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Pediatrik öncü B-ALL’ye Moleküler Yaklaşım

Yıl 2019, , 91 - 101, 15.06.2019
https://doi.org/10.16948/zktipb.425982

Öz

Lösemi, çocukluk çağında en sık görülen malign
hastalıktır. Bu hastalık yaklaşık 150 yıl önce tanımlanmıştır, ancak son 30
yıllık süreçte tedavide %90’lara varan bir başarı oranına ulaşılabilmiştir. Bu
başarılı sonuçlara ulaşılmasında çoklu ilaç uygulamaları, santral sinir sistemi
profilaksisi, idame ve destek tedavi uygulamaları etkili olmuştur. Tedavide bu
kadar başarılı sonuçların alınmasına rağmen nüks lösemi için bir risk olmaya
devam etmekte ve ALL hastalarının %20’sinde görülmektedir. Tedaviden alınan
farklı sonuçlar diğer bütün kanser tiplerinde olduğu gibi lösemi’nin de
heterojen bir yapıya sahip olduğunu işaret etmektedir. Bu nedenle erken, doğru
bir teşhis ile daha etkin bir tedavinin ancak kişiye özgü (hastalık alt
gruplarına) tedavi, yöntem ve müdahale stratejilerinin geliştirilmesi ile
mümkün olabileceği öngörülmektedir. Bu kapsamda diğer bütün kanser tiplerinde
olduğu gibi “lösemi genomunda” yapısal ve/veya işlevsel bozukluk gösteren
genler, lösemi tanısı, tedavisi ve nüksünün önlenebilmesi için yeni prognostik
araçlar olabilme potansiyeli taşımaktadır.

Kaynakça

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Molecular Approach to Pediatric Precursor B-ALL

Yıl 2019, , 91 - 101, 15.06.2019
https://doi.org/10.16948/zktipb.425982

Öz

Leukemia is the most common malignant disease in
childhood. This disease was identified almost 150 years ago, but in the last 30
years, treatment processes have achieved a success rate of up to 90%. These
successful outcomes were supported by multi-drug treatments, central nervous
system prophylaxis, maintainability and therapeutic applications. Although
successful treatment outcome relapse continues to be a risk for leukemia and is
seen in 20% of patients with leukemia. In this case, all other types of cancers
as well as leukemia have a structure that is heterogeneous. Therefore,
individualized treatment methods are more effective than early accurate
diagnosis, hence the development of individualised treatment methods and
intervention strategies have become necessary. In this context, as in all other
types of cancer the leukemia genome contain structural abnormalities several
genes leading to their functional dysfunction. These genes have the potential
to become novel biomarkers for diagnosis, prognosis, treatment and prevention
of relapse.

Kaynakça

  • 1. Roberts KG, Mullighan CG. Genomics in acute lymphoblastic leukaemia: insights and treatment implications. Nature reviews Clinical oncology, 2015;12(6):344-57.
  • 2. Mullighan CG, Downing JR. Genome-wide profiling of genetic alterations in acute lymphoblastic leukemia: recent insights and future directions. Leukemia, 2009 J;23(7):1209-18.
  • 3. Berg SL, Steuber P, Poplack DG. Clinical manifestations of acute lymphoblastic leukemia. In: Hoffman R, Benz EJ, Shattil SJ, et al., editors. Hematology Basic principles and practice. Philadelphia; 2005. p. 1155-62.
  • 4. Smith M, Arthur D, Camitta B, et al. Uniform approach to risk classification and treatment assignment for children with acute lymphoblastic leukemia. Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 1996;14(1):18-24.
  • 5. Gokbuget N, Hoelzer D. Recent approaches in acute lymphoblastic leukemia in adults. Reviews in clinical and experimental hematology, 2002;6(2):114-41; discussion 200-2.
  • 6. Durmaz ÖE. B hücre aktivasyonu ve antikor üretimi B cell activation and antibody. Türkderm, 2013;47(1):24-7.
  • 7. Schwab CJ, Chilton L, Morrison H, et al. Genes commonly deleted in childhood B-cell precursor acute lymphoblastic leukemia: association with cytogenetics and clinical features. Haematologica, 2013 ;98(7):1081-8.
  • 8. Harrison CJ. Targeting signaling pathways in acute lymphoblastic leukemia: new insights. Hematology / the Education Program of the American Society of Hematology American Society of Hematology Education Program. 2013;:118-25.
  • 9. Parikh NI, Vasan RS. Assessing the clinical utility of biomarkers in medicine. Biomarkers in medicine, 2007;1(3):419-36.
  • 10. Strimbu K, Tavel JA. What are biomarkers? Current opinion in HIV and AIDS, 2010;5(6):463-6.
  • 11. Oikawa T. ETS transcription factors: possible targets for cancer therapy. Cancer science. 2004;95(8):626-33.
  • 12. Rashed RA, Kadry DY, El Taweel M, Abd El Wahab N, Abd El Hameed T. Relation of BAALC and ERG Gene Expression with Overall Survival in Acute Myeloid Leukemia Cases. Asian Pacific journal of cancer prevention : APJCP. 2015;16(17):7875-82.
  • 13. http://www.ensembl.org/index.html. [cited; Available from:
  • 14. Siddique HR, Rao VN, Lee L, Reddy ES. Characterization of the DNA binding and transcriptional activation domains of the erg protein. Oncogene. 1993 Jul;8(7):1751-5.
  • 15. Bock J, Mochmann LH, Schlee C, et al. ERG transcriptional networks in primary acute leukemia cells implicate a role for ERG in deregulated kinase signaling. PloS one. 2013;8(1):e52872.
  • 16. Eid MA, Attia M, Abdou S, et al. BAALC and ERG expression in acute myeloid leukemia with normal karyotype: impact on prognosis. International journal of laboratory hematology. 2010 Apr;32(2):197-205.
  • 17. Pigazzi M, Masetti R, Martinolli F, et al. Presence of high-ERG expression is an independent unfavorable prognostic marker in MLL-rearranged childhood myeloid leukemia. Blood. 2012 Jan 26;119(4):1086-7; author reply 7-8.
  • 18. Salek-Ardakani S, Smooha G, de Boer J, et al. ERG is a megakaryocytic oncogene. Cancer research. 2009 Jun 1;69(11):4665-73.
  • 19. Marcucci G, Baldus CD, Ruppert AS, et al. Overexpression of the ETS-related gene, ERG, predicts a worse outcome in acute myeloid leukemia with normal karyotype: a Cancer and Leukemia Group B study. Journal of clinical oncology : official journal of the American Society of Clinical Oncology. 2005 Dec 20;23(36):9234-42.
  • 20. Huber RG, Fan H, Bond PJ. The Structural Basis for Activation and Inhibition of ZAP-70 Kinase Domain. PLoS computational biology. 2015 Oct;11(10):e1004560.
  • 21. Saito T, Matsuda Y, Ito H, Fusaki N, Hori T, Yamamoto T. Localization of Zap70, the gene for a T cell-specific protein tyrosine kinase, to mouse and rat chromosomes by fluorescence in situ hybridization and molecular genetic linkage analyses. Mammalian genome : official journal of the International Mammalian Genome Society. 1997 Jan;8(1):45-6.
  • 22. Chen L, Widhopf G, Huynh L, et al. Expression of ZAP-70 is associated with increased B-cell receptor signaling in chronic lymphocytic leukemia. Blood. 2002 Dec 15;100(13):4609-14.
  • 23. Chakupurakal G, Bell A, Griffiths M, Wandroo F, Moss P. Analysis of ZAP70 expression in adult acute lymphoblastic leukaemia by real time quantitative PCR. Molecular cytogenetics. 2012;5(1):22.
  • 24. Kong GH, Bu JY, Kurosaki T, Shaw AS, Chan AC. Reconstitution of Syk function by the ZAP-70 protein tyrosine kinase. Immunity. 1995 May;2(5):485-92.
  • 25. Ebeid E, Kamel M, Moussa H, Galal U. ZAP-70 as a possible prognostic factor in childhood acute lymphoblastic leukemia. Journal of the Egyptian National Cancer Institute. 2008 Jun;20(2):121-6.
  • 26. Wandroo F, Bell A, Darbyshire P, et al. ZAP-70 is highly expressed in most cases of childhood pre-B cell acute lymphoblastic leukemia. International journal of laboratory hematology. 2008 Apr;30(2):149-57.
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  • 65. Shah S, Schrader KA, Waanders E, et al. A recurrent germline PAX5 mutation confers susceptibility to pre-B cell acute lymphoblastic leukemia. Nature genetics. 2013 Oct;45(10):1226-31.
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  • 73. Liao D. Emerging roles of the EBF family of transcription factors in tumor suppression. Molecular cancer research : MCR. 2009 Dec;7(12):1893-901.
  • 74. Prasad MA, Ungerback J, Ahsberg J, et al. Ebf1 heterozygosity results in increased DNA damage in pro-B cells and their synergistic transformation by Pax5 haploinsufficiency. Blood. 2015 Jun 25;125(26):4052-9.
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  • 81. Inthal A, Zeitlhofer P, Zeginigg M, et al. CREBBP HAT domain mutations prevail in relapse cases of high hyperdiploid childhood acute lymphoblastic leukemia. Leukemia. 2012 Aug;26(8):1797-803.82. Ma X, Edmonson M, Yergeau D, et al. Rise and fall of subclones from diagnosis to relapse in pediatric B-acute lymphoblastic leukaemia. Nature communications. 2015;6:6604.83. Huether R, Dong L, Chen X, et al. The landscape of somatic mutations in epigenetic regulators across 1,000 paediatric cancer genomes. Nature communications. 2014;5:3630.84. Zhang Z, Burch PE, Cooney AJ, et al. Genomic analysis of the nuclear receptor family: new insights into structure, regulation, and evolution from the rat genome. Genome research. 2004 Apr;14(4):580-90.
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  • 87. Hayashi R, Wada H, Ito K, Adcock IM. Effects of glucocorticoids on gene transcription. European journal of pharmacology. 2004 Oct 1;500(1-3):51-62.
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  • 89. Longui CA, Vottero A, Adamson PC, et al. Low glucocorticoid receptor alpha/beta ratio in T-cell lymphoblastic leukemia. Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme. 2000 Oct;32(10):401-6.
  • 90. Ray A, Prefontaine KE. Physical association and functional antagonism between the p65 subunit of transcription factor NF-kappa B and the glucocorticoid receptor. Proceedings of the National Academy of Sciences of the United States of America. 1994 Jan 18;91(2):752-6.
  • 91. Haarman EG, Kaspers GJ, Pieters R, Rottier MM, Veerman AJ. Glucocorticoid receptor alpha, beta and gamma expression vs in vitro glucocorticod resistance in childhood leukemia. Leukemia. 2004 Mar;18(3):530-7.
  • 92. Bhadri VA, Trahair TN, Lock RB. Glucocorticoid resistance in paediatric acute lymphoblastic leukaemia. Journal of paediatrics and child health. 2012 Aug;48(8):634-40.
  • 93. Ho GA, Odenwald E, Reiter A, Sauter S, Riehm H. Lack of correlation between glucocorticoid receptor levels, response to prednisone monotherapy and relapse-free survival in childhood leukemia. Proc Am Soc Clin Oncol. 1991;18(3):530-7.
  • 94. Haarman EG, Kaspers GJ, Pieters R, et al. In vitro glucocorticoid resistance in childhood leukemia correlates with receptor affinity determined at 37 degrees C, but not with affinity determined at room temperature. Leukemia. 2002 Sep;16(9):1882-4.
  • 95. Longui CA, Vottero A, Adamson PC, et al. Low glucocorticoid receptor alpha/beta ratio in T-cell lymphoblastic leukemia. Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme. 2000 Oct;32(10):401-6.
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Toplam 92 adet kaynakça vardır.

Ayrıntılar

Birincil Dil Türkçe
Konular Sağlık Kurumları Yönetimi
Bölüm Derleme / Review
Yazarlar

Dilara Fatma Akın Balı

Yayımlanma Tarihi 15 Haziran 2019
Yayımlandığı Sayı Yıl 2019

Kaynak Göster

APA Akın Balı, D. F. (2019). Pediatrik öncü B-ALL’ye Moleküler Yaklaşım. Zeynep Kamil Tıp Bülteni, 50(2), 91-101. https://doi.org/10.16948/zktipb.425982
AMA Akın Balı DF. Pediatrik öncü B-ALL’ye Moleküler Yaklaşım. Zeynep Kamil Tıp Bülteni. Haziran 2019;50(2):91-101. doi:10.16948/zktipb.425982
Chicago Akın Balı, Dilara Fatma. “Pediatrik öncü B-ALL’ye Moleküler Yaklaşım”. Zeynep Kamil Tıp Bülteni 50, sy. 2 (Haziran 2019): 91-101. https://doi.org/10.16948/zktipb.425982.
EndNote Akın Balı DF (01 Haziran 2019) Pediatrik öncü B-ALL’ye Moleküler Yaklaşım. Zeynep Kamil Tıp Bülteni 50 2 91–101.
IEEE D. F. Akın Balı, “Pediatrik öncü B-ALL’ye Moleküler Yaklaşım”, Zeynep Kamil Tıp Bülteni, c. 50, sy. 2, ss. 91–101, 2019, doi: 10.16948/zktipb.425982.
ISNAD Akın Balı, Dilara Fatma. “Pediatrik öncü B-ALL’ye Moleküler Yaklaşım”. Zeynep Kamil Tıp Bülteni 50/2 (Haziran 2019), 91-101. https://doi.org/10.16948/zktipb.425982.
JAMA Akın Balı DF. Pediatrik öncü B-ALL’ye Moleküler Yaklaşım. Zeynep Kamil Tıp Bülteni. 2019;50:91–101.
MLA Akın Balı, Dilara Fatma. “Pediatrik öncü B-ALL’ye Moleküler Yaklaşım”. Zeynep Kamil Tıp Bülteni, c. 50, sy. 2, 2019, ss. 91-101, doi:10.16948/zktipb.425982.
Vancouver Akın Balı DF. Pediatrik öncü B-ALL’ye Moleküler Yaklaşım. Zeynep Kamil Tıp Bülteni. 2019;50(2):91-101.