Sorted By Test Name - Mayo Medical Laboratories

TREC
87959
(T-ALL), T-cell prolymphocytic leukemia (T-PLL), T-cell large granular lymphocytic leukemia (T-LGL),
anaplastic large cell lymphoma (ALCL), peripheral T-cell lymphoma, and various other cutaneous, nodal,
and extrandodal lymphoma subtypes. The 2 most prevalent lymphoma subtypes are unspecified peripheral
T-cell lymphoma (3.7%) and ALCL (2.4%). A few common chromosome abnormalities are associated
with specific T-cell lymphoma subtypes, including: -inv (14)(q11q32) and t(14;14)(q11;q32) involving
the T-cell leukemia/lymphoma 1 gene (TCL1A) at 14Q32 -Translocations involving the ALK gene at
2p23 in ALCL -Isochromosome 7q and trisomy 8 in hepatosplenic T-cell lymphoma T-ALL is a
neoplastic disorder of lymphoblasts committed to the T-cell lineage. These malignancies comprise 15% to
20% of acute leukemias. While half of T-ALL patients have normal chromosome studies, molecular
cytogenetic analysis can identify abnormalities including: -Episomal amplification involving the
ABL1/NUP214 fusion gene. These abnormalities may be seen in tissues (ie, lymph nodes), as well as in
blood and bone marrow. This tissue-based assay detects the common chromosome abnormalities observed
in T-cell lymphoma and T-ALL (for blood and bone marrow in patients with T-ALL, see FRTAL/88783
T-Cell Acute Lymphoblastic Leukemia [T-ALL], FISH; for all other T-cell lymphomas, see
FRTLP/89040 T-Cell Lymphoma, FISH, Blood or Bone Marrow). These probes have diagnostic
relevance and can also be used to track response to therapy.
Useful For: Detecting a neoplastic clone associated with the common chromosome abnormalities seen
in patients with various T-cell lymphomas Tracking known chromosome abnormalities and response to
therapy in patients with T-cell neoplasms
Interpretation: A neoplastic clone is detected when the percent of cells with an abnormality exceeds
the normal reference range for any given probe. Detection of an abnormal clone is supportive of a
diagnosis of a T-cell lymphoma or T-cell acute lymphoblastic leukemia. The specific anomaly detected
may help subtype the neoplasm. The absence of an abnormal clone does not rule out the presence of a
neoplastic disorder.
Reference Values:
An interpretive report will be provided.
Clinical References: 1. World Health Organization Classification of Tumours. Pathology and
Genetics of Tumours of aematopoietic and Lymphoid Tissues. Edited by ES Jaffe, NL Harris, H Stein,
JW Vardiman. Lyon, IARC Press, 2001 2. Gesk S, Martin-Subero JI, Harder L, et al: Molecular
cytogenetic detection of chromosomal breakpoints in T-cell receptor gene loci. Leukemia
2003;17:738-745 3. Chin M, Mugishima H, Takamura M, et al: Hemophagocytic syndrome and
hepatosplenic (gamma)(delta) T-cell lymphoma with isochromosome 7q and 8 trisomy. J Pediatr Hematol
Oncol 2004;26(6):375-378 4. Graux C, Cools J, Michaux L, et al: Cytogenetics and molecular genetics of
T-cell acute lymphoblastic leukemia: from thymocyte to lymphoblast. Leukemia 2006;20:1496-1510 5.
Cayuela JM, Madani A, Sanhes L, et al: Multiple tumor-suppressor gene 1 inactivation is the most
frequent genetic in T-cell lymphoblastic leukemia. Blood 1996;87:3180-3186 6. Hayette S, Tigaud I,
Maguer-Satta V, et al: Recurrent involvement of the MLL gene in adult T-lineage acute lymphoblastic
leukemia. Blood 2002;99:4647-4649 7. Graux C, Cools J, Melotte C, et al: Fusion of NUP214 to ABL1
on amplified episomes in T-cell acute lymphoblastic leukemia. Nat Genet 2004;36:1084-1089
T-Cell Receptor Excision Circles (TREC) Analysis for Immune
Reconstitution
Clinical Information: T cell reconstitution is a critical feature of the recovery of the adaptive
immune response and has 2 main components: thymic output of new T cells and peripheral homeostatic
expansion of preexisting T cells. It has been shown that though thymic function declines with age,
substantial output is still maintained into late adult life.(1) In many clinical situations, thymic output is
crucial to the maintenance and competence of the T cell effector immune response. Thymic function can
be determined by T cell receptor excision circle (TREC) analysis. TRECs are episomal DNA by-products
of T cell receptor (TCR) rearrangement, which are nonreplicative. TRECs are expressed only in T cells of
thymic origin and each cell contains a single copy of TREC. Hence, TREC analysis provides a very
specific assessment of T cell recovery (eg, during human immunodeficiency virus [HIV] treatment or
after hematopoietic stem cell transplantation) or T cell competence. There are several TRECs generated
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