1. Volume 136, Issue 7, Pages 2137-2148 (June 2009)
Quantification of Epigenetic and Genetic 2nd Hits in CDH1 During Hereditary Diffuse Gastric Cancer Syndrome Progression 
Carla Oliveira, Sónia Sousa, Hugo Pinheiro, Rachid Karam, Renata Bordeira–Carriço, Janine Senz, Pardeep Kaurah, Joana Carvalho, Rui Pereira, Leonor Gusmão, Xiaogang Wen, Maria Augusta Cipriano, Jun Yokota, Fátima Carneiro, David Huntsman, Raquel Seruca 
Gastroenterology 
Volume 136, Issue 7, Pages (June 2009)
DOI: /j.gastro
Copyright © 2009 AGA Institute Terms and Conditions

2. Figure 1
Examples of 2nd-hit inactivating mechanisms in HDGC tumors from 2 family members from family 4. LOH analysis using CDH1 flanking markers, intragenic markers, and the mutation site, and CDH1 promoter hypermethylation analysis are depicted for every case. Variation sites, in sequencing schemes, are marked with arrowheads; CpG sites at the CDH1 promoter are underlined in the sequencing scheme. Whenever a LOH marker was not informative, NI, replaced the LOH pick. N, normal; T, primary tumor; M, metastases.
Gastroenterology  , DOI: ( /j.gastro )
Copyright © 2009 AGA Institute Terms and Conditions

3. Figure 2
Genetic profiling of 4 individuals from 3 families for which multiple samples were analyzed. Analysis of 32 in/del markers in 20 chromosomes, 3 dinucleotide LOH markers flanking CDH1 and CDH1 intragenic markers. Chromosome 16 markers are flanked by 2 vertical black lines; markers displaying LOH are inside darker squares.
Gastroenterology  , DOI: ( /j.gastro )
Copyright © 2009 AGA Institute Terms and Conditions

4. Figure 3
Schematic representation of 2nd-hit inactivating mechanisms superimposed with germline mutations type and site. CDH1 germline mutations are preceded by letters indicating the type of mutation N (nonsense), F (frameshift), M (missense), and M/S (missense/splicing), and are aligned according to the 2nd-hit inactivating mechanism.
Gastroenterology  , DOI: ( /j.gastro )
Copyright © 2009 AGA Institute Terms and Conditions