Telomerase activity in human leukemic cells with or without monosomy 7 or 7q-

Serakıncı, Nedime; Koch, Jørn

doi:10.1186/1471-2350-3-11

Cited by 2 publications

(3 citation statements)

References 14 publications

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“…Other study done by Serakinci and Koch, (2002) also found there was no evidence of TERC gene amplification in human leukaemic cells. Our study showed almost all of study participants did not have TERC gene amplification and support the fact that haematologic disorders dissimilar from other cancers as they might originate from a cell with low-level of telomerase activity.…”

Section: Discussionmentioning

confidence: 77%

Low Level of TERC Gene Amplification between Chronic Myeloid Leukaemia Patients Resistant and Respond to Imatinib Mesylate Treatment

Ashari

Sulong

Hassan

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Section: Discussionmentioning

confidence: 77%

Low Level of TERC Gene Amplification between Chronic Myeloid Leukaemia Patients Resistant and Respond to Imatinib Mesylate Treatment

Ashari

Sulong

Hassan

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…One study that included patients with different types of leukemia subgroups reported that amplification of hTERC and hTERT genes was associated with increased telomerase activity and expression in leukemia cells [12]. Hematologic malignancies differ from other cancers, as they do not originate from cells with low-level telomerase activity.…”

Section: Discussionmentioning

confidence: 99%

“…FISH is a useful method for observing gene amplification and was used in the present study to determine hTERC gene amplification. Previous studies have reported that amplification of hTERT and hTERC genes in acute leukemia cells exhibit a variable number of copies-as many as 12-based on FISH analysis [12].…”

Section: Discussionmentioning

confidence: 99%

Fluorescence in situ hybridization analysis of the hTERC region in acute myeloid leukemia patients

Özer¹,

Balci²,

Yılmaz³

et al. 2011

Turk J Hematol

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Objective: The telomerase RNA component (hTERC) gene is located at 3q26. Increased hTERC gene expression has been frequently observed and amplification was shown using fluorescence in situ hybridization (FISH) in different cancers. The aim of this study was to determine whether hTERC gene amplification is detectable by FISH in acute myeloid leukemia (AML) cells. Material and Methods: FISH and karyotype results at the time of diagnosis of 23 adult AML patients were retrospectively evaluated. Additionally, fixed cells were hybridized with an hTERC region-specific FISH probe to determine gene amplification. Results: Ten of the 23 patients had a normal karyotype and 6 had an abnormal karyotype. hTERC region amplification was not observed in any of the patients. Conclusion: Although it was reported that hTERC gene amplification may partially contribute to increased telomerase expression and activity in leukemic cells, it is not possible to make such a conclusion based on the results of the this study, as hTERC amplification was not observed in the study group. This suggests that increased telomerase activity via gene amplification in the development of AML may not be as important a factor as it is in solid tumors. (Turk J Hematol 2011; 28: 103-6) IntroductionAcute myeloid leukemia (AML) originates from myeloid cells. The disease is characterized by rapid proliferation of abnormal cells, which accumulate in the bone marrow and interfere with the production of normal blood cells. AML is the most common form of acute leukemia in adults and its incidence increases with age [1]. Morphological, cytochemical, immunophenotypic, cytogenetic, and molecular features of the blasts are important factors in the classification of AML patients [2].Telomeres, located at the ends of chromosomes, determine the replication capacity of cells. They shorten during each cell division and it is generally thought that telomere length serves as a clock for cells. Telomerase is a ribonucleoprotein complex, consisting of human transcriptase reverse transcriptase (hTERT), proteins (hTP1), and RNA template for telomeric DNA synthesis (hTERC) [3]; this complex synthesizes telomeres and stabilizes their length. Mutations in any of these components may result in a rare bone marrow failure syndrome known as dyskeratosis congenita [4].Telomerase activity was reported to be low in normal human somatic cells [3]. Proliferating cells become senescent when telomeres are short and when there is no telomerase activity. Cancer cells are known to overcome this senescence pathway and become immortalized. Immortalization is almost always accompanied by expression of telomerase, which is most likely necessary for the continued growth of cancer cells. Telomerase is activated in most malignant tumours, but is usually inactive in normal somatic cells [3]. Despite the questionable role of telomerase reactivation in cell immortalization and carcinogenesis, telomerase may serve as a diagnostic marker for tumor development [5]. Several studies have shown tha...

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Telomerase activity in human leukemic cells with or without monosomy 7 or 7q-

Cited by 2 publications

References 14 publications

Low Level of TERC Gene Amplification between Chronic Myeloid Leukaemia Patients Resistant and Respond to Imatinib Mesylate Treatment

Low Level of TERC Gene Amplification between Chronic Myeloid Leukaemia Patients Resistant and Respond to Imatinib Mesylate Treatment

Fluorescence in situ hybridization analysis of the hTERC region in acute myeloid leukemia patients

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