For more information, contact Abbott.
For more information, contact Abbott.
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The Vysis CLL FISH Probe Kit uses FISH DNA probe technology to determine deletion status of probe targets for locus-specific identifier (LSI) TP53 (containing tumor protein p53 gene, located on chromosome 17p), LSI ATM (containing ataxia telangiectasia mutated gene, located on chromosome 11q), and LSI D13S319 (containing marker D13S319, located on chromosome 13q), as well as determining trisomy 12 with CEP12 (D12Z3 alpha satellite, located on chromosome 12). The Vysis CLL FISH Probe Kit includes LSI 13q34 (containing lysosomal-associated membrane protein 1 gene, located on chromosome 13q) as a control probe.
Explanation of the Test
Chronic lymphocytic leukemia (CLL) is the most common form of adult leukemia in the developed world. Approximately 1 in 202 men and women will be diagnosed with CLL during their lifetime. The median age at diagnosis is approximately 70 years of age. Incidence rates are higher for males (6.44 per 100,000 population) than females (3.51 per 100,000 population). Leukemia incidence is highest among non-Hispanic whites (13.6 per 100,000 population); incidence is lowest among Asian and Pacific Islander populations (7.4 per 100,000 population) and American Indian and Alaska Native populations (7.3 per 100,000 population).
Probe Targets Information
The tumor suppressor protein, p53, has been shown to play a critical role in oncogenesis and response to chemotherapy in a variety of human cancers. In humans, the TP53 gene is found on the short arm of chromosome 17 (17p13) and is reported to be suppressed or mutated in a large number of human cancers. Deletions of the 17p region resulting in abnormalities of the tumor suppressor protein p53 have been identified as one of the poorest prognostic factors for CLL as it is predictive of short time to disease progression, short response duration, lack of response to therapy and short overall survival (OS).
The 17p deletion is more frequently observed in treated patients than in previously untreated patients, increasing in frequency during the course of the disease with up to 50% of patients with relapsed or refractory disease having the deletion. Approximately 8 to 12% of patients with CLL in the first line treatment carry del 17p.6 It is widely accepted that treatment outcomes in patients with del 17p are poor.
Once patients fail purine analog based chemoimmunotherapy, subsequent therapies provide shorter progression-free survival (PFS). 8 The outcome to treatment is strongly impacted by several molecular biologic features and several nonrandom cytogenetic alterations and oncogenes. In particular, an ultra-high risk group of CLL patients has been defined who have deletion of the short arm of chromosome 17 (del17p) with a median life expectancy of less than 2 to 3 years.
Patient Impact
Currently, most patients diagnosed with CLL have early stage-disease (Rai stage 0 or 1). Patients with early-stage CLL are a heterogeneous group; approximately 30% to 50% are at high risk of accelerated disease progression, and the remainder may live for decades and possibly never require therapy. Recent insights into the biological characteristics of leukemic B cells have led to the discovery of new prognostic tools (immunoglobulin variable-region heavy chain gene mutation status, cytogenetic abnormalities assessed by fluorescence in situ hybridization [FISH], and Z-chain-associated protein kinase-70 protein expression) that can contribute to the identification of patients with early-stage disease who are at high risk for early disease progression.
Routine karyotype analysis only detects chromosomal aberrations associated with CLL in 40% to 50% of the cases. Use of FISH and other technologies have detected genomic abnormalities in over 80% of cases of CLL. The common genomic aberrations seen are trisomy 12 and deletions of 13q, 17p, and 11q.
Several published studies suggest that some of these chromosomal abnormalities may be correlated with various disease parameters.
To learn more about the Vysis CLL FISH Probe Kit please visit: https://www.molecular.abbott/int/en/products/oncology/vysis-cll-fish-probe-kit
Each probe produces a single FISH signal for each copy of its target sequence.
Hybridization of Vysis LSI TP53 SpectrumOrange/ATM SpectrumGreen Probes is expected to produce two orange p53 and two green ATM signals in cells with two normal copies of chromosomes 17 and 11.
Hybridization of Vysis LSI D13S319 SpectrumOrange/13q34 SpectrumAqua/CEP 12 SpectrumGreen Probes is expected to produce two orange D13S319, two green CEP12, and two aqua LSI 13q34 signals in cells having two normal copies of chromosomes 12 and 13.
Gains or losses of a specific probe target sequence will be observed as cells with either greater than or less than, respectively, two signals for that probe.
While some abnormal CLL specimens are aberrant for only one probe locus, others may be abnormal for two or more loci. Other abnormal signal patterns may also occur.
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Please be aware that the website you have requested is intended for the residents of a particular country or countries, as noted on that site. As a result, the site may contain information on pharmaceuticals, medical devices and other products or uses of those products that are not approved in other countries or regions.