preparation-formalin-fixed-paraffin-embedded-tissue-cores-for-both

Preparation of Formalin-fixed Paraffin-embedded Tissue Cores for both RNA and DNA Extraction

Formalin-fixed paraffin embedded tissue (FFPET) represents a valuable, well-annotated substrate for molecular investigations. The utility of FFPET in ...

Queen's University

&#x9AA8;&#x8089;&#x7624; (OS) &#x7684;&#x7279;&#x70B9;&#x662F;&#x67D3;&#x8272;&#x4F53;&#x4E0D;&#x7A33;&#x5B9A;&#x548C;&#x9AD8;&#x62F7;&#x8D1D;&#x6570;&#x57FA;&#x56E0;&#x6269;&#x589E;&#x3002;&#x8BE5;&#x65AD;&#x88C2;&#x878D;&#x5408;&#x6865; &#xFF08;BFB&#xFF09; &#x5468;&#x671F;&#x662F;&#x80BF;&#x7624;&#x548C;&#x4F53;&#x5916;&#x6A21;&#x578B;&#x7528;&#x4E8E;&#x7814;&#x7A76;&#x7684;&#x8D77;&#x6E90;&#x590D;&#x6742;&#x67D3;&#x8272;&#x4F53;&#x91CD;&#x6392;&#x548C;&#x764C;&#x75C7;&#x57FA;&#x56E0;&#x7EC4;&#x6269;&#x589E;&#x7684;&#x57FA;&#x56E0;&#x7EC4;&#x4E0D;&#x7A33;&#x5B9A;&#x7684;&#x4E00;&#x4E2A;&#x884C;&#x4E4B;&#x6709;&#x6548;&#x7684;&#x673A;&#x5236;&#x3002;&#x7136;&#x800C;&#xFF0C;&#x5230;&#x76EE;&#x524D;&#x4E3A;&#x6B62;&#xFF0C;&#x6CA1;&#x6709;&#x9AD8;&#x5206;&#x8FA8;&#x7387;&#x7684;&#x7EC6;&#x80DE;&#x9057;&#x4F20;&#x6216;&#x57FA;&#x56E0;&#x7EC4;&#x9635;&#x5217;&#x7814;&#x7A76; BFB &#x4E8B;&#x4EF6;&#x7684; OS&#x3002;&#x5728;&#x672C;&#x7814;&#x7A76;&#x4E2D;&#xFF0C;&#x591A;&#x8272;&#x6761;&#x7EB9;&#x5E73;&#x94FA;&#x96C6; (mBAND) &#x9C7C;&#x548C; submegabase &#x53F7;&#x51B3;&#x8BAE; &#xFF08;&#x516C;&#x53F8;&#xFF09; &#x9635;&#x5217;&#x6BD4;&#x8F83;&#x57FA;&#x56E0;&#x7EC4;&#x6742;&#x4EA4; &#xFF08;&#x5168;&#x606F;&#xFF09; &#x88AB;&#x7528;&#x6765;&#x8BC6;&#x522B;&#x548C;&#x6620;&#x5C04;&#x7684; BFB &#x4E8B;&#x4EF6;&#x4E2D;&#x56DB;&#x4E2A; OS &#x7EC6;&#x80DE;&#x682A;&#x548C;&#x4E00;&#x4E2A;&#x75C5;&#x4EBA;&#x80BF;&#x7624;&#x57FA;&#x56E0;&#x7EC4;&#x7B7E;&#x540D;&#x3002;BFB &#x67D3;&#x8272;&#x4F53;&#x67D3;&#x8272;&#x4F53;&#x3001; &#x5012;&#x7ACB;&#x91CD;&#x53E0;&#x7684;&#x60C5;&#x51B5;&#xFF0C;&#x548C;&#x5185;&#x90E8;&#x548C; interchromosomal &#x7684;&#x653E;&#x5927;&#x4E0E;&#x76F8;&#x5173;&#x8054;&#x7684;&#x9884;&#x671F;&#x4E2D;&#x95F4;&#x4F53;-&#x786E;&#x5B9A;&#x4E86;&#x3002;mBAND &#x5206;&#x6790;&#x63D0;&#x4F9B;&#x8BE6;&#x7EC6;&#x7684;&#x91CD;&#x6392; 1 p&#x3001; 6 p &#x548C; 8q &#x7684;&#x6620;&#x5C04;&#x548C;&#x663E;&#x793A;&#x6613;&#x4F4D;&#x8DEF;&#x53E3;&#x5F80;&#x5F80;&#x662F;&#x8106;&#x5F31;&#x7684;&#x5730;&#x70B9;&#x9760;&#x8FD1;&#x3002;&#x66F4;&#x8BE6;&#x7EC6;&#x7684; OS &#x7684;&#x5355;&#x5143;&#x683C;&#x884C;&#x6BEB;&#x514B; 63 &#x7684; mBAND &#x7814;&#x7A76;&#x63ED;&#x793A;&#x9636;&#x68AF;&#x5F62;&#x9C7C;&#x4FE1;&#x53F7;&#x540C;&#x6837;&#x95F4;&#x8DDD; interchromosomal coamplifications 6 p 21&#x3001; 8q24&#xFF0C;&#x548C; 9 p 21 p22 &#x5747;&#x5300;&#x67D3;&#x8272; (hsr) &#x5730;&#x533A;&#x3002;Concordantly &#x6620;&#x5C04;&#x5230; hsr &#x7684;&#x7126;&#x653E;&#x5927;&#x4E86;&#x516C;&#x53F8;&#x6570;&#x7EC4;&#x8BA1;&#x7B97;&#x5168;&#x606F;&#x56FE;&#x7684;&#x5C40;&#x9650;&#x4E8E;&#x79BB;&#x6563;&#x57FA;&#x56E0;&#x7EC4;&#x7684;&#x65F6;&#x95F4;&#x95F4;&#x9694;&#x3002;&#x5728;&#x6B64; hsr &#x7684;&#x590D;&#x6742;&#x6269;&#x589E;&#x5B50;&#x7ED3;&#x6784;&#x8868;&#x660E;&#x7D27;&#x90BB;&#x5FAE;&#x7F3A;&#x5931;&#x7684;&#x7126;&#x653E;&#x5927;&#x3002;&#x6B64;&#x5916;&#xFF0C;&#x5728;&#x5220;&#x9664;/&#x6269;&#x589E;&#x7684;&#x57FA;&#x56E0;&#x7EC4;&#x533A;&#x57DF;&#x5DF2;&#x7ECF;&#x8106;&#x5F31;&#x7684;&#x7AD9;&#x70B9;&#x7684;&#x4F18;&#x52BF;&#x3002;&#x603B;&#x4E4B;&#xFF0C;&#x8FD9;&#x9879;&#x7814;&#x7A76;&#x63D0;&#x4F9B;&#x4E86;&#x8FDB;&#x4E00;&#x6B65;&#x652F;&#x6301; BFB &#x673A;&#x5236;&#x548C;&#x8106;&#x5F31;&#x7AD9;&#x70B9;&#x5728;&#x4FC3;&#x8FDB;&#x57FA;&#x56E0;&#x6269;&#x589E;&#x548C;&#x67D3;&#x8272;&#x4F53;&#x91CD;&#x6392;&#x5728; OS &#x4E2D;&#x7684;&#x4F5C;&#x7528;&#x3002;

&#x7EFC;&#x5408; mBAND &#x548C; submegabase &#x51B3;&#x8BAE;&#x5E73;&#x94FA;&#x96C6; (&#x516C;&#x53F8;) &#x8BA1;&#x7B97;&#x5168;&#x606F;&#x56FE;&#x9635;&#x5217;&#x5206;&#x6790;&#x7126;&#x653E;&#x5927;&#x7684;&#x5FAE;&#x7F3A;&#x5931;&#xFF0C;&#x68AF;&#x5B50;&#x7ED3;&#x6784;&#x7B26;&#x5408;&#x65AD;&#x88C2;&#x878D;&#x5408;&#x6865;&#x5FAA;&#x73AF;&#x548C;&#x9AA8;&#x8089;&#x7624;&#x4E2D;&#x7684;&#x4E8B;&#x4EF6;&#x3002;

Osteosarcoma (OS) is characterized by chromosomal instability and high-copy-number gene amplification. The breakage-fusion-bridge (BFB) cycle is a well-established mechanism of genomic instability in tumors and in vitro models used to study the origins of complex chromosomal rearrangements and cancer genome amplification. However, until now, there have been no high-resolution cytogenetic or genomic array studies of BFB events in OS. In the present study, multicolor banding (mBAND) FISH and submegabase resolution tiling set (SMRT) array comparative genomic hybridization (CGH) were used to identify and map genomic signatures of BFB events in four OS cell lines and one patient tumor. The expected intermediates associated with BFB-dicentric chromosomes, inverted duplications, and intra- and interchromosomal amplifications-were identified. mBAND analysis provided detailed mapping of rearrangements in 1p, 6p, and 8q and showed that translocation junctions were often in close proximity to fragile sites. More detailed mBAND studies of OS cell line MG-63 revealed ladderlike FISH signals of equally spaced interchromosomal coamplifications of 6p21, 8q24, and 9p21-p22 in a homogeneously staining region (hsr). Focal amplifications that concordantly mapped to the hsr were localized to discrete genomic intervals by SMRT array CGH. The complex amplicon structure in this hsr suggests focal amplifications immediately adjacent to microdeletions. Moreover, the genomic regions in which there was deletion/amplification had a preponderance of fragile sites. In summary, this study has provided further support for the role of the BFB mechanism and fragile sites in facilitating gene amplification and chromosomal rearrangement in OS.

An integrated mBAND and submegabase resolution tiling set (SMRT) CGH array analysis of focal amplification, microdeletions, and ladder structures consistent with breakage-fusion-bridge cycle events in osteosarcoma.

Ost&#xE9;osarcome (OS) est caract&#xE9;ris&#xE9; par une instabilit&#xE9; chromosomique et haute nombre de copies d&#x26;#39;amplification g&#xE9;nique. La cassure-fusion-pont (BFB) du cycle est un m&#xE9;canisme bien &#xE9;tabli de l&#x26;#39;instabilit&#xE9; g&#xE9;nomique dans les tumeurs et dans des mod&#xE8;les in vitro utilis&#xE9;s pour &#xE9;tudier les origines de complexes r&#xE9;arrangements chromosomiques et l&#x26;#39;amplification du g&#xE9;nome du cancer. Toutefois, jusqu&#x26;#39;&#xE0; pr&#xE9;sent, il n&#x26;#39;ya pas eu cytog&#xE9;n&#xE9;tique &#xE0; haute r&#xE9;solution ou des &#xE9;tudes g&#xE9;nomiques tableau des &#xE9;v&#xE9;nements BFB dans OS. Dans la pr&#xE9;sente &#xE9;tude, multicolore baguage (mBAND) FISH et ensemble la r&#xE9;solution submegabase carrelage (SMRT) hybridation g&#xE9;nomique comparative (CGH) ont &#xE9;t&#xE9; utilis&#xE9;s pour identifier et cartographier les signatures g&#xE9;nomiques d&#x26;#39;&#xE9;v&#xE9;nements BFB dans quatre lign&#xE9;es cellulaires tumorales OS et un patient. Les interm&#xE9;diaires attendus associ&#xE9;s &#xE0; BFB-dicentriques chromosomes, les duplications invers&#xE9;es, et intra-et interchromosomique amplifications des ont &#xE9;t&#xE9; identifi&#xE9;s. analyse mBAND fourni une cartographie d&#xE9;taill&#xE9;e des r&#xE9;arrangements dans 1p, 6p, 8q et et a montr&#xE9; que les jonctions de translocation sont souvent &#xE0; proximit&#xE9; de sites fragiles. Des &#xE9;tudes plus d&#xE9;taill&#xE9;es mBAND de la lign&#xE9;e cellulaire OS MG-63 a r&#xE9;v&#xE9;l&#xE9; signaux FISH ladderlike de &#xE9;quidistants coamplifications interchromosomiques de 6p21, 8q24, 9p21-p22 et dans une r&#xE9;gion homog&#xE8;ne coloration (HSR). Amplifications focaux qui concordante mapp&#xE9;s &#xE0; l&#x26;#39;HSR ont &#xE9;t&#xE9; localis&#xE9;es &#xE0; intervalles discrets g&#xE9;nomiques par CGH tableau SMRT. La structure complexe amplicon dans ce hsr sugg&#xE8;re amplifications focaux imm&#xE9;diatement adjacentes &#xE0; des microd&#xE9;l&#xE9;tions. En outre, les r&#xE9;gions g&#xE9;nomiques dans lequel il y avait suppression / amplification eu une pr&#xE9;pond&#xE9;rance des sites fragiles. En r&#xE9;sum&#xE9;, cette &#xE9;tude a fourni un appui suppl&#xE9;mentaire pour le r&#xF4;le du m&#xE9;canisme de BFB et des sites fragiles en vue de faciliter l&#x26;#39;amplification du g&#xE8;ne et de r&#xE9;arrangement chromosomique dans OS.

Une d&#xE9;marche int&#xE9;gr&#xE9;e et MBAND Submegabase R&#xE9;solution Tiling Set (SMRT) Analyse de la CGH array Amplification focale, microd&#xE9;l&#xE9;tions, et des structures coh&#xE9;rentes avec Ladder &#xE9;v&#xE9;nements du cycle de cassure-fusion-pont dans l&#x26;#39;ost&#xE9;osarcome

Ein integrierter mBAND und submegabase Aufl&#xF6;sung Fliesen-Set (SMRT) CGH-Array-Analysen von fokalen Verst&#xE4;rkung, Mikrodeletionen und Leiter-Strukturen im Einklang mit Bruch-Fusions-Br&#xFC;cken-Zyklus Ereignisse in Osteosarkom.

L&#39;osteosarcoma (OS) &egrave; caratterizzata da instabilit&agrave; cromosomica e amplificazione ad alto numero di copie del gene. Il ciclo di rottura-fusione-bridge (BFB) &egrave; un meccanismo consolidato di instabilit&agrave; genomica in modelli in vitro utilizzati per studiare le origini del complessi riarrangiamenti cromosomici e amplificazione del genoma di cancro e tumori. Tuttavia, fino ad ora, ci sono stati studi ad alta risoluzione matrice genomica o citogenetica di eventi BFB in OS. Nel presente studio, multicolor banding (mBAND) risoluzione di pesce e submegabase affiancamento insieme il (SMRT) matrice ibridazione genomic comparativa (CGH) sono stati utilizzati per identificare e mappare genomiche firme degli eventi BFB in quattro linee di cellule di OS e un paziente tumorale. Intermedi attesi associati cromosomi BFB-dicentrico, duplicazione invertite e intra - e amplificazioni interchromosomal-sono stati identificati. mBAND analisi dettagliata mappatura dei riarrangiamenti in 1 p p 6 e 8q e ha mostrato che le giunzioni di traslocazione erano spesso in prossimit&agrave; di siti fragili. Studi pi&ugrave; dettagliati del mBAND della linea cellulare OS MG-63 ha rivelato ladderlike segnali di pesce di ugualmente distanziati interchromosomal coamplifications di p22 6 p 21, 8q24 e 9 p 21 - in una regione omogenea colorazione (hsr). Amplificazioni focale che concordemente mappato l&#39;hsr erano localizzati a intervalli discreti di genomici di matrice SMRT CGH. La struttura complessa ampliconi in questo hsr suggerisce focale amplificazioni immediatamente adiacenti a microdelezioni. Inoltre, le regioni genomiche in cui c&#39;era la cancellazione/amplificazione avevano una preponderanza di siti fragili. In sintesi, questo studio ha fornito un ulteriore supporto per il ruolo del meccanismo di BFB e siti fragili nell&#39;agevolare l&#39;amplificazione del gene e riarrangiamento cromosomico in OS.

Un&#39;integrato risoluzione mBAND e submegabase affiancamento analisi set (SMRT) CGH array focale amplificazione, microdelezioni e le strutture di scaletta coerente con rottura-fusione-ponte ciclo di eventi nell&#39;osteosarcoma.

&#x9AA8;&#x8089;&#x816B;&#xFF08;OS&#xFF09;&#x306F;&#x67D3;&#x8272;&#x4F53;&#x4E0D;&#x5B89;&#x5B9A;&#x6027;&#x3068;&#x9AD8;&#x30B3;&#x30D4;&#x30FC;&#x6570;&#x306E;&#x907A;&#x4F1D;&#x5B50;&#x5897;&#x5E45;&#x306B;&#x3088;&#x3063;&#x3066;&#x7279;&#x5FB4;&#x4ED8;&#x3051;&#x3089;&#x308C;&#x308B;&#x3002;&#x7834;&#x640D;&#x878D;&#x5408;&#x30D6;&#x30EA;&#x30C3;&#x30B8;&#xFF08;BFB&#xFF09;&#x30B5;&#x30A4;&#x30AF;&#x30EB;&#x306F;&#x3001;&#x816B;&#x760D;&#x3067;&#x3001;&#x8907;&#x96D1;&#x306A;&#x67D3;&#x8272;&#x4F53;&#x518D;&#x914D;&#x5217;&#x3068;&#x764C;&#x306E;&#x30B2;&#x30CE;&#x30E0;&#x5897;&#x5E45;&#x306E;&#x8D77;&#x6E90;&#x3092;&#x7814;&#x7A76;&#x3059;&#x308B;&#x305F;&#x3081;&#x306B;&#x4F7F;&#x7528;&#x3055;&#x308C;&#x308B;in vitro&#x30E2;&#x30C7;&#x30EB;&#x306B;&#x304A;&#x3051;&#x308B;&#x30B2;&#x30CE;&#x30E0;&#x4E0D;&#x5B89;&#x5B9A;&#x6027;&#x306E;&#x5341;&#x5206;&#x306B;&#x78BA;&#x7ACB;&#x3055;&#x308C;&#x305F;&#x30E1;&#x30AB;&#x30CB;&#x30BA;&#x30E0;&#x3067;&#x3059;&#x3002;&#x3057;&#x304B;&#x3057;&#x3001;&#x4ECA;&#x307E;&#x3067;&#x3001;&#x306A;&#x3044;&#x9AD8;&#x89E3;&#x50CF;&#x5EA6;&#x306E;&#x7D30;&#x80DE;&#x907A;&#x4F1D;&#x5B66;&#x7684;&#x307E;&#x305F;&#x306F;OS&#x306E;BFB&#x30A4;&#x30D9;&#x30F3;&#x30C8;&#x306E;&#x30B2;&#x30CE;&#x30E0;&#x914D;&#x5217;&#x306E;&#x7814;&#x7A76;&#x304C;&#x884C;&#x308F;&#x308C;&#x3066;&#x3044;&#x306A;&#x3044;&#x3002;&#x672C;&#x7814;&#x7A76;&#x3067;&#x306F;&#x3001;&#x30BB;&#x30C3;&#x30C8;&#xFF08;SMRT&#xFF09;&#x30A2;&#x30EC;&#x30A4;&#x6BD4;&#x8F03;&#x30B2;&#x30CE;&#x30E0;&#x30CF;&#x30A4;&#x30D6;&#x30EA;&#x30C0;&#x30A4;&#x30BC;&#x30FC;&#x30B7;&#x30E7;&#x30F3;&#xFF08;CGH&#xFF09;&#x3092;&#x30BF;&#x30A4;&#x30EB;&#x591A;&#x8272;&#x30D0;&#x30F3;&#x30C7;&#x30A3;&#x30F3;&#x30B0;&#xFF08;mBAND&#xFF09;FISH&#x3068;submegabase&#x306E;&#x89E3;&#x50CF;&#x5EA6;&#x306F;&#x3001;4&#x3064;&#x306E;OS&#x306E;&#x7D30;&#x80DE;&#x682A;&#x3068;&#x4E00;&#x4EBA;&#x306E;&#x60A3;&#x8005;&#x306E;&#x816B;&#x760D;&#x3067;BFB&#x30A4;&#x30D9;&#x30F3;&#x30C8;&#x306E;&#x30B2;&#x30CE;&#x30E0;&#x7F72;&#x540D;&#x3092;&#x8B58;&#x5225;&#x3057;&#x3066;&#x30DE;&#x30C3;&#x30D4;&#x30F3;&#x30B0;&#x3059;&#x308B;&#x305F;&#x3081;&#x306B;&#x4F7F;&#x7528;&#x3055;&#x308C;&#x307E;&#x3057;&#x305F;&#x3002; BFB-&#x4E8C;&#x52D5;&#x539F;&#x4F53;&#x67D3;&#x8272;&#x4F53;&#x3001;&#x53CD;&#x8EE2;&#x8907;&#x88FD;&#x3001;&#x30A4;&#x30F3;&#x30C8;&#x30E9;&#x3068;&#x67D3;&#x8272;&#x4F53;&#x9593;&#x306B;&#x95A2;&#x9023;&#x4ED8;&#x3051;&#x3089;&#x308C;&#x3066;&#x3044;&#x308B;&#x671F;&#x5F85;&#x3055;&#x308C;&#x308B;&#x4E2D;&#x9593;&#x4F53;&#x3092;&#x540C;&#x5B9A;&#x3057;&#x5897;&#x5E45;&#x306F;&#x3001;&#x3055;&#x308C;&#x307E;&#x3057;&#x305F;&#x3002; mBAND&#x5206;&#x6790;&#x3067;&#x306F;&#x3001;1P&#x3001;6P&#x3001;&#x3068;&#x200B;&#x200B;8Q&#x306E;&#x518D;&#x7DE8;&#x6210;&#x306E;&#x8A73;&#x7D30;&#x306A;&#x30DE;&#x30C3;&#x30D4;&#x30F3;&#x30B0;&#x3092;&#x63D0;&#x4F9B;&#x3057;&#x3001;&#x8EE2;&#x5EA7;&#x63A5;&#x5408;&#x304C;&#x8106;&#x5F31;&#x90E8;&#x4F4D;&#x306B;&#x8FD1;&#x63A5;&#x3057;&#x3066;&#x983B;&#x7E41;&#x306B;&#x3042;&#x308B;&#x3053;&#x3068;&#x3092;&#x793A;&#x3057;&#x305F;&#x3002; OS&#x306E;&#x7D30;&#x80DE;&#x682A;MG-63&#x306E;&#x8A73;&#x7D30;mBAND&#x7814;&#x7A76;&#x3067;&#x306F;&#x3001;&#x5747;&#x4E00;&#x67D3;&#x8272;&#x9818;&#x57DF;&#xFF08;HSR&#xFF09;&#x306E;6p21&#x3001;8q24&#x306E;&#x3001;&#x3068;&#x4F53;9p21-P22&#x306E;&#x7B49;&#x9593;&#x9694;&#x306E;&#x67D3;&#x8272;&#x4F53;&#x9593;coamplifications&#x306E;ladderlike&#x306E;FISH&#x30B7;&#x30B0;&#x30CA;&#x30EB;&#x3092;&#x660E;&#x3089;&#x304B;&#x306B;&#x3057;&#x305F;&#x3002; concordantly HSR&#x306B;&#x30DE;&#x30C3;&#x30D7;&#x3055;&#x308C;&#x305F;&#x30D5;&#x30A9;&#x30FC;&#x30AB;&#x30EB;&#x5897;&#x5E45;&#x306F;SMRT&#x306E;&#x30A2;&#x30EC;&#x30A4;CGH&#x306B;&#x3088;&#x3063;&#x3066;&#x96E2;&#x6563;&#x7684;&#x30B2;&#x30CE;&#x30E0;&#x9593;&#x9694;&#x306B;&#x5C40;&#x5728;&#x3057;&#x3066;&#x3044;&#x305F;&#x3002;&#x3053;&#x306E;HSR&#x306E;&#x8907;&#x96D1;&#x306A;&#x30A2;&#x30F3;&#x30D7;&#x30EA;&#x30B3;&#x30F3;&#x306E;&#x69CB;&#x9020;&#x306F;&#x3001;&#x5FAE;&#x5C0F;&#x6B20;&#x5931;&#x306B;&#x96A3;&#x63A5;&#x7126;&#x70B9;&#x5897;&#x5E45;&#x3092;&#x793A;&#x5506;&#x3057;&#x3066;&#x3044;&#x308B;&#x3002;&#x307E;&#x305F;&#x3001;&#x6B20;&#x5931;/&#x5897;&#x5E45;&#x304C;&#x3055;&#x308C;&#x305F;&#x30B2;&#x30CE;&#x30E0;&#x9818;&#x57DF;&#x306F;&#x3001;&#x8106;&#x5F31;&#x30B5;&#x30A4;&#x30C8;&#x306E;&#x512A;&#x4F4D;&#x6027;&#x3092;&#x6301;&#x3063;&#x3066;&#x3044;&#x305F;&#x3002;&#x8981;&#x7D04;&#x3059;&#x308B;&#x3068;&#x3001;&#x672C;&#x7814;&#x7A76;&#x3067;&#x306F;BFB&#x306E;&#x30E1;&#x30AB;&#x30CB;&#x30BA;&#x30E0;&#x3068;OS&#x3067;&#x306E;&#x907A;&#x4F1D;&#x5B50;&#x5897;&#x5E45;&#x3068;&#x67D3;&#x8272;&#x4F53;&#x518D;&#x914D;&#x5217;&#x3092;&#x5BB9;&#x6613;&#x306B;&#x3059;&#x308B;&#x8106;&#x5F31;&#x90E8;&#x4F4D;&#x306E;&#x5F79;&#x5272;&#x306E;&#x3055;&#x3089;&#x306A;&#x308B;&#x30B5;&#x30DD;&#x30FC;&#x30C8;&#x3092;&#x63D0;&#x4F9B;&#x3057;&#x3066;&#x3044;&#x307E;&#x3059;&#x3002;

&#x30D5;&#x30A9;&#x30FC;&#x30AB;&#x30EB;&#x5897;&#x5E45;&#x3001;&#x5FAE;&#x5C0F;&#x6B20;&#x5931;&#x3001;&#x304A;&#x3088;&#x3073;&#x9AA8;&#x8089;&#x816B;&#x306E;&#x7834;&#x640D;&#x878D;&#x5408;&#x30D6;&#x30EA;&#x30C3;&#x30B8;&#x30B5;&#x30A4;&#x30AF;&#x30EB;&#x30A4;&#x30D9;&#x30F3;&#x30C8;&#x3068;&#x4E00;&#x81F4;&#x3057;&#x3066;&#x30E9;&#x30C0;&#x30FC;&#x69CB;&#x9020;&#x306E;&#x7D71;&#x5408;MBAND&#x3068;Submegabase&#x89E3;&#x50CF;&#x5EA6;&#x30BF;&#x30A4;&#x30EB;&#x30BB;&#x30C3;&#x30C8;&#xFF08;SMRT&#xFF09;&#x306E;CGH&#x30A2;&#x30EC;&#x30A4;&#x89E3;&#x6790;

&#xB2E4;&#xB9AC; (OS) &#xC5FC;&#xC0C9;&#xCCB4; &#xBD88;&#xC548;&#xC815;&#xACFC; &#xB192;&#xC740; &#xBCF5;&#xC0AC; &#xBC88;&#xD638; &#xC720;&#xC804;&#xC790; &#xC99D;&#xD3ED;&#xC5D0; &#xC758;&#xD574; &#xD2B9;&#xC9D5;&#xC785;&#xB2C8;&#xB2E4;. &#xD30C;&#xC190; &#xD4E8;&#xC804; &#xBE0C;&#xB9AC;&#xC9C0; (BFB) &#xC0AC;&#xC774;&#xD074; &#xC885;&#xC591; &#xBC0F; &#xBCF5;&#xC7A1; &#xD55C; &#xC5FC;&#xC0C9;&#xCCB4; &#xC7AC;&#xBC30;&#xC5F4; &#xBC0F; &#xC554; &#xAC8C;&#xB188; &#xC99D;&#xD3ED;&#xC758; &#xAE30;&#xC6D0;&#xC744; &#xC5F0;&#xAD6C; &#xD558;&#xB294; &#xB370; &#xC0AC;&#xC6A9; &#xD558;&#xB294; &#xCCB4; &#xC678; &#xBAA8;&#xB378; genomic &#xBD88;&#xC548;&#xC815;&#xC131;&#xC758; &#xC798; &#xC124;&#xB9BD; &#xBA54;&#xCEE4;&#xB2C8;&#xC998;&#xC785;&#xB2C8;&#xB2E4;. &#xADF8;&#xB7EC;&#xB098;, &#xC9C0;&#xAE08;&#xAE4C;&#xC9C0; OS&#xC5D0; BFB &#xC0AC;&#xAC74;&#xC758; &#xC544;&#xBB34; &#xACE0;&#xD574;&#xC0C1;&#xB3C4; cytogenetic &#xB610;&#xB294; &#xAC8C;&#xB188; &#xBC30;&#xC5F4; &#xC5F0;&#xAD6C; &#xB418;&#xC5C8;&#xC2B5;&#xB2C8;&#xB2E4;. &#xD604;&#xC7AC;&#xC758; &#xC5F0;&#xAD6C;&#xC5D0; &#xBA40;&#xD2F0; &#xCEEC;&#xB7EC; &#xBC34;&#xB529; &#xAE30;&#xC640; &#xC138;&#xD2B8; (mBAND) &#xBB3C;&#xACE0;&#xAE30;&#xC640; submegabase &#xD574;&#xC0C1;&#xB3C4; (SMRT) &#xBC30;&#xC5F4; &#xBE44;&#xAD50; genomic &#xAD50; &#xC7A1; (CGH) &#xB370; &#xC2DD;&#xBCC4; &#xD558; &#xACE0; 4 &#xAC1C;&#xC758; OS &#xC140; &#xB77C;&#xC778;&#xACFC; &#xD55C; &#xD658;&#xC790; &#xC885;&#xC591;&#xC5D0; BFB &#xC774;&#xBCA4;&#xD2B8;&#xC758; &#xAC8C;&#xB188; &#xC11C;&#xBA85;&#xC744; &#xC9C0;&#xB3C4;. BFB dicentric &#xC5FC;&#xC0C9;&#xCCB4;, &#xAC70;&#xAFB8;&#xB85C; &#xC911;&#xBCF5; &#xBC0F; &#xB0B4;&#xBD80;&#xC640; interchromosomal &#xD655;&#xB300;&#xC640; &#xAD00;&#xB828; &#xB41C; &#xC608;&#xC0C1;&#xB41C; &#xC911;&#xAC04;&#xCCB4;-&#xBC1C;&#xACAC; &#xD588;&#xB2E4;. &#xC81C;&#xACF5; &#xD558;&#xB294; mBAND &#xBD84;&#xC11D; 1 p, 6p, &#xADF8;&#xB9AC;&#xACE0; 8q &#xC7AC;&#xBC30;&#xC5F4;&#xC758; &#xB9E4;&#xD551; &#xC0C1;&#xC138; &#xD558; &#xACE0; &#xAE68;&#xC9C0;&#xAE30; &#xC26C;&#xC6B4; &#xC0AC;&#xC774;&#xD2B8; &#xADFC;&#xC811;&#xC5D0;&#xC11C; &#xC804; &#xC811;&#xD569; &#xC790;&#xC8FC; &#xD588;&#xB2E4; &#xBCF4;&#xC5EC;&#xC8FC;&#xC5C8;&#xB2E4;. OS &#xC140; &#xC120; MG-63&#xC758; &#xB354; &#xC790;&#xC138;&#xD55C; mBAND &#xC5F0;&#xAD6C; 6 p 21, 8q24, &#xBC0F; homogeneously &#xC5BC;&#xB8E9; &#xC9C0;&#xC5ED; (hsr) 9 p 21-p22 &#xB3D9;&#xB4F1; &#xD558; &#xAC8C; &#xAC04;&#xACA9; &#xB454;&#xB41C; interchromosomal coamplifications&#xC758; ladderlike &#xBB3C;&#xACE0;&#xAE30; &#xC2E0;&#xD638;&#xB97C; &#xBC1D;&#xD614;&#xB2E4;. Hsr&#xC5D0; &#xB9E4;&#xD551;&#xB41C; concordantly &#xCD08;&#xC810; &#xD655;&#xB300; SMRT &#xBC30;&#xC5F4; CGH &#xC5EC; &#xC774;&#xC0B0; &#xAC8C;&#xB188; &#xAC04;&#xACA9;&#xC5D0; &#xC9C0;&#xC5ED;&#xD654; &#xB41C; &#xD588;&#xB2E4;. &#xC774; hsr&#xC5D0; &#xBCF5;&#xC7A1; &#xD55C; amplicon &#xAD6C;&#xC870; &#xCD08;&#xC810; &#xD655;&#xB300; &#xBC14;&#xB85C; &#xC606; microdeletions&#xC5D0; &#xC81C;&#xC548;&#xD569;&#xB2C8;&#xB2E4;. &#xB610;&#xD55C;, &#xAC8C;&#xB188; &#xC601;&#xC5ED; &#xD588;&#xB2E4; &#xC0AD;&#xC81C;/&#xC99D;&#xD3ED; &#xAE68;&#xC9C0;&#xAE30; &#xC26C;&#xC6B4; &#xC704;&#xCE58;&#xC758; &#xC911;&#xB7C9;&#xC5D0; &#xC788;&#xC5B4;&#xC11C; &#xC6B0;&#xC138;&#xB97C; &#xD588;&#xB2E4;. &#xC694;&#xC57D; &#xD558;&#xC790;&#xBA74;,&#xC774; &#xC5F0;&#xAD6C; BFB &#xBA54;&#xCEE4;&#xB2C8;&#xC998; &#xBC0F; &#xC720;&#xC804;&#xC790; &#xC99D;&#xD3ED; &#xBC0F; &#xC6B4;&#xC601; &#xCCB4;&#xC81C;&#xC5D0;&#xC11C; &#xC5FC;&#xC0C9;&#xCCB4; &#xC7AC;&#xBC30;&#xCE58; &#xCD09;&#xC9C4;&#xC5D0; &#xAE68;&#xC9C0;&#xAE30; &#xC26C;&#xC6B4; &#xC0AC;&#xC774;&#xD2B8;&#xC758; &#xC5ED;&#xD560;&#xC5D0; &#xB300; &#xD55C; &#xCD94;&#xAC00; &#xC9C0;&#xC6D0;&#xC744; &#xC81C;&#xACF5; &#xD558;&#xACE0;&#xC788;&#xB2E4;.

&#xD1B5;&#xD569; &#xB41C; mBAND &#xBC0F; submegabase &#xD574;&#xC0C1;&#xB3C4; &#xC9D1;&#xD569; (SMRT) CGH &#xBC30;&#xC5F4; &#xBD84;&#xC11D; &#xCD08;&#xC810; &#xD655;&#xB300;&#xC758; &#xAE30;&#xC640;, microdeletions, &#xC0AC;&#xB2E4;&#xB9AC; &#xAD6C;&#xC870; &#xD30C;&#xC190; &#xD4E8;&#xC804; &#xBE0C;&#xB9AC;&#xC9C0;&#xC640; &#xC77C;&#xCE58; &#xB2E4;&#xB9AC;&#xC5D0;&#xC11C; &#xC774;&#xBCA4;&#xD2B8;&#xB97C; &#xC8FC;&#xAE30;.

El osteosarcoma (OS) se caracteriza por la inestabilidad cromos&#xF3;mica y de gran n&#xFA;mero de copias de amplificaci&#xF3;n de genes. La rotura-fusi&#xF3;n-puente (CBA) del ciclo es un mecanismo bien establecido de la inestabilidad gen&#xF3;mica en tumores y en modelos in vitro para estudiar los or&#xED;genes de complejos reordenamientos cromos&#xF3;micos y la amplificaci&#xF3;n del genoma del c&#xE1;ncer. Sin embargo, hasta ahora, no ha habido citogen&#xE9;tico de alta resoluci&#xF3;n o los estudios de gen&#xF3;mica de la matriz de eventos de BFB en OS. En el presente estudio, multicolor bandas (mBAND) de pescado y submegabase resoluci&#xF3;n de impresi&#xF3;n en mosaico (SMRT) variedad de hibridaci&#xF3;n gen&#xF3;mica comparada (CGH) fueron utilizados para identificar y mapear las firmas gen&#xF3;micas de eventos BFB en cuatro l&#xED;neas celulares del sistema operativo y un tumor del paciente. Los productos intermedios esperados asociados con BFB-dic&#xE9;ntricos cromosomas, duplicaciones invertidas, y las intra e interchromosomal amplificaciones fueron identificados. an&#xE1;lisis de mBAND siempre un mapeo detallado de reordenamientos en 1p, 6p, y 8q y mostr&#xF3; que las uniones translocaci&#xF3;n eran a menudo muy cerca de los sitios fr&#xE1;giles. Los estudios m&#xE1;s detallados de mBAND l&#xED;nea celular OS MG-63 revel&#xF3; se&#xF1;ales de escalera de FISH equidistantes coamplifications interchromosomal de 6p21, 8q24, 9p21 y p22-en una regi&#xF3;n homog&#xE9;nea tinci&#xF3;n (RSS). Amplificaciones focales que concordantemente asignadas a la ISS fueron localizados a intervalos discretos gen&#xF3;micas por CGH array SMRT. La estructura de amplificaci&#xF3;n en este complejo de la ISS sugiere ampliaciones de actividad inmediatamente adyacentes a microdeleciones. Adem&#xE1;s, las regiones gen&#xF3;micas en el que no hab&#xED;a supresi&#xF3;n / amplificaci&#xF3;n ten&#xED;an una preponderancia de sitios fr&#xE1;giles. En resumen, este estudio ha proporcionado apoyo adicional a la funci&#xF3;n del mecanismo de BFB y los sitios fr&#xE1;giles en la facilitaci&#xF3;n de la amplificaci&#xF3;n de genes y el reordenamiento cromos&#xF3;mico en el sistema operativo.

Un sistema integrado de MBAND y Submegabase Set Resoluci&#xF3;n Mosaico (SMRT) CGH array an&#xE1;lisis de amplificaci&#xF3;n focal, microdeleciones y Estructuras escalera consistente con los acontecimientos del ciclo de rotura de puente de fusi&#xF3;n en el osteosarcoma

Adult somatic tissue, and the tumours that arise therein, are maintained by a small population of stem cells. In addition to the self-renewal potential and pluripotency, these stem cells express several phenotypic traits that can be used in isolation and enrichment strategies. Since most of the traits are not exclusive to the stem cells however, the resultant populations are typically heterogeneous and variable from one isolation to another. In this article, we review the strategies for isolation of stem cells, and the limitations thereof, with emphasis on mesenchymal tissue and bone tumours. The emerging evidence suggests that stem cell is not a distinct entity, but rather an indefinite state along a spectrum, characterized by phenotypic traits, epigenetic factors and the microenvironment.

Stem cell enrichment approaches.

The recent description of novel recurrent gene fusions in approximately 80% of prostate cancer (PCa) cases has generated increased interest in the search for new translocations in other epithelial cancers and emphasizes the importance of understanding the origins and biologic implications of these genomic rearrangements. Analysis of 15 PCa cases by reverse transcription-polymerase chain reaction was used to detect six ERG-related gene fusion transcripts with TMPRSS2. No TMPRSS2/ETV1 chimeric fusion was detected in this series. Three-color fluorescence in situ hybridization confirms that TMPRSS2/ERG fusion may be accompanied by a small hemizygous sequence deletion on chromosome 21 between ERG and TMPRSS2 genes. Analysis of genomic architecture in the region of genomic rearrangement suggests that tracts of microhomology could facilitate TMPRSS2/ERG fusion events.

Three-color FISH analysis of TMPRSS2/ERG fusions in prostate cancer indicates that genomic microdeletion of chromosome 21 is associated with rearrangement.

Osteosarcoma (OS) is characterized by chromosomal instability and high copy number gene amplification. The breakage-fusion-bridge (BFB) cycle is a well-established mechanism of genome instability in tumors and in vitro models used to study the origins of complex chromosomal rearrangements and cancer genome amplification. To determine whether the BFB cycle could be increasing the de novo rate of formation of cytogenetic aberrations in OS, the frequency of anaphase bridge configurations and dicentric chromosomes in four OS cell lines was quantified. An increased level of anaphase bridges and dicentrics was observed in all the OS cell lines. There was also a strong association between the frequencies of anaphase bridges, dicentrics, centrosomal anomalies, and multipolar mitotic figures in all the OS cell lines, indicating a possible link in the mechanisms that led to the structural and numerical instabilities observed in OS. In summary, this study has provided strong support for the role of the BFB cycle in generating the extensive structural chromosome aberrations, as well as cell-to-cell cytogenetic variation observed in OS, thus conferring the genetic diversity for OS tumor progression.

The breakage-fusion-bridge (BFB) cycle as a mechanism for generating genetic heterogeneity in osteosarcoma.

The progression to cancer is often associated with instability and the acquisition of genomic heterogeneity, generating both clonal and non-clonal populations. Chromosomal instability (CIN) describes the excessive rate of numerical and structural genomic change in tumors. Mitotic segregation errors strongly influences copy number, while structural aberrations can occur at unstable genomic regions, or through aberrant DNA repair or methylation. Combined molecular cytogenetic analyses can evaluate cell-to-cell variation, and define the complexity of numerical and structural alterations. Because structural change may occur independently of numerical alteration, we propose the term structural chromosomal instability [(S)-CIN] to distinguish numerical from structural CIN.

Genomic mechanisms and measurement of structural and numerical instability in cancer cells.

Pediatric undifferentiated soft tissue sarcomas (USTS) are a rare group of neoplasms that are unclassifiable despite the application of immunohistochemical, cytogenetic, and molecular techniques. To date, there is a dearth of studies looking at the cytogenetic and molecular genetic alterations in such tumors. Trisomy 8, a frequent molecular alteration in neoplasia, is seen in several soft tissue sarcomas, including Ewing sarcoma/primitive neuroectodermal tumor (ES/PNET), synovial sarcoma, and leiomyosarcoma. Because USTS share several clinicobiological features with the aforementioned tumors, the occurrence of alterations in chromosome 8 was studied in 11 pediatric USTS using a combination of interphase fluorescence in situ hybridization (FISH), spectral karyotyping (SKY), and genomic profiling with oligonucleotide array comparative genomic hybridization (aCGH). The copy number status of MYC was also assessed on the same tumors using dual-color FISH, with the aim of delineating the degree and intratumoral distribution of MYC amplification in this tumor. A near-uniform presence of an increase in MYC copy number was observed, along with an increase in chromosome 8 copy number in all the tumors. SKY and aCGH analysis of tumors exhibiting trisomy 8 confirmed the numerical imbalances. The occurrence of trisomy 8 in a subset of pediatric USTS confirms a shared genomic alteration with several other soft tissue sarcomas. Further studies are required to determine the clinical implications of such a finding.

Characterization of trisomy 8 in pediatric undifferentiated sarcomas using advanced molecular cytogenetic techniques.

Osteosarcoma (OS) is an aggressive bone tumor characterized by complex abnormal karyotypes and a high level of genomic instability. Using high-resolution array comparative genomic hybridization (aCGH), a novel class of localized copy number variations called microaberrations has been detected. These genomic anomalies typically involve DNA imbalances affecting 700 kb to 1 Mb DNA, and are often associated with some type of genetic syndromes. Because the origin of instability in OS is poorly understood, we used aCGH to determine whether microaberrations were a characteristic of four OS cell lines: U-2 OS, HOS, MG-63, and SAOS-2. TP53 is mutated in SAOS-2, a line in which 17 microaberrations were found. In contrast, U-2 OS, which has a wild-type TP53, had only six such anomalies, the lowest incidence. A 500-kb microaberration within a region of gain at 5p15.33 in SAOS-2 was confirmed by fluorescence in situ hybridization. Significantly, this genomic location is close to the TERT gene, a region of gain in all four cell lines. To our knowledge, this is the first systematic analysis of the incidence of microaberrations in OS. The high levels of these anomalies detected suggest that the instability processes in OS that lead to a highly abnormal karyotypes may also be associated with acquisition of genomic microaberrations.

Identification of cryptic microaberrations in osteosarcoma by high-definition oligonucleotide array comparative genomic hybridization.

Osteosarcoma, the most frequent primary bone tumor, is a malignant mesenchymal sarcoma with a peak incidence in young children and adolescents. Left untreated, it progresses relentlessly to local and systemic disease, ultimately leading to death within months. Genomically, osteosarcomas are aneuploid with chaotic karyotypes, lacking the pathognomonic genetic rearrangements characteristic of most sarcomas. The familial genetics of osteosarcoma helped in elucidating some of the etiological molecular disruptions, such as the tumor suppressor genes RB1 in retinoblastoma and TP53 in Li-Fraumeni, and RECQL4 involved in DNA repair/replication in Rothmund-Thomson syndrome. Genomic profiling approaches such as array comparative genomic hybridization (aCGH) have provided additional insights concerning the mechanisms responsible for generating complex osteosarcoma genomes. This chapter provides a brief introduction to the clinical features of conventional osteosarcoma, the predominant subtypes, and a general overview of materials and analytical methods of osteosarcoma aCGH, followed by a more detailed literature overview of aCGH studies and a discussion of emerging genes, molecular mechanisms, and their clinical implications, as well as more recent application of integrative genomics in osteosarcoma. aCHG is helping elucidate genomic events leading to tumor development and evolution as well as identification of prognostic markers and therapeutic targets in osteosarcoma.

Array comparative genomic hybridization in osteosarcoma.

Metastatic urothelial carcinoma of the bladder is associated with multiple somatic copy-number alterations (SCNAs). We evaluated SCNAs to identify predictors of poor survival in patients with metastatic urothelial carcinoma treated with platinum-based chemotherapy.

Integrative analysis of 1q23.3 copy-number gain in metastatic urothelial carcinoma.

Alveolar soft part sarcoma (ASPS) is a soft tissue sarcoma with poor prognosis, and little molecular evidence exists for its origin, initiation, and progression. The aim of this study was to elucidate candidate molecular pathways involved in tumor pathogenesis.

High-resolution array CGH and gene expression profiling of alveolar soft part sarcoma.

Anaplastic lymphoma kinase (ALK) genomic alterations have emerged as a potent predictor of benefit from treatment with ALK inhibitors in several cancers. Currently, there is no information about ALK gene alterations in urothelial carcinoma (UC) and its correlation with clinical or pathologic features and outcome.

Identification of ALK gene alterations in urothelial carcinoma.

We investigated the prevalence of germline mutations in APC, ATM, BRCA1, BRCA2, CDKN2A, MLH1, MSH2, MSH6, PALB2, PMS2, PRSS1, STK11, and TP53 in patients with pancreatic cancer.

Prevalence of germline mutations in cancer predisposition genes in patients with pancreatic cancer.

We evaluated primary tumors from two cohorts, Spain (N = 111) and Greece (N = 102), for patients who were treated with platinum-based chemotherapy. Patients were tested for HER2 status (IHC score of 3+ or FISH ratio of ≥ 2.2) by immunohistochemistry (IHC), fluorescence in situ hybridization (FISH), DNA copy number, mRNA expression, and mutation status in patients with metastatic urothelial carcinoma (UC), and its impact on survival. ERBB2 mutation was determined by hotspot sequencing. mRNA expression was assessed using NanoString counting. Association of overall survival (OS) and HER2 status was assessed by a Cox regression model. NIH-3T3 cells containing HER2 V777L were assessed for growth, invasion, and HER2 kinase activation. In all, 22% of Spanish and 4% of Greek cohorts had 3+ HER2 staining by IHC. FISH amplification was identified in 20% of Spanish and 4% of Greek cohorts. Kappa coefficient between FISH and IHC was 0.47. HER2 status was not associated with OS in univariate (Spanish P = 0.34; Greek P = 0.11) or multivariate (Spanish P = 0.49; Greek P = 0.12) analysis. HER2-positive tumors expressed higher levels of HER2 mRNA than HER2-negative tumors (P < 0.001). HER2 mutations (V777L and L755S) were identified in two (2%) patients. In vitro analysis of V777L results in transformation of NIH-3T3 cells, leading to increased growth, invasion on soft agar, and HER2 kinase constitutive activation. In summary, HER2 overexpression or amplification in the primary tumor did not predict OS in patients with metastatic UC. HER2 positivity rates can differ between different populations. Further trials in genomically screened patients are needed to assess HER2-targeted therapies in UC.

HER2 as a target in invasive urothelial carcinoma.

Gleason scores (GS) 3+3 and 3+4 prostate cancers (PCa) differ greatly in their clinical courses, with Gleason pattern (GP) 4 representing a major independent risk factor for cancer progression. However, Gleason grade is not reliably ascertained by diagnostic biopsy, largely due to sampling inadequacies, subjectivity in the Gleason grading procedure, and a lack of more objective biomarker assays to stratify prostate cancer aggressiveness. In most aggressive cancer types, the tumor microenvironment exhibits a reciprocal pro-tumorigenic metabolic phenotype consistent with the reverse Warburg effect (RWE). The RWE can be viewed as a physiologic response to the epithelial phenotype that is independent of both the epithelial genotype and of direct tumor sampling. We hypothesize that differential expression of RWE-associated genes can be used to classify Gleason pattern, distinguishing GP3 from GP4 PCa foci.

Article	Year
An integrated mBAND and submegabase resolution tiling set (SMRT) CGH array analysis of focal amplification, microdeletions, and ladder structures consistent with breakage-fusion-bridge cycle... Genes, chromosomes & cancer\| PubMed ID: 15660435	2005
Stem cell enrichment approaches. Seminars in cancer biology\| PubMed ID: 16814562	2007
Three-color FISH analysis of TMPRSS2/ERG fusions in prostate cancer indicates that genomic microdeletion of chromosome 21 is associated with rearrangement. Neoplasia (New York, N.Y.)\| PubMed ID: 16820092	2006
The breakage-fusion-bridge (BFB) cycle as a mechanism for generating genetic heterogeneity in osteosarcoma. Chromosoma\| PubMed ID: 16897100	2006
Genomic mechanisms and measurement of structural and numerical instability in cancer cells. Seminars in cancer biology\| PubMed ID: 17126026	2007
Characterization of trisomy 8 in pediatric undifferentiated sarcomas using advanced molecular cytogenetic techniques. Cancer genetics and cytogenetics\| PubMed ID: 17350464	2007
Identification of cryptic microaberrations in osteosarcoma by high-definition oligonucleotide array comparative genomic hybridization. Cancer genetics and cytogenetics\| PubMed ID: 17981215	2007
Array comparative genomic hybridization in osteosarcoma. Methods in molecular biology (Clifton, N.J.)\| PubMed ID: 23412794	2013
Integrative analysis of 1q23.3 copy-number gain in metastatic urothelial carcinoma. Clinical cancer research : an official journal of the American Association for Cancer Research\| PubMed ID: 24486590	2014
High-resolution array CGH and gene expression profiling of alveolar soft part sarcoma. Clinical cancer research : an official journal of the American Association for Cancer Research\| PubMed ID: 24493828	2014
Identification of ALK gene alterations in urothelial carcinoma. PloS one\| PubMed ID: 25083769	2014
Prevalence of germline mutations in cancer predisposition genes in patients with pancreatic cancer. Gastroenterology\| PubMed ID: 25479140	2015
HER2 as a target in invasive urothelial carcinoma. Cancer medicine\| PubMed ID: 25720673	2015
Molecular characterization of Gleason patterns 3 and 4 prostate cancer using reverse Warburg effect-associated genes. Cancer & metabolism\| PubMed ID: 27152194	2016

Shamini Selvarajah

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