Journals / Turkish Journal of Hematology / 2011 / Cilt: 28 - Sayı: 2

Akut myeloid lösemi olgularında floresan in situ hibridizasyon yöntemi ile hTERC bölgesinin analizi

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

Pages
103–106
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

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.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Objective: The telomerase RNA component (hTERC) gene is located at 3q26.
📊
Key Findings & Data:Increased hTERC gene expression has been frequently observed and amplification was shown using fluorescence in situ hybridization (FISH) in different cancers.
💡
Conclusion & Impact: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.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

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-specif- ic 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.

Özet

Amaç: Telomeraz RNA komponenti (hTERC) geni 3q26 bölgesinde yer alır. Çeşitli kanserlerde artmış hTERC gen anlatımı sıklıkla saptanmış ve FISH yöntemi ile gen amplifikasyonu gösterilmiştir. Bu çalışmanın amacı akut miyeloid lösemi (AML) hücrelerinde hTERC gen amplifikasyonunun FISH yöntemi ile saptanabilirliğinin araştırılmasıdır. Yöntem ve Gereçler: Bu çalışmada 23 yeni tanı erişkin AML olgusunun FISH ve karyotip sonuçları geriye dönük olarak değerlendirildi. Ayrıca gen amplifikasyonunu değerlendirebilmek için tespit edilmiş hücreler hTERC bölgesine özgül FISH probu ile melezlendi. Bulgular: Çalışma kapsamına alınan 23 hastanın 10’unda normal karyotip; 6 hastada anormal karyo- tip bulundu. Hastaların hiçbirinde hTERC bölgesinde gen amplifikasyonu saptanamadı. Tartışma: Hasta grubumuzda hTERC amplifikasyonu bulmadık. Bu nedenle, hTERC gen amplifikasyonunun lösemik hücrelerde telomeraz anlatımı ve aktivitesini arttırmada kısmen etkili olduğunun bildirilmesine karşın, çalışmamızın sonuçları ile benzer bir sonuca ulaşmak mümkün olmamıştır. Bu sonuç, AML gelişiminde gen amplifikasyonu yoluyla telomeraz aktivite artışının, solid tümörlerde olduğu kadar önemli bir faktör olmadığı görüşünü destekler niteliktedir.

🔖

Cite This Article

ÖZER, Ö., BULAKBAŞI, T. B., YILMAZ, Z., ŞAHİN, F. İ. (2011). Akut myeloid lösemi olgularında floresan in situ hibridizasyon yöntemi ile hTERC bölgesinin analizi. Turkish Journal of Hematology, Cilt: 28 - Sayı: 2, 103–106. https://ajindex.com/articles/412905

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (11)

  1. Jemal A, Siegel R, Ward E, Murray T, Xu J, Smigal C, Thun MJ. Cancer statistics. CA Cancer J Clin 2006;56:106-30
  2. Flandrin G. Classification of acute myeloid leukemias. Atlas Genet Cytogenet Oncol Haematol. May 2002. URL: http://AtlasGeneticsOncology.org/Anomalies/ ClassifAMLID1238.html 3. Norrback KF and Roos G. Telomeres and telomerase in normal and malignant haematopoietic cells. Eur J Cancer 1997;33:774-80
  3. Kirwan M, Dokal I. Dyskeratosis congenita: a genetic disorder of many faces. Clin Genet 2008;73:103-12
  4. Ohyashiki JH, Sashida G, Tauchi T, Ohyashiki K. Telomeres and telomerase in hematologic neoplasia. Oncogene 2002;21:680-7
  5. Ohyashiki JH, Ohyashiki K, Iwama H, Hayashi S, Toyama K, Shay JW. Clinical implications of telomer- ase activity levels in acute leukemia. Clin Cancer Res 1997;3:619-25
  6. Davison GM. Telomeres and telomerase in leukaemia and lymphoma. Transfusion and Apheresis Science 2007;37:43-7
  7. Januszkiewicz D, Wysoki J, Lewandowski K, Pernak M, Nowicka K, Rembowska J, Nowak J. Lack of cor- relation between telomere length and telomerase activity and expression in leukemic cells. Int J Mol Med 2003;12:935-8
  8. Cao Y, Bryan TM, Reddel RR. Increased copy number of the TERT and TERC telomerase subunit genes in cancer cells. Cancer Sci 2008;99:1092-9
  9. Cairney CJ, Keith WN. Telomerase redefined: inte- grated regulation of hTR and hTERT for telomere maintenance and telomerase activity. Biochimie 2008;90:3-23
  10. Nowak T, Januszkiewicz D, Zawada M, Pernak M, Lewandowski K, Rembowska J, Nowicka K, Mankowski P, Nowak J. Amplification of hTERT and hTERC genes in leukemic cells with high expression and activity of telomerase. Oncology Reports 2006;16:301-5
  11. Serakinci N, Koch JE. Telomerase activity in human leukemic cells with or without monosomy 7 or 7q-. BMC Med Genet 2002;29:3-11