Journal
AMERICAN JOURNAL OF HEMATOLOGY
Volume 96, Issue 3, Pages 312-319Publisher
WILEY
DOI: 10.1002/ajh.26069
Keywords
-
Categories
Funding
- National Natural Science Foundation of China [81400080]
Ask authors/readers for more resources
The study investigated the characteristics and prognostic value of CDKN2A gene deletions in T-ALL patients, finding an association with younger age, higher white blood cell count, and higher lactate dehydrogenase levels. Patients with CDKN2A deletion had lower survival rates and it was identified as an independent adverse prognostic factor for overall survival. These patients may benefit from intensive chemotherapy or stem-cell transplantation.
The identification of genetic risk subgroups of T-cell acute lymphoblastic leukemia (T-ALL) may provide evidence for risk stratification and individualized treatment. We investigated the characteristics and prognostic value of tumor suppressor gene CDKN2A deletions in 101 patients with T-ALL. The CDKN2A deletion was present in 23% (23/101) of T-ALL by fluorescence in situ hybridization (FISH). The most common type of CDKN2A deletion was homozygous deletion (70%, 16/23). A lower frequency of CDKN2A deletion was found in patients with early T-cell precursor (ETP) ALL than in patients with non-ETP-ALL (10.4% vs 34.0%; P = .008). Deletion of CDKN2A was significantly associated with younger age (P = .001), higher white blood cell (WBC) count (P < .001) and higher lactate dehydrogenase (LDH) level (P = .002). Patients with CDKN2A deletion had lower 2-year overall survival (OS) and event-free survival (EFS) rates than patients without CDKN2A deletion (2-year OS: 18.6% +/- 8.9% vs 47.4% +/- 6.2%, P = .032; EFS: 16.4 +/- 8.3 vs 38.6 +/- 5.9%, P = .022). In multivariable analysis, CDKN2A deletion was an independent adverse prognostic factor for OS (P = .016). In conclusion, adult T-ALL patients with CDKN2A deletion had a poor prognosis, and these patients might benefit from intensive chemotherapy or allogeneic hematopoietic stem-cell transplantation.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available