
distinct proteins, ETS-1 p51 encoded by a full-length mRNA, ETS-1 p42
and ETS-1 p27 encoded by an alternatively spliced mRNA lacking exon
VII and exons III–VI, respectively. Even though ETS-1 p42 and p27 have
been investigated in functional terms, the presence and roles of ETS-1