24 colour multifish karyotype showing the complexity of the genomic rearrangements with rearranged chromosomes in most pairs and several unidentified marker chromosomes (bottom left)

<p><b>Copyright information:</b></p><p>Taken from "Biological characterization of two xenografts derived from human CUPs (carcinomas of unknown primary)"</p><p>http://www.biomedcentral.com/1471-2407/7/225</p><p>BMC Cancer 2007;7():225-225.</p><p>Published online 18 Dec 2007</p><p>PMCID:PMC2241840.</p><p></p> Of particular interest are the translocation of chromosome 21 (in green) to the distal chromosome 4 (in grey) and the loss of chromosomes 9. In this cell, there were 2 der(3)t(3, 15) instead of one in most other cells which were analyzed

Microsatellite tracking assay linking DNA from patient peripheral blood mononuclear cells (PBMC), tumor surgical specimen (Surg

<p><b>Copyright information:</b></p><p>Taken from "Biological characterization of two xenografts derived from human CUPs (carcinomas of unknown primary)"</p><p>http://www.biomedcentral.com/1471-2407/7/225</p><p>BMC Cancer 2007;7():225-225.</p><p>Published online 18 Dec 2007</p><p>PMCID:PMC2241840.</p><p></p> Spec.) and xenograft to the Capi3 cell line

aCGH karyogram of patient t-8 and MCR delineation of RUNX1.

<p>A = A del (7q) and trisomy 13 are obvious. Cryptic deletions from 21q22.1 (corresponding to RUNX1) and from Xp11.4, that are smaller than 60kb, are nullosomic. On 22q11, the loss is a constitutive CNV of GGT1. B = A UCSC map (build 18) of the RUNX1 gene. C = The deletions of RUNX in four patients at the molecular level are labeled in orange and the smallest in red. The location of the breakpoints are indicated at the ends of the colored lines. Patient t-8 exhibits a homozygous 590 Kb deletion that encompassed the entire RUNX1 gene and could have occurred by an acquired isodisomy. Patient t-11 had the smallest deletion (40Kb) that was internal to RUNX1; t-29 had a deletion limited to RUNX1.</p

p-AML (case p24) with a complex karyotype.

<p>See the amplification of 15q23q24 and of 21q11.2q22.1 that are enlarged at the gene level. Multiple abnormalities (cf <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016623#pone-0016623-t005" target="_blank">table 5</a>) are asterisked.</p

Details of critical rearrangements concerning MCRs.

<p>A = gain on 8q24.3 in a t-AML; B = loss of 12 p13 in t-AML (patients t-4 and t-5); C loss of 3p21.3 in a p-AML.</p

Minimal critical regions in the literature including the present work: losses.

<p>The first column lists the chromosomal losses and gains. The second lists the absolute number of each rearrangement (excluding a single rearrangement). The third and the fourth are the absolute numbers in p-AML and t-AML respectively and the percentage is indicated between parenthesis. The chromosomal location is listed. The references are indicated by letters: A <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016623#pone.0016623-Akagi1" target="_blank">[32]</a>, B <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016623#pone.0016623-Akagi2" target="_blank">[33]</a>, C <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016623#pone.0016623-Akagi3" target="_blank">[34]</a>, D <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016623#pone.0016623-Parkin1" target="_blank">[18]</a>, E <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016623#pone.0016623-Parkin2" target="_blank">[19]</a>, F <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016623#pone.0016623-Paulsson1" target="_blank">[28]</a>, G <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016623#pone.0016623-Rucker1" target="_blank">[29]</a>, H <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016623#pone.0016623-Suela1" target="_blank">[30]</a>, I <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016623#pone.0016623-Tyybakinoja1" target="_blank">[31]</a>, J <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016623#pone.0016623-Walter1" target="_blank">[20]</a>, K present work. The last column lists the genes included in those MCR.</p

Minimal critical regions in the literature including the present work: gains.

<p>The first column lists the chromosomal losses and gains. The second lists the absolute number of each rearrangement (excluding a single rearrangement). The third and the fourth are the absolute numbers in p-AML and t-AML respectively and the percentage is indicated between parenthesis. The chromosomal location is listed. The references are indicated by letters: A <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016623#pone.0016623-Akagi1" target="_blank">[32]</a>, B <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016623#pone.0016623-Akagi2" target="_blank">[33]</a>, C <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016623#pone.0016623-Akagi3" target="_blank">[34]</a>, D <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016623#pone.0016623-Parkin1" target="_blank">[18]</a>, E <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016623#pone.0016623-Parkin2" target="_blank">[19]</a>, F <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016623#pone.0016623-Paulsson1" target="_blank">[28]</a>, G <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016623#pone.0016623-Rucker1" target="_blank">[29]</a>, H <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016623#pone.0016623-Suela1" target="_blank">[30]</a>, I <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016623#pone.0016623-Tyybakinoja1" target="_blank">[31]</a>, J <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016623#pone.0016623-Walter1" target="_blank">[20]</a>, K present work. The last column lists the genes included in those MCR.</p

Single CNA of interest.

<p>Column 2: The CNA were either lost or gained as indicated by a “−” or a “+”; the locations on chromosomes are described following the ISCN 2009 with slight modifications: sequence numbers are included between <> and expressed in Mb, with a resolution of 10kb; linear ratios are written between brackets after an “×”; chromosomes with a linear ratio >2 (low level of amplification) or losses <0.25 are labeled in <b>bold</b> and <b><i>italics</i></b>.</p

Germinal and immunoglobulin genes related CNVs.

<p>The CNVs are either lost or gained as indicated by a “−” or a “+”. Locations on chromosomes are described according to the ISCN 2009 with slight modifications: sequence numbers are included between <> and expressed in Mb, with a resolution of 10kb. Column 2: coding genes included in the CNVs: Column 3; miRNA genes included in the CNVs.</p

Minimal Critical Region in the two groups of patients.

<p>Column 1, the location of the MCR that follows the rules of <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016623#pone-0016623-t004" target="_blank">tables 4</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016623#pone-0016623-t005" target="_blank">5</a>; the figures in brackets and in bold are the ratios of the amplified regions. Column 2, patients; the figures in bold indicate the smaller CNA.</p