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Increased telomerase activity is associated with shorter survival in patients with chronic phase chronic myeloid leukemia
Author(s) -
Verstovsek Srdan,
Kantarjian Hagop,
Manshouri Taghi,
Cortes Jorge,
Faderl Stefan,
Giles Francis J.,
Keating Michael,
Albitar Maher
Publication year - 2003
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/cncr.11217
Subject(s) - medicine , myeloid leukemia , telomerase , oncology , cancer research , leukemia , immunology , gene , genetics , biology
BACKGROUND Significantly elevated telomerase activity (TA) has been found in samples from patients with many malignant hematologic diseases. However, the impact of elevated TA on the course of patients with chronic phase chronic myeloid leukemia (CP‐CML) is unknown. METHODS Using a modified polymerase chain reaction‐based telomeric repeat amplification protocol assay, the authors measured TA in bone marrow samples from 93 patients with CP‐CML and correlated it with patient characteristics and survival. TA also was measured in bone marrow samples from 29 patients with accelerated/blastic phase CML. RESULTS Patients with accelerated/blastic phase CML were found to have somewhat higher levels of TA compared with patients with CP‐CML ( P = 0.07). Among patients with CP‐CML, those with high TA progressed to advanced stages of disease sooner ( P = 0.05) and had a significantly shorter survival ( P = 0.04) than patients with low TA. No correlation was found between TA and patient age, hemoglobin, platelet and leukocyte counts, percentage of peripheral or bone marrow blasts or basophils, or bone marrow cellularity. On multivariate analysis, high TA retained its significance as a factor associated with shorter patient survival ( P = 0.02). CONCLUSIONS The current study data suggest that TA plays a role in the propagation of CP‐CML and that the potential of telomerase inhibitors in patients with CML should be explored, even in those with early phase disease. Cancer 2003;97:1248–52. © 2003 American Cancer Society. DOI 10.1002/cncr.11217