CGI Italia announces the release of new CE-marked TP53/RARA DNA-FISH Probe

By admin on January 10 2011

PRESS RELEASEwww.cancergeneticsitalia.com)– Cancer Genetics Italia S.r.l. (CGI Italia) has released a new CE marked DNA-FISH Probe designed to detect the deletion of the TP53 gene [del(TP53)] on 17p13 relative to the control gene RARA on 17q21 using fluorescence in situ hybridization (FISH). CGI Italia’s TP53/RARA DNA-FISH Probe will aid in the diagnosis and prognosis of several hematological malignancies and solid tumors. CGI Italia includes the TP53/RARA DNA-FISH Probe in the chronic lymphocytic leukemia (CLL), multiple myeloma (MM), myelodysplastic syndrome (MDS), and solid tumor panels. The TP53 gene is a known tumor suppressor gene[1]. In CLL, del(TP53) is associated with lower overall survival[2]. In MM patients, del(TP53) is associated with an advanced stage of MM, shortened survival, and a poor prognosis[3],[4]. Similarly, in MDS patients, del(TP53) is associated with a poor prognosis and is linked with the progression to a leukemic transformation[5]. The TP53 deletion has prognostic value in many solid tumors, including breast cancer, brain glioma, gastric adenocarcinoma, urinary bladder malignancies and esophageal adenocarcinoma.

Overview

CLL arises through clonal expansion of CD5+ B lymphocytes. CLL is the most common form of adult leukemia in Western countries and accounts for approximately 30–40% of all leukemias[6]. Western Europe has the highest number of patients with CLL, with a higher prevalence in males[7]. Accurate prognostication for treatment options is highly desirable in CLL considering that it occurs almost exclusively in adults (median age at diagnosis is 65 to 68 years) and chromosomal changes in patients with CLL vary, which affects the prognosis.

MM is a cancer of the plasma cells found primarily in bone marrow. MM is the second most common hematological cancer in Europe and accounts for almost 10% of all hematological cancers[8],[9]. In Europe, it is estimated that 5.7 out of 100,000 people will be newly diagnosed with MM each year[10]. Accurate prognostication for treatment options is highly desirable because patients display great clinical heterogeneity in the course of their disease[11].

MDS is a general term used to describe cancer in the blood and bone marrow. There are different types of MDS and types require different levels of attention. MDS is difficult to diagnose and accurate diagnosis is crucial to prognosis.

The del(TP53) has been found in several solid tumors, including esophageal adenocarcinoma. In recent years, incidence of esophageal adenocarcinoma has been increasing in Western Europe[12]. Esophageal adenocarcinoma is cancer of the epithelia originating in glandular tissue in the esophagus. Barrett’s esophagus (BE) is a known precursor to esophageal adenocarcinoma.

CGI Italia’s TP53/RARA DNA-FISH Probe is designed to clearly detect the deletion of TP53 on chromosome 17p13. The TP53 gene is known to regulate different cell processes, and the deletion is found in several different cancers. The DNA-FISH Probe can be used on peripheral blood and bone marrow as well as formalin fixed paraffin embedded (FFPE) tissue. CGI Italia DNA-FISH Probes are expertly designed with robust signal intensity and are distributed in a ready-to-use format that is competitively priced.

 

About Cancer Genetics Italia S.r.l.,

CGI Italia is a subsidiary of Cancer Genetics, Inc. (CGI) located in Rutherford, New Jersey, USA. CGI was founded in by Dr. R.S.K. Chaganti in 1999 on the principal to provide leading clinical cytogenetic and molecular genetics services. The mission of CGI Italia is to provide state-of-the-art DNA-based reagents of the highest sensitivity and specificity to enable clinicians to conduct assays with the highest degree of confidence outside the United States. CGI Italia Probes are CE marked, certifying the product complies with EU requirements for effectiveness and safety.


[1]Bertheau P, et al. Pathobiology. 2008; 75(2):132-9.

[2] Haferlach C, et al. Genes Chromosomes Cancer. 2010 Sep; 49(9):851-9.

[3] Carlebach M, et al. Cancer Genet Cytogenet. 2000 Feb; 117(1):57-60.

[4] Terpos E, et al.  Leuk Lymphoma. 2006 May; 47(5):803-14.

[5] Kaneko H, et al. Blood. 1995 April 15; 85(8): 2189-2193.

[6] Cheson BD, et al. Blood, 1996 Jan 4; 87:4990–7.

[7] Louise Watson, et al. European Journal of Haematology, 2008; 18:253-258

[8] Boyle P, et al. Ann Oncol. 2005; 16: 481-488.

[9] Parker SL, et al. CA Cancer J Clin. 1998; 48:31–48.

[10] Ferlay J, et al. IARC Cancer Base No 4. Lyon, France: IARC Press, 1999.

[11] Avet-Loiseau H, et al. Blood. 2002 Mar 15; 99(6): 2185-2191.

[12] Botterweck AA, et al. . Epidemiol. 2000; 29: 645-54.