S1115 A Prognostic/Diagnostic DNA Fluorescent in Situ Hybridization Probe Set for Identifying Patients At Risk and (Early) Neoplasia in Barrett's Esophagus

2008 ◽  
Vol 134 (4) ◽  
pp. A-181
Author(s):  
Rygiel M. Agnieszka ◽  
Francesca Milano ◽  
Wytske Westra ◽  
Brenda Elzer ◽  
Annet Schaap ◽  
...  
Keyword(s):  
At Risk ◽  
In Situ Hybridization ◽  
Barrett’S Esophagus ◽  
Barrett's Esophagus ◽  
Fluorescent In Situ Hybridization ◽  
Hybridization Probe ◽  
Patients At Risk ◽  
Probe Set

scholarly journals Low Level ofHer-2Locus Amplification by Fluorescent In Situ Hybridization Does Not Correlate with Her-2 Protein Overexpression by Immunohistochemistry in Barrett's Esophagus

2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Agnieszka M. Rygiel ◽  
Francesca Milano ◽  
Fiebo J. ten Kate ◽  
Jacques J. G. H. M. Bergman ◽  
Kausillia K. Krishnadath
Keyword(s):  
In Situ Hybridization ◽  
Barrett’S Esophagus ◽  
Barrett's Esophagus ◽  
Fluorescent In Situ Hybridization ◽  
Chromosome 17 ◽  
Protein Overexpression ◽  
Therapeutic Implications ◽  
Low Level ◽  
Her 2

An accurate evaluation of theHer-2status has important prognostic and therapeutic implications in many carcinomas. The aim of the study was to correlateHer-2locus (17q11.2) amplification and chromosome 17 gains as assessed by fluorescent in situ hybridization (FISH) with Her-2 protein overexpression by immunohistochemistry (IHC) in patients with Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC). We analyzed 34 patients withHer-2amplification and/or chromosome 17gains using FISH on brush cytology specimens. Seven patients (21%) showed highHer-2locus amplification (Her-2: Cep17≥5 : 1), 5 (15%) showed lowHer-2locus amplification (Her-2: Cep17≥2<5 : 1), and 22 (65%) displayed gains of chromosome 17 only. Further, we confirmedHer-2amplification on corresponding biopsies that were taken at the same occasion as the cytologybrushings. Then, we compared the FISH results with IHC data obtained from the corresponding biopsies and showed that low level of Her-2 amplification does not correlate with Her-2 protein overexpression (score+3/+2;P=1), in contrast to the high amplification level (P=.001). Thus, in our population of BE and EAC patients, low level ofHer-2amplification does not result in detectable level of Her-2 protein as assessed by IHC.

Perilobar Nephrogenic Rests and Chromosome 22

2011 ◽  
Vol 14 (6) ◽  
pp. 485-492 ◽  
Author(s):  
Reena MdZIN ◽  
Marianne Phillips ◽  
Caitlin Edwards ◽  
Ashleigh Murch ◽  
Adrian Charles
Keyword(s):  
In Situ Hybridization ◽  
Fluorescent In Situ Hybridization ◽  
Wilms Tumor ◽  
Microsatellite Analysis ◽  
Chromosome 22 ◽  
Hybridization Probe ◽  
Genetic Changes ◽  
Preferential Loss ◽  
Nephrogenic Rests

Perilobar nephrogenic rests (NR) are precursor lesions that may display genetic changes similar to their associated Wilms tumor (WT). Two patients presented with WT, both with perilobar NR and 1 with bilateral, multifocal metachronous WT. Both patients' WT displayed monosomy 22 as the predominant cytogenetic change, and the constitutional cytogenetic analysis was normal. The purpose of our study was to identify at what stage in the morphologic progression from NR to WT the monosomy 22 occurred by using a fluorescent in situ hybridization probe for chromosome 22 in the subtypes of perilobar NR and WT present in both cases. Section and core fluorescent in situ hybridization with a chromosome 22 probe was performed on formalin-fixed, paraffin-embedded tissues containing WT and perilobar NR. We also performed fluorescent-based microsatellite analysis on some of the WT in the bilateral case to determine whether there was a preferential loss of the same allele of chromosome 22. Sclerotic and dormant perilobar NR showed a rate of monosomy 22 of only approximately 30%, but this increased to approximately 50% in hyperplastic and adenomatous NR. Monosomy 22 was present in 60%-80% of nuclei in WT. Microsatellite analysis showed loss of homozygosity, with preferential loss of the same allele of chromosome 22 in the tumors examined. There are differences in the rate of detection of monosomy 22 in perilobar NR and WT, suggesting loss of chromosome 22 in the progression of perilobar NR to WT in a subset of tumors.

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