Interleukin 3 (IL-3) induces transcription from nonrearranged T cell receptor gamma loci in IL-3-dependent cell lines.

The expression of the murine TCR-gamma genes was examined in a series of IL-3-dependent and growth factor-independent cell lines. All of the IL-3-dependent cell lines, but none of the IL-3-independent lines, expressed high levels of one or more of the gamma genes but did not express the TCR-beta genes. None of the cell lines expressing the gamma loci contained detectable genomic gamma gene rearrangements. Sequencing of cDNA clones from two of the cell lines demonstrated that transcription was from nonrearranged gamma loci based on the presence of sequences in the cDNAs that are found immediately 5' of the J gamma 4 and J gamma 2 genes. The expression of gamma transcripts was dependent upon IL-3 and no transcripts were detectable within 6-8 h after the removal of IL-3. Readdition of IL-3, but not granulocyte CSF, resulted in the reappearance of gamma transcripts within 30 min. The results demonstrate that IL-3 regulates the expression of nonrearranged gamma loci. Since expression is required for rearrangement, it can be hypothesized that IL-3 may influence the ability of lymphoid/myeloid progenitors to commit to the T cell lineage.

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Validation of Sixteen Leukemia and Lymphoma Cell Lines as Controls for Molecular Gene Rearrangement Assays

Clinical Chemistry ◽

10.1093/clinchem/48.8.1344 ◽

2002 ◽

Vol 48 (8) ◽

pp. 1344-1351 ◽

Cited By ~ 3

Author(s):

Rong Yao ◽

Steven A Rich ◽

Erasmus Schneider

Keyword(s):

T Cell ◽

Southern Blot ◽

T Cell Receptor ◽

Cell Lines ◽

Gene Rearrangement ◽

Cell Receptor ◽

Lymphoma Cell ◽

Clinical Samples ◽

Gene Rearrangements ◽

Positive Controls

Abstract Background: Assays for rearrangement of the immunoglobulin, T-cell receptor, bcr/abl, and bcl-2 genes are valuable tools to aid in the diagnosis of leukemias and lymphomas and are now offered by many pathology laboratories. However, there is a lack of well-characterized and validated calibrators and positive controls for these assays. We therefore evaluated 16 readily available leukemia and lymphoma cell lines for their potential use as controls. Methods: DNA and RNA were isolated from each cell line and analyzed by Southern blot and PCR or reverse transcription-PCR (RT-PCR). Rearrangements in the IgJH, IgJκ, TcR-β or TcR-γ, bcr/abl, and bcl-2 genes were detected by commercially available probes and primers. Cell lineages were confirmed by immunophenotyping. Results: Immunoglobulin and T-cell receptor gene rearrangements were identified in five B- and three T-cell lines, respectively. Two cell lines tested positive for the bcr/abl gene, and one was positive for the bcl-2 gene rearrangement by Southern blot. Conclusions: The 16 cell lines studied can be used as positive controls in molecular detection assays for gene rearrangements. The parallel processing of these cell lines with clinical samples can serve to quality control the experimental procedures from the first step of DNA or RNA extraction to the final step of result analysis.

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T cell receptor (TCR) gene rearrangements in the assignment of tumour cell lineage.

Journal of Clinical Pathology ◽

10.1136/jcp.44.3.262-c ◽

1991 ◽

Vol 44 (3) ◽

pp. 262-262

Author(s):

N O'Connor

Keyword(s):

T Cell ◽

T Cell Receptor ◽

Tumour Cell ◽

Cell Lineage ◽

Cell Receptor ◽

Gene Rearrangements

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T-cell receptor beta chain gene rearrangements: Genetic markers of T-cell lineage and clonality

Human Pathology ◽

10.1016/s0046-8177(86)80125-3 ◽

1986 ◽

Vol 17 (6) ◽

pp. 546-551 ◽

Cited By ~ 29

Author(s):

Daniel M. Knowles ◽

Pier-Giuseppe Pelicci ◽

Riccardo Dalla-Favera

Keyword(s):

T Cell ◽

T Cell Receptor ◽

Genetic Markers ◽

Cell Lineage ◽

Cell Receptor ◽

Chain Gene ◽

Gene Rearrangements ◽

Beta Chain ◽

T Cell Receptor Beta ◽

Receptor Beta

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Detection of clonal T-cell receptor gamma gene rearrangements with the use of the polymerase chain reaction in cutaneous lesions of mycosis fungoides and Sezary syndrome

Archives of Dermatology ◽

10.1001/archderm.131.9.1027 ◽

1995 ◽

Vol 131 (9) ◽

pp. 1027-1031 ◽

Cited By ~ 17

Author(s):

H. Bachelez

Keyword(s):

Polymerase Chain Reaction ◽

T Cell ◽

Mycosis Fungoides ◽

T Cell Receptor ◽

Cell Receptor ◽

Sézary Syndrome ◽

Gene Rearrangements ◽

Chain Reaction ◽

Cutaneous Lesions ◽

Polymerase Chain

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Detection of Clonal T-cell Receptor ?? Gene Rearrangements Using Fluorescent-based PCR and Automated High-resolution Capillary Electrophoresis

Molecular Diagnosis ◽

10.2165/00066982-200106030-00004 ◽

2001 ◽

Vol 6 (3) ◽

pp. 169-179

Author(s):

VIVIAN LUO ◽

STUART R. LESSIN ◽

ROBERT B. WILSON ◽

HANNA RENNERT ◽

CINDY TOZER ◽

...

Keyword(s):

Capillary Electrophoresis ◽

T Cell ◽

High Resolution ◽

T Cell Receptor ◽

Receptor Gene ◽

Cell Receptor ◽

Gene Rearrangements ◽

T Cell Receptor Gene ◽

Cell Receptor Gene

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Clonal Diversity of Ig and T-Cell–Receptor Gene Rearrangements Identifies a Subset of Childhood B-Precursor Acute Lymphoblastic Leukemia With Increased Risk of Relapse

Blood ◽

10.1182/blood.v92.3.952 ◽

1998 ◽

Vol 92 (3) ◽

pp. 952-958 ◽

Cited By ~ 27

Author(s):

Elaine Green ◽

Carmel M. McConville ◽

Judith E. Powell ◽

Jillian R. Mann ◽

Philip J. Darbyshire ◽

...

Keyword(s):

Acute Lymphoblastic Leukemia ◽

T Cell ◽

T Cell Receptor ◽

Lymphoblastic Leukemia ◽

Clonal Diversity ◽

Cell Receptor ◽

Prognostic Indicators ◽

Gene Rearrangements ◽

Risk Patients ◽

Standard Risk

Abstract Current prognostic indicators such as age, sex, and white blood cell count (WBC) fail to identify all children with more aggressive forms of B-precursor acute lymphoblastic leukemia (ALL), and a proportion of patients without poor prognostic indicators still relapse. Results obtained from an analysis of 65 pediatic B-precursor ALL patients indicated that subclone formation leading to clonal diversity, as detected by Ig and T-cell receptor (TCR) gene rearrangements, may represent a very useful prognostic indicator, independent of age, sex, and WBC. Disease-free survival was significantly shorter in those patients showing clonal diversity at presentation. Furthermore, clonal diversity was detected not only in the majority of high-risk patients who relapsed but was also associated with a high probability of relapse in standard-risk patients. Sixty-five percent (13/20) of standard-risk patients who also showed clonal diversity subsequently relapsed, whereas the percentage of relapses among standard-risk patients without clonal diversity was much lower at 19% (7/36). Continued clonal evolution during disease progression is an important feature of aggressive B-precursor ALL. All 5 patients with clonal diversity who were followed up in our study showed a change in the pattern of clonality between presentation and relapse. This implies an important role for clonal diversity as a mechanism of disease progression through the process of clonal variation and clonal selection. © 1998 by The American Society of Hematology.

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