quantitative-multispectral-analysis-following-fluorescent-tissue

Quantitative Multispectral Analysis Following Fluorescent Tissue Transplant for Visualization of Cell Origins, Types, and Interactions

With the desire to understand the contributions of multiple cellular elements to the development of a complex tissue; such as the numerous cell types that ...

MD Anderson Cancer Center

Women visiting Estonian STD clinics were subjected to PCR assay for human papillomavirus (HPV), Chlamydia trachomatis and Ureaplasma urealyticum biovar 2. The overall prevalence of coinfection was 8%. The chlamydial infection was found to be associated with HPV, especially with high-risk HPV (OR=2.5, p<0.005) and most significantly in women over 41 y of age. C. trachomatis infection also occurred more frequently in U. urealyticum-infected than in U. urealyticum-free patients (OR=2.6, p=0.02). U. urealyticum infection did not associate with HPV status. The clinical significance of the association between C. trachomatis and U. urelyticum infection remains to be elucidated.

Coinfection of Chlamydia trachomatis, Ureaplasma urealyticum and human papillomavirus among patients attending STD clinics in Estonia.

Mesenchymal stem cells (MSC) migrate to and proliferate within sites of inflammation and tumors as part of the tissue remodeling process. Radiation increases the expression of inflammatory mediators that could enhance the recruitment of MSC into the tumor microenvironment. To investigate this, bilateral murine 4T1 breast carcinomas (expressing renilla luciferase) were irradiated unilaterally (1 or 2 Gy). Twenty-four hours later, 2 x 10(5) MSC-expressing firefly luciferase were injected i.v. Mice were then monitored with bioluminescent imaging for expression of both renilla (tumor) and firefly (MSC) luciferase. Forty-eight hours postirradiation, levels of MSC engraftment were 34% higher in tumors receiving 2 Gy (P = 0.004) than in the contralateral unirradiated limb. Immunohistochemical staining of tumor sections from mice treated unilaterally with 2 Gy revealed higher levels of MSC in the parenchyma of radiated tumors, whereas a higher proportion of MSC remained vasculature-associated in unirradiated tumors. To discern the potential mediators involved in MSC attraction, in vitro migration assays showed a 50% to 80% increase in MSC migration towards conditioned media from 1 to 5 Gy-irradiated 4T1 cells compared with unirradiated 4T1 cells. Irradiated 4T1 cells had increased expression of the cytokines, transforming growth factor-beta1, vascular endothelial growth factor, and platelet-derived growth factor-BB, and this up-regulation was confirmed by immunohistochemistry in tumors irradiated in vivo. Interestingly, the chemokine receptor CCR2 was found to be up-regulated in MSC exposed to irradiated tumor cells and inhibition of CCR2 led to a marked decrease of MSC migration in vitro. In conclusion, clinically relevant low doses of irradiation increase the tropism for and engraftment of MSC in the tumor microenvironment.

Tumor irradiation increases the recruitment of circulating mesenchymal stem cells into the tumor microenvironment.

&#x80BF;&#x7624;&#x76F8;&#x5173;&#x6210;&#x7EA4;&#x7EF4;&#x7EC6;&#x80DE; (TAF)&#xFF0C;&#x5BF9;&#x4E8E;&#x80BF;&#x7624;&#x7684;&#x5F62;&#x6210;&#x8FC7;&#x7A0B;&#x63D0;&#x4F9B;&#x65E2;&#x529F;&#x80FD;&#x548C;&#x7ED3;&#x6784;&#x7684;&#x6709;&#x5229;&#x73AF;&#x5883;&#x81F3;&#x5173;&#x91CD;&#x8981;&#x3002;TAF&#xFF0C;&#x79F0;&#x4E3A;&#x6FC0;&#x6D3B;&#x6210;&#x7EA4;&#x7EF4;&#x7EC6;&#x80DE;&#xFF0C;&#x5BF9;&#x4F5C;&#x4E3A;&#x77E9;&#x9635;&#x5408;&#x6210;&#x6216;&#x6709;&#x8FB1;&#x4EBA;&#x683C;&#x7684;&#x7EC6;&#x80DE;&#x3001; &#x7EC6;&#x80DE;&#x6536;&#x7F29;&#x548C;&#x751A;&#x81F3;&#x8840;&#x7BA1;&#x76F8;&#x5173;&#x7EC6;&#x80DE;&#x57FA;&#x8D28;&#x80BF;&#x7624;&#x7684;&#x53D1;&#x751F;&#x6709;&#x65E2;&#x5B9A;&#x7684;&#x751F;&#x7269;&#x4EA7;&#x751F;&#x5F71;&#x54CD;&#x3002;&#x751F;&#x957F;&#x56E0;&#x5B50;&#x3001; &#x7EC6;&#x80DE;&#x56E0;&#x5B50;&#x3001; &#x8D8B;&#x5316;&#x56E0;&#x5B50;&#x3001; &#x77E9;&#x9635;&#x964D;&#x89E3;&#x7684;&#x9176;&#xFF0C;&#x548C;&#x7531;&#x8FD9;&#x4E9B;&#x7EC6;&#x80DE;&#x514D;&#x75AB;&#x8C03;&#x8282;&#x673A;&#x5236;&#x751F;&#x4EA7;&#x589E;&#x52A0;&#x80BF;&#x7624;&#x7684;&#x5F62;&#x6210;&#x8FC7;&#x7A0B;&#x63D0;&#x4F9B;&#x4E00;&#x4E2A;&#x5408;&#x9002;&#x7684;&#x73AF;&#x5883;&#x3002;&#x6709;&#x51E0;&#x4E2A;&#x5EFA;&#x8BAE;&#x7684;&#x8D77;&#x6E90;&#x7684; TAF &#x5305;&#x62EC;&#x7EC4;&#x7EC7;&#x9A7B;&#x5730;&#x3001; &#x5FAA;&#x73AF;&#xFF0C;&#x548C;&#x4E0A;&#x76AE;-&#x5230;-&#x95F4;&#x5145;&#x8D28;-&#x8F6C;&#x6362;&#x7684;&#x5355;&#x5143;&#x683C;&#x3002;

&#x9AA8;&#x9AD3;&#x95F4;&#x5145;&#x8D28;&#x5E72;&#x7EC6;&#x80DE;&#x5411;&#x80BF;&#x7624;&#x76F8;&#x5173;&#x6210;&#x7EA4;&#x7EF4;&#x7EC6;&#x80DE;&#x7684;&#x8FC7;&#x6E21;&#x5230;&#x7EA4;&#x7EF4;&#x8840;&#x7BA1;&#x7F51;&#x7EDC;&#x6269;&#x5F20;&#x4E0E;&#x80BF;&#x7624;&#x8FDB;&#x5C55;&#x4F5C;&#x51FA;&#x8D21;&#x732E;&#x3002;

Tumor associated fibroblasts (TAF), are essential for tumor progression providing both a functional and structural supportive environment. TAF, known as activated fibroblasts, have an established biological impact on tumorigenesis as matrix synthesizing or matrix degrading cells, contractile cells, and even blood vessel associated cells. The production of growth factors, cytokines, chemokines, matrix-degrading enzymes, and immunomodulatory mechanisms by these cells augment tumor progression by providing a suitable environment. There are several suggested origins of the TAF including tissue-resident, circulating, and epithelial-to-mesenchymal-transitioned cells.

Mesenchymal stem cell transition to tumor-associated fibroblasts contributes to fibrovascular network expansion and tumor progression.

Fibroblastes tumeur associ&eacute;e (TAF), sont essentiels pour fournir aussi bien un environnement de soutien fonctionnel et structurel de la progression tumorale. TAF, connu sous le nom activ&eacute; fibroblastes, avoir des r&eacute;percussions biologiques &eacute;tablies sur tumorigen&egrave;se comme la synth&egrave;se de la matrice ou matrice d&eacute;gradant les cellules, cellules contractiles et m&ecirc;me les cellules des vaisseaux sanguins associ&eacute;. La production de facteurs de croissance, cytokines, chimiokines, enzymes d&eacute;gradant la matrice et m&eacute;canismes immunomodulateurs par ces cellules augmenter la progression tumorale en fournissant un environnement ad&eacute;quat. Il y a plusieurs origines sugg&eacute;r&eacute;es du TAF y compris les cellules de tissu-r&eacute;sident, circulation et &eacute;pith&eacute;liales-&agrave;-m&eacute;senchymateuses-pass&eacute;s.

Cellules souches m&eacute;senchymateuses transition aux fibroblastes associ&eacute;es aux tumeurs contribue au r&eacute;seau fibrovasculaire expansion et la progression tumorale.

Tumor-assoziierten Fibroblasten (TAF), sind wesentlich f&uuml;r Tumor Fortschreiten bietet sowohl eine funktionale und strukturelle unterst&uuml;tzende Umgebung. TAF, bekannt als aktiviert die Fibroblasten, etablierte biologische Auswirkungen auf Tumorentstehung als Synthese von Matrix oder Matrix erniedrigende Zellen, kontraktilen Zellen und sogar Blutgef&auml;&szlig; verbundenen Zellen haben. Die Produktion von Wachstumsfaktoren, Zytokine, Chemokine, Matrix-entw&uuml;rdigende Enzyme und immunmodulatorische Mechanismen durch diese Zellen vermehren Tumor Fortschreiten durch die Bereitstellung eines geeigneten Umfelds. Es gibt mehrere vorgeschlagene Urspr&uuml;nge der die TAF, einschlie&szlig;lich Gewebe-Resident, zirkulierende und den Epithel--mesenchymal-&Uuml;bergang in Zellen.

Mesenchymale Stammzellen &Uuml;bergang zur Tumor-assoziierte Fibroblasten tr&auml;gt zur Erweiterung und Tumor Fortschreiten der fibrovascular Netzwerk.

Fibroblasti tumore associato (TAF), sono essenziali per la progressione del tumore che fornisce sia un ambiente di sostegno strutturale e funzionale. TAF, noto come attivazione dei fibroblasti, hanno un impatto biologico stabilito su tumorigenesi come sintesi di matrice o matrice degradanti, cellule contrattili e anche cellule dei vasi sanguigni associati. La produzione di fattori di crescita, citochine, chemochine, enzimi degradanti matrix e meccanismi immunomodulatori da queste cellule aumentare la progressione del tumore fornendo un ambiente adatto. Ci sono diverse origini suggeriti di TAF comprese cellule tessuto-residente, circolanti ed epiteliali-a-mesenchimali-transizione.

Transizione delle cellule staminali mesenchimali di fibroblasti tumore-associati contribuisce alla progressione di tumore e di espansione di rete fibrovascolare.

&#x95A2;&#x9023;&#x4ED8;&#x3051;&#x3089;&#x308C;&#x305F;&#x816B;&#x760D;&#x7E4A;&#x7DAD;&#x82BD;&#x7D30;&#x80DE; (TAF) &#x304C;&#x816B;&#x760D;&#x306E;&#x9032;&#x884C;&#x306E;&#x4E21;&#x65B9;&#x69CB;&#x9020;&#x3068;&#x6A5F;&#x80FD;&#x306E;&#x652F;&#x63F4;&#x74B0;&#x5883;&#x3092;&#x63D0;&#x4F9B;&#x3059;&#x308B;&#x305F;&#x3081;&#x306B;&#x4E0D;&#x53EF;&#x6B20;&#x3067;&#x3059;&#x3002;TAF &#x3068;&#x3057;&#x3066;&#x77E5;&#x3089;&#x308C;&#x3066;, &#x7DDA;&#x7DAD;&#x82BD;&#x7D30;&#x80DE;&#x6D3B;&#x6027;&#x5316;&#x3001;&#x816B;&#x760D;&#x5F62;&#x6210;&#x5408;&#x6210;&#x30DE;&#x30C8;&#x30EA;&#x30C3;&#x30AF;&#x30B9;&#x307E;&#x305F;&#x306F;&#x30DE;&#x30C8;&#x30EA;&#x30C3;&#x30AF;&#x30B9;&#x306E;&#x30BB;&#x30EB;&#x3001;&#x53CE;&#x7E2E;&#x7D30;&#x80DE;&#x304A;&#x3088;&#x3073;&#x8840;&#x7BA1;&#x306B;&#x95A2;&#x9023;&#x4ED8;&#x3051;&#x3089;&#x308C;&#x305F;&#x30BB;&#x30EB;&#x3082;&#x4F4E;&#x4E0B;&#x3068;&#x3057;&#x3066;&#x4E0A;&#x78BA;&#x7ACB;&#x3055;&#x308C;&#x305F;&#x751F;&#x7269;&#x5B66;&#x7684;&#x5F71;&#x97FF;&#x3092;&#x6301;&#x3063;&#x3066;&#x3044;&#x307E;&#x3059;&#x3002;&#x6210;&#x9577;&#x56E0;&#x5B50;&#x3001;&#x30B5;&#x30A4;&#x30C8;&#x30AB;&#x30A4;&#x30F3;&#x3001;&#x30B1;&#x30E2;&#x30AB;&#x30A4;&#x30F3;&#x3001;&#x30DE;&#x30C8;&#x30EA;&#x30C3;&#x30AF;&#x30B9;&#x5206;&#x89E3;&#x9175;&#x7D20;&#x3068;&#x3053;&#x308C;&#x3089;&#x306E;&#x7D30;&#x80DE;&#x306B;&#x3088;&#x3063;&#x3066;&#x514D;&#x75AB;&#x8ABF;&#x7BC0;&#x6A5F;&#x69CB;&#x306E;&#x751F;&#x7523;&#x306B;&#x9069;&#x3057;&#x305F;&#x74B0;&#x5883;&#x3092;&#x63D0;&#x4F9B;&#x3059;&#x308B;&#x3053;&#x3068;&#x306B;&#x3088;&#x308A;&#x3001;&#x816B;&#x760D;&#x306E;&#x9032;&#x884C;&#x3092;&#x5897;&#x5927;&#x3055;&#x305B;&#x307E;&#x3059;&#x3002;&#x7D44;&#x7E54;&#x306E;&#x5C45;&#x4F4F;&#x8005;&#x3001;&#x5FAA;&#x74B0;&#x3001;&#x304A;&#x3088;&#x3073;&#x9077;&#x79FB;&#x4E0A;&#x76AE;--&#x9593;&#x8449;&#x7CFB;-&#x5F8C;&#x306E;&#x7D30;&#x80DE;&#x3092;&#x542B;&#x3080; TAF &#x306E;&#x3044;&#x304F;&#x3064;&#x304B;&#x306E;&#x63A8;&#x5968;&#x8D77;&#x6E90;&#x3067;&#x3059;&#x3002;

&#x9593;&#x8449;&#x7CFB;&#x5E79;&#x7D30;&#x80DE;&#x306E;&#x8EE2;&#x79FB;&#x816B;&#x760D;&#x95A2;&#x9023;&#x7DDA;&#x7DAD;&#x82BD;&#x7D30;&#x80DE;&#x306B;&#x7DDA;&#x7DAD;&#x8840;&#x7BA1;&#x30CD;&#x30C3;&#x30C8;&#x30EF;&#x30FC;&#x30AF;&#x306E;&#x62E1;&#x5927;&#x3068;&#x816B;&#x760D;&#x306E;&#x9032;&#x884C;&#x306B;&#x8CA2;&#x732E;&#x3057;&#x3066;&#x3044;&#x307E;&#x3059;&#x3002;

&#xC885;&#xC591; &#xAD00;&#xB828; &#xAC8C;&#xC7AC; (TAF) &#xBAA8;&#xB450; &#xAE30;&#xB2A5; &#xBC0F; &#xAD6C;&#xC870; &#xC9C0;&#xC6D0; &#xD658;&#xACBD;&#xC744; &#xC81C;&#xACF5; &#xD558;&#xB294; &#xC885;&#xC591; &#xC9C4;&#xD589;&#xC5D0; &#xD544;&#xC218;&#xC801;&#xC785;&#xB2C8;&#xB2E4;. TAF&#xB85C; &#xC54C;&#xB824;&#xC9C4; &#xC12C;&#xC720; &#xC544; &#xC138;&#xD3EC; &#xD65C;&#xC131;&#xD654;, &#xB9E4;&#xD2B8;&#xB9AD;&#xC2A4; &#xD569;&#xC131; &#xB610;&#xB294; &#xD589;&#xB82C; &#xC140;, &#xC218;&#xCD95; &#xC138;&#xD3EC;&#xC640; &#xAD00;&#xB828; &#xB41C; &#xD608;&#xAD00; &#xC138;&#xD3EC;&#xB3C4; &#xC800;&#xD558;&#xB85C; tumorigenesis&#xC5D0; &#xC124;&#xC815; &#xB41C; &#xC0DD;&#xBB3C; &#xD559;&#xC801; &#xC601;&#xD5A5;&#xC744; &#xBBF8;&#xCE60;. &#xC131;&#xC7A5; &#xC778;&#xC790;, cytokines, chemokines, &#xB9E4;&#xD2B8;&#xB9AD;&#xC2A4; &#xC800;&#xD558; &#xD6A8;&#xC18C; &#xBC0F;&#xC774; &#xC138;&#xD3EC;&#xC5D0; &#xC758;&#xD574; immunomodulatory &#xBA54;&#xCEE4;&#xB2C8;&#xC998;&#xC758; &#xC0DD;&#xC0B0; &#xC885;&#xC591; &#xC9C4;&#xD589;&#xC744; &#xC99D;&#xAC00; &#xC2DC;&#xD0A4;&#xAE30; &#xC704;&#xD574; &#xC801;&#xD569; &#xD55C; &#xD658;&#xACBD;&#xC744; &#xC81C;&#xACF5; &#xD558; &#xC5EC;. &#xC5EC;&#xB7EC; &#xC81C;&#xC548;&#xB41C; &#xAE30;&#xC6D0;&#xC758; &#xC870;&#xC9C1; &#xC0C1;&#xC8FC;, &#xC21C;&#xD658;, &#xBC0F; &#xC0C1;&#xD53C;-&#xD558;-&#xC5FD;-&#xC804;&#xD658; &#xC138;&#xD3EC;&#xB97C; &#xD3EC;&#xD568; &#xD55C; TAF&#xB294;.

&#xC885;&#xC591; &#xAD00;&#xB828; &#xAC8C;&#xC7AC; &#xC911;&#xAC04; &#xC5FD; &#xC904;&#xAE30; &#xC138;&#xD3EC; &#xC804;&#xD658; fibrovascular &#xB124;&#xD2B8;&#xC6CC;&#xD06C; &#xD655;&#xC7A5; &#xBC0F; &#xC885;&#xC591; &#xC9C4;&#xD589;&#xC5D0; &#xAE30;&#xC5EC; &#xD55C;&#xB2E4;.

Los fibroblastos asociados tumor (TAF), son esenciales para proporcionar tanto un ambiente de apoyo funcional y estructural de la progresi&oacute;n del tumor. TAF, conocido como activa los fibroblastos, tienen un impacto biol&oacute;gico establecido en tumorigenesis como s&iacute;ntesis de la matriz o matriz degradantes de las c&eacute;lulas, las c&eacute;lulas contr&aacute;ctiles e incluso las c&eacute;lulas de los vasos sangu&iacute;neos asociados. La producci&oacute;n de factores de crecimiento, citoquinas, quimioquinas, enzimas degradadoras de matriz y mecanismos inmunomoduladores por estas c&eacute;lulas aumentar la progresi&oacute;n del tumor por proporcionar un ambiente adecuado. Hay varios or&iacute;genes sugeridos de la TAF, incluyendo las c&eacute;lulas de tejido-residente, circulaci&oacute;n y epitelial-a-mesenquimal-transici&oacute;n.

C&eacute;lulas madre mesenquimales transici&oacute;n a fibroblastos asociados tumor contribuye a red fibrovascular expansi&oacute;n y progresi&oacute;n tumoral.

Because of the inflammatory nature and extensive stromal compartment in pancreatic tumors, we investigated the role of mesenchymal stromal cells (MSC) to engraft selectively in pancreatic carcinomas and serve as anti-tumor drug delivery vehicles to control pancreatic cancer progression.

Mesenchymal stromal cells alone or expressing interferon-beta suppress pancreatic tumors in vivo, an effect countered by anti-inflammatory treatment.

Targeted migration is a necessary attribute for any gene delivery vehicle. Mesenchymal stem cells (MSC) have been used as effective delivery vehicles for treatments against cancer, graft versus host disease, -arthritis, multiple sclerosis, and many other diseases. MSC migrate toward sites of inflammation, however, the true migratory mechanism has yet to be elucidated. There are several receptors and respective chemokines known to be involved in the migration of the MSC. Further insight to MSC migration will be revealed both in vivo and in vitro through the application of migration assays from the most simple, to the more technologically demanding.

Dissecting mesenchymal stem cell movement: migration assays for tracing and deducing cell migration.

Cancer stem cells (CSCs) are a small subpopulation of cancer cells that have increased resistance to conventional therapies and are capable of establishing metastasis. However, only a few biomarkers of CSCs have been identified. Here, we report that ganglioside GD2 (a glycosphingolipid) identifies a small fraction of cells in human breast cancer cell lines and patient samples that are capable of forming mammospheres and initiating tumors with as few as 10 GD2+ cells. In addition, the majority of GD2+ cells are also CD44hiCD24lo, the previously established CSC-associated cell surface phenotype. Gene expression analysis revealed that GD3 synthase (GD3S) is highly expressed in GD2+ as well as in CD44hiCD24lo cells and that interference with GD3S expression, either by shRNA or using a pharmacological inhibitor, reduced the CSC population and CSC-associated properties. GD3S knockdown completely abrogated tumor formation in vivo. Also, induction of epithelial-mesenchymal transition (EMT) in transformed human mammary epithelial cells (HMLER cells) dramatically increased GD2 as well as GD3S expression in these cells, suggesting a role of EMT in the origin of GD2+ breast CSCs. In summary, we identified GD2 as a new CSC-specific cell surface marker and GD3S as a potential therapeutic target for CSCs, with the possibility of improving survival and cure rates in patients with breast cancer.

Ganglioside GD2 identifies breast cancer stem cells and promotes tumorigenesis.

The act of migration is similar for many cell types. The migratory mechanism of mesenchymal stem cells (MSC) is not completely elucidated, yet many of the initial studies have been based on current understanding of the leukocyte migration. A normal function of MSC is the ability of the cell to migrate to and repair wounded tissue. This wound healing property of MSC originates with migration towards inflammatory signals produced by the wounded environment [1]. A tumor and its microenvironment are capable of eliciting a similar inflammatory response from the MSC, thus resulting in migration of the MSC towards the tumor microenvironment. We have shown MSC migration both in vitro and in vivo. In this chapter, we elucidate several in vivo methods to study MSC migration and mobilization to the tumor microenvironment. The first model is an exogenous model of MSC migration that can be performed in both xenograft and syngenic systems with in vitro expanded MSC. The second model utilizes transgenic-fluorescent--colored mice to follow endogenous bone marrow components including MSC. The third technique enables us to analyze data from the transgenic model through multispectral imaging. Furthermore, the migratory phenotype of MSC can be exploited for use in tumor-targeted gene delivery therapy has been efficacious in animal model studies and is an anticipated therapeutic device in clinical trials.

Tracking inflammation-induced mobilization of mesenchymal stem cells.

Many ovarian cancers originate from ovarian surface epithelium, where they develop from cysts intermixed with stroma. The stromal layer is critical to the progression and survival of the neoplasm and consequently is recruited into the tumor microenvironment.

Tumor stroma engraftment of gene-modified mesenchymal stem cells as anti-tumor therapy against ovarian cancer.

Tumor-stroma interactions play a crucial role in cancer progression by eliciting factors that promote proliferative, angiogenic, and invasive supports to the tumor microenvironment. Mesenchymal stromal/stem cells (MSC) contribute to stroma in part as cancer-associated fibroblasts (CAF), but a complete understanding of how MSC contribute to the tumor stroma is lacking. In this study, we show how CAF phenotypes rely upon MSC expression of the multifunctional cell surface glycoprotein CD44, a putative stem cell marker. Through bone marrow transplantation experiments in a transgenic mouse model of cancer, we determined that CD44 deficiency leads to a relative reduction in the contribution of bone marrow-derived cells to tumor stroma. CD44 attenuation in MSC limited their expression of CAF markers induced by tumor conditioning, and these MSC migrated poorly and provided weak angiogenic support compared with wild-type MSC. These defects were linked to deficiencies in the ability of CD44-attenuated MSC to transcriptionally upregulate Twist expression. Together, our results establish that CD44 expression contributes to critical functions in the tumor stroma. Cancer Res; 73(17); 5347-59. Â©2013 AACR.

Erika L. Spaeth

Department of Leukemia

MD Anderson Cancer Center

Quantitative Multispectral Analysis Following Fluorescent Tissue Transplant for Visualization of Cell Origins, Types, and Interactions

Erika L. Spaeth

.css-o250i3{font-size:18px;font-family:Open Sans,sans-serif;line-height:21.6px;}Department of Leukemia

MD Anderson Cancer Center

Quantitative Multispectral Analysis Following Fluorescent Tissue Transplant for Visualization of Cell Origins, Types, and Interactions

Department of Leukemia