scholarly journals Detection of circulating tumor cells using GeneScan analysis for antigen receptor gene rearrangements in canine lymphoma patients

2016 ◽  
Vol 78 (5) ◽  
pp. 877-881 ◽  
Author(s):  
Saaya HIYOSHI-KANEMOTO ◽  
Yuko GOTO-KOSHINO ◽  
Kenjiro FUKUSHIMA ◽  
Masashi TAKAHASHI ◽  
Hideyuki KANEMOTO ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Circulating Tumor Cells ◽  
Receptor Gene ◽  
Antigen Receptor ◽  
Gene Rearrangements ◽  
Canine Lymphoma ◽  
Genescan Analysis

scholarly journals Rearrangement and expression of T cell antigen receptor and gamma genes during thymic development.

1986 ◽  
Vol 164 (1) ◽  
pp. 1-24 ◽  
Author(s):  
R Haars ◽  
M Kronenberg ◽  
W M Gallatin ◽  
I L Weissman ◽  
F L Owen ◽  
...  
Keyword(s):  
T Cell ◽  
Fetal Liver ◽  
Receptor Gene ◽  
Gene Segment ◽  
Antigen Receptor ◽  
Gene Rearrangements ◽  
T Cell Antigen Receptor ◽  
Cell Antigen Receptor ◽  
Cell Antigen ◽  
Beta Gene

Rearrangement and expression of the T cell antigen receptor and the gamma genes during T cell ontogeny is a regulated process; the gamma genes are rearranged and expressed first, followed by the beta and then the alpha genes. Expression of both functional alpha and beta gene RNA first occurs at day 17 of gestation, along with the expression of T3 delta chain RNA. T cell antigen receptor gene rearrangements occur primarily or exclusively in the thymus, although some gamma gene rearrangements occur outside the thymus in fetal liver cells that may be committed T cell progenitors. There is no gross difference in the extent of beta and gamma gene rearrangements in the adult thymocyte subpopulations that were analyzed, despite the fact that some of these populations cannot respond to antigen and never emigrate from the thymus. Quantitative analysis of rearrangements in total adult thymocyte DNA shows that beta gene rearrangements generally occur on both chromosomal homologs, and that rearrangements occur preferentially to the J beta 2 gene segment cluster.

Presence of clone-specific antigen receptor gene rearrangements at birth indicates an in utero origin of diverse types of early childhood acute lymphoblastic leukemia

Blood ◽  
2000 ◽  
Vol 95 (8) ◽  
pp. 2722-2724 ◽  
Author(s):  
Karin Fasching ◽  
Simon Panzer ◽  
Oskar A. Haas ◽  
Rolf Marschalek ◽  
Helmut Gadner ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Fusion Gene ◽  
Lymphoblastic Leukemia ◽  
Receptor Gene ◽  
Specific Antigen ◽  
Antigen Receptor ◽  
In Utero ◽  
Gene Rearrangements ◽  
Fetal Life ◽  
Childhood All

Abstract There is strong evidence that infant leukemias with a t(4;11) translocation originate in utero. To test whether other subtypes of childhood leukemias are also initiated during fetal life, we used clone-specific genetic markers for the analysis of neonatal blood spots from 5 children aged 6 months to 4 years 8 months at diagnosis of pro-B, common acute lymphoblastic leukemia (ALL), and T-ALL. In all children, the clonotypic antigen receptor gene rearrangements were already present at birth. The estimated amount of clonotypic cells was in the range of 10 to 100 cells per blood spot. In 2 infants with a t(4;11) positive ALL, we detected similar amounts of the fusion gene sequences compared with the clonal antigen receptor gene rearrangements, suggesting the presence of both markers in the same cells. Our data indicate that the first leukemogenic event of diverse types of childhood ALL may already occur in utero.

Presence of clone-specific antigen receptor gene rearrangements at birth indicates an in utero origin of diverse types of early childhood acute lymphoblastic leukemia

Blood ◽  
2000 ◽  
Vol 95 (8) ◽  
pp. 2722-2724
Author(s):  
Karin Fasching ◽  
Simon Panzer ◽  
Oskar A. Haas ◽  
Rolf Marschalek ◽  
Helmut Gadner ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Fusion Gene ◽  
Lymphoblastic Leukemia ◽  
Receptor Gene ◽  
Specific Antigen ◽  
Antigen Receptor ◽  
In Utero ◽  
Gene Rearrangements ◽  
Fetal Life ◽  
Childhood All

There is strong evidence that infant leukemias with a t(4;11) translocation originate in utero. To test whether other subtypes of childhood leukemias are also initiated during fetal life, we used clone-specific genetic markers for the analysis of neonatal blood spots from 5 children aged 6 months to 4 years 8 months at diagnosis of pro-B, common acute lymphoblastic leukemia (ALL), and T-ALL. In all children, the clonotypic antigen receptor gene rearrangements were already present at birth. The estimated amount of clonotypic cells was in the range of 10 to 100 cells per blood spot. In 2 infants with a t(4;11) positive ALL, we detected similar amounts of the fusion gene sequences compared with the clonal antigen receptor gene rearrangements, suggesting the presence of both markers in the same cells. Our data indicate that the first leukemogenic event of diverse types of childhood ALL may already occur in utero.

scholarly journals Detection of Activating Estrogen Receptor Gene (ESR1) Mutations in Single Circulating Tumor Cells

2017 ◽  
Vol 23 (20) ◽  
pp. 6086-6093 ◽  
Author(s):  
Carmela Paolillo ◽  
Zhaomei Mu ◽  
Giovanna Rossi ◽  
Matthew J. Schiewer ◽  
Thomas Nguyen ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Tumor Cells ◽  
Circulating Tumor Cells ◽  
Receptor Gene ◽  
Estrogen Receptor Gene ◽  
Esr1 Mutations

scholarly journals Detection of Androgen Receptor Mutations in Circulating Tumor Cells in Castration-Resistant Prostate Cancer

2010 ◽  
Vol 56 (9) ◽  
pp. 1492-1495 ◽  
Author(s):  
Yuqiu Jiang ◽  
John F Palma ◽  
David B Agus ◽  
Yixin Wang ◽  
Mitchell E Gross
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Tumor Cells ◽  
Circulating Tumor Cells ◽  
Relative Abundance ◽  
Direct Sequencing ◽  
Receptor Gene ◽  
Missense Mutations ◽  
Castration Resistant Prostate Cancer ◽  
Castration Resistant

BACKGROUND Coding mutations in the AR (androgen receptor) gene have been identified in tissue samples from patients with advanced prostate cancer and represent a possible mechanism underlying the development of castration-resistant prostate cancer (CRPC). There is a paucity of tumor-derived tissue available for molecular studies of CRPC patients. Circulating tumor cells (CTCs) in the blood of CRPC patients represent a possible avenue for interrogating the disease of such patients. METHODS Circulating tumor cells were captured with the CellSearch® Circulating Tumor Cell (CTC) Kit and with the CellSearch Profile Kit plus Qiagen's AllPrep DNA/RNA Micro Kit for the measurement of the CTC count per 7.5 mL of blood and for the isolation of nucleic acids, respectively. The AR gene was amplified by the PCR, and mutation status and relative abundance were analyzed by applying Transgenomic's WAVE® denaturing HPLC technology followed by direct sequencing. RESULTS AR mutations were detected in 20 of 35 CRPC patients; 19 missense mutations, 2 silent mutations, 5 deletions, and 1 insertion were observed. The relative abundance of the mutants in the amplified products ranged from 5% to 50%. Many of the AR mutations were identified in surgical biopsies or at autopsy and were associated with resistance to androgen-directed therapies. CONCLUSIONS AR mutations can be identified in CTC-enriched peripheral blood samples from CRPC patients. This approach has the potential to open new perspectives in understanding CTCs and the mechanisms for tumor progression and metastasis in CRPC.

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