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

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(AMACR, FASN, GOLM1, GSP-pi, ERG) that aid in the differential diagnosis<br />

are presented and discussed here.<br />

The clinical decision of urologists or radiooncologists, whom and how<br />

to treat these men, still rests predominantly on histological parameters.<br />

This urges us to increase standardization of the way we handle and diagnose<br />

our specimens. Processing and diagnosing of prostatectomy specimens<br />

has been the topic of the 2009 consensus conference of the International<br />

Society of Urologic Pathology (ISUP) and the most important<br />

recommendations of this conference will be discussed in comparison to<br />

the current S3-guidelines.<br />

As Gleason Score is one of the strongest prognostic parameters in prostate<br />

cancer, standardization is particularly important. The long overdue<br />

update on Gleason scoring by the ISUP 2005 recommendations has generally<br />

increased awareness, but has also led to some confusion among<br />

pathologists and clinicians and has possibly even induced a systematic<br />

over-grading of biopsies. A recent study conducted by the European Network<br />

of Urinary Pathologists focussed on particularly challenging cases<br />

to discriminate problematic areas in the differentiation of Gleason patterns<br />

3 and 4 in or<strong>der</strong> to establish helpful diagnostic guidelines.<br />

Despite the clinical need to identify insignificant and lethal prostate cancer<br />

at the biopsy stage, this estimation is still left exclusively to conventional<br />

clinical and histological parameters and no molecular biomarker has<br />

entered clinical practice yet. A critical overview of recent developments<br />

of prognostic biomarkers in prostate cancer is given.<br />

Finally, a brief outline of the PREFERE study, a prospective therapy study<br />

beginning in late 2012 in Germany, that aims to compare the outcomes<br />

of 7600 patients over a period of nearly 20 years, will be presented.<br />

Gastric Cancer – English<br />

VO-024<br />

Hereditary gastric cancer<br />

F . Carneiro1 1Institute of Molecular Pathology and Immunology of the University of<br />

Porto (IPATIMUP) and Medical Faculty of Porto/Centro Hospitalar S . João,<br />

Porto, Portugal, Porto, Portugal<br />

Familial aggregation of gastric cancer (GC), both of the diffuse and of<br />

the intestinal type, occurs in a variable proportion of cases, pointing to<br />

genetic predisposition in these settings.<br />

In 1998, Guilford et al identified the first inherited gastric cancer syndrome,<br />

designated as Hereditary Diffuse Gastric Cancer (HDGC), caused<br />

by germline alterations at the CDH1 (E-cadherin) gene. In 1999, the<br />

International Gastric Cancer Linkage Consortium (IGCLC) defined the<br />

criteria for the different types of familial gastric cancer syndromes: 1)<br />

two GC cases in a family, one confirmed DGC 80% at the age of 80<br />

in both gen<strong>der</strong>s, and lobular breast cancer is 60% in women by age 80.<br />

About one third of families fulfilling the criteria for HDGC carry germline<br />

alterations of the CDH1 gene. To date, about 100 different germline<br />

CDH1 alterations have been identified in HDGC families, mainly point<br />

mutations and large deletions. In 2010, the IGCLC updated the recommendations<br />

for CDH1 testing, including: 1) histological confirmation of<br />

DGC only required for one family member; 2) DGC

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