2004 Summer Meeting - Amsterdam - The Pathological Society of ...

117
Expression of hTERT in gastrointestinal stromal tumours
occurs preferentially in malignant neoplasms
M Sabah , R Cummins , M Leader , E Kay
Royal College of Surgeons in Ireland, Dublin 9, Ireland
Background: Telomerase is expressed in many human cancers and cell lines
and is thought to contribute to their immortality. To date, little is known about
the expression of telomerase in non-epithelial tumours. The objective of this
study was to evaluate the expression of human telomerase reverse transcriptase
(hTERT) in gastrointestinal stromal tumours (GISTs).
Methods: Twenty three GISTs (9 low malignant potential, 10 primary
malignant and 4 intra-abdominal recurrences) were evaluated for hTERT
expression using immunohistochemistry on tissue microarray. Tissue blocks
were retrieved and H&E stains were performed to evaluate the histologic
tumour type. All cases were strongly positive for KIT (CD117).
Immunohistochemistry for hTERT was performed.
Results: Eighty nine percent (8/9) of the low malignant potential group were
negative for hTERT immunoexpression whereas all malignant GISTs showed
positive staining which varied from weak to strong immunoreactivity. 60%
(6/10) of the primary malignant GISTs were strongly positive. The remaining
40% (4/10) showed weak staining. All recurrent GISTs (4/4) exhibited strong
positive immunostaining for hTERT.
Conclusions: Telomerase expression occurs during the progression of GISTs
and immunohistochemical staining for hTERT may be a useful marker for the
prognostication of GISTs
118
Metastatic Lymph Node Deposits Originating From A
Different Primary To That Of The Resection Specimen
R Swamy , H M Kamel
Department of Histopathology, Royal Infirmary, 51, Little France
Crescent, Edinburgh, United Kingdom
We describe an unusual finding in a resection specimen for colonic carcinoma.
The primary tumour in the resection specimen was a moderately differentiated
adenocarcinoma of the sigmoid colon. Ten out of sixteen lymph nodes
retrieved from the specimen including the apical lymph node showed metastatic
adenocarcinoma with a morphological pattern different to that of the primary
cancer. A close examination of the colonic cancer showed no evidence of a
similar phenotype in any part of the tumour. The morphology of a micro-acinar
architecture raised the suspicion of metastases from a primary prostatic
adenocarcinoma. Immunohistochemistry was performed which showed positive
staining for PSA and negative staining for CK20 and CEA markers, confirming
our suspicion.
This case highlights the importance of proper histological comparison and
evaluation of any variations in the phenotypes between the primary tumour and
their metastases in the draining lymph nodes. While tumour de-differentiation
in nodal metastases is common, unusual variations in tumour phenotype must
be diligently recorded since this can have significant implications on patient
management, staging and prognosis. It can also lead to identification of new
pathology or another primary as in this case.
119
Chromosomal Changes in Colorectal Adenomas: Specific
Relation to Gene Mutation and Clinical Utility in Screening
A Leslie , A Stewart , DU Baty , NR Pratt , RJC Steele , FA
Carey
University of Dundee, Dundee, United Kingdom
We have previously shown that the model of colorectal carcinogenesis
involving sequential changes in the APC, K-ras and p53 genes is not supported
by the mutational profile of cancers (PNAS 2002; 99:9433). We have also
demonstrated specific associations between gene mutations and chromosomal
abnormalities (eg p53 with 20q+, 18q-, 13q+, K-ras with 12p+. Cancer Res
2003; 63:4656).
We have now analysed APC, K-ras and p53 mutations and chromosomal
change by comparative genomic hybridisation (CGH) in 79 colorectal
adenomas. APC (52%) and K-ras (27%) mutations were seen at a similar
frequency to that observed in cancer. p53 mutation (3 cases, 4%) was rare. As
in cancers we did not see any cases with both K-ras and p53 mutation
supporting our previous contention that these mutations may define separate
pathways to colorectal carcinoma.
Many of the important CGH changes seen in cancer were also present in
adenomas. The 2 most frequent cancer changes, 20q+ (80%) and 18q- (76%),
were much less common in adenomas (11% and 10% respectively). However
both abnormalities were significantly associated with histological severe
dysplasia (p