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Chronic Lymphocytic Leukemia (CLL) Panel by FISH

Test Code


Test Synonyms

MYB (6q23), ATM (11q22.3), +12, DLEU1 (13q14.3), TP53 (17p13)


Chronic Lymphocytic Leukemia(CLL)

The Vysis CLL Fish probe kit is indicated for detecting deletion of the LSI TP53 probe target (17p-) as an aid in identifying those patients with CLL for whom treatment with VENCLEXTA® (venetoclax) is indicated. Vysis CLL FISH Probe Kit is not intended for monitoring of residual disease


Fluorescence in situ Hybridization (FISH)

Turnaround Time

3-5 days

Specimen Requirements

2.0 mL (min. 1.0 mL) peripheral blood in sodium heparin preferred, EDTA accepted
1.0 mL (min. 0.5 mL) bone marrow in sodium heparin preferred, EDTA accepted
5 mm^3 fresh tissue in MPLN RPMI media

Specimen Stability
Peripheral blood and bone marrow stable at 18-25°C for 72 hours
Fresh tissue stable at 2-8°C for 72 hours
Storage & Handling

Whole blood and bone marrow, ship ambient
Fresh tissue ship in a Styrofoam container with a cool/refrigerated pack (Do not allow cool pack to directly contact sample.)

Causes for Rejection

Clotted specimen; Specimens exposed to extreme temperature; Anticoagulant toxic to cells; Insufficient number of cells

Reference Range

See report


Leukemias are a diverse group of diseases often characterized by multiple genetic aberrations distributed across the genome. In some cases, the same genetic aberrations are shared by different types of leukemia. Fluorescence in situ hybridization (FISH) has improved the detection of genomic aberrations in chronic lymphocytic leukemia. Chromosomal aberrations are detected in approximately 82% of patients. The most frequent changes are deletion 13q (55%), deletion 11q (18%), trisomy 12 (16 %), deletion 17p (7%) and deletion 6q (6%). FISH can detect these abnormalities in either interphase or metaphase cells.

  1. Emili Montserrat. (2002). Classical and new prognostic factors in chronic lymphocytic leukemia: where to now? The Hematology Journal. 3:7.
  2. Stilgenbauer S et al. (2002). Genetics of chronic lymphocytic leukemia: genomic aberrations and V(H) gene mutation status in pathogenesis and clinical course. Leukemia. 16(6):993-1007.
  3. Pettitt A.R. et al. (2001). Dysfunction in B-cell chronic lymphocytic leukemia: inactivation of ATM as an alternative to TP53 mutation. Blood. 98(3):814-822. 
  4. Dohner et al. (2000). Chromosomal Abnormalities in Chronic Lymphocytic Leukemia. NEJM. 343:1910.