Journals / Zeynep Kamil Tıp Bülteni / 2019 / Cilt: 50 - Sayı: 3

A MOLECULAR VIEW OF RAS /RAF/MEK /ERK IN PEDIATRIC ALL

PEDİATRİK ALL’DE RAS/RAF/MEK/ERK YOLAĞINA MOLEKÜLER BİR BAKIŞ

Pages
162–166
Publication Date
2019-09-15
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)

It provied that treatment of chemotherapy-resistant and relapsing leukemia and the development of personalized treatment modalities In this review, we aimed to reveal the approach of the RAS / RAF / MEK / ERK pathway revealed in the studies that are important in the development of cancer in Acute Lymphoblastic Leukemia (ALL), a subtype of pediatric leukemia.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Pediatric leukemia is thought to be a multifactorial disease that can be treated.In leukemia there are genetic changes like many other types of cancer.
📊
Key Findings & Data:These genetic changes are effective in the activation of oncogenes or inactivation of tumor suppressor genes; can lead to the development of leukemia by causing damage to regulatory mechanisms of cell death, differentiation or division.
💡
Conclusion & Impact:It provied that treatment of chemotherapy-resistant and relapsing leukemia and the development of personalized treatment modalities In this review, we aimed to reveal the approach of the RAS / RAF / MEK / ERK pathway revealed in the studies that are important in the development of cancer in Acute Lymphoblastic Leukemia (ALL), a subtype of pediatric leukemia.
🔬Design:Review & Systematic Survey
📍Scope:Comprehensive Sample
⚙️Variables:Lösemi · pediatri · biyobelirteç

Abstract

Pediatric leukemia is thought to be a multifactorial disease that can be treated.In leukemia there are genetic changes like many other types of cancer. These genetic changes are effective in the activation of oncogenes or inactivation of tumor suppressor genes; can lead to the development of leukemia by causing damage to regulatory mechanisms of cell death, differentiation or division. Unspecified genetic anomalies provide the availability of treatment options that affect these steps of cell cycle. It provied that treatment of chemotherapy-resistant and relapsing leukemia and the development of personalized treatment modalities In this review, we aimed to reveal the approach of the RAS / RAF / MEK / ERK pathway revealed in the studies that are important in the development of cancer in Acute Lymphoblastic Leukemia (ALL), a subtype of pediatric leukemia.

Özet

Pediatrik löseminin henüz sebebi kesin olarak bilinmeyen ancak tedavi edilebilen, multifaktöriyel bir hastalık olduğu düşünülmektedir. Lösemilerde diğer birçok kanser türü gibi genetik değişimler söz konusudur. Onkogenlerin aktivasyonu ya da tümör baskılayıcı genlerin inaktivasyonunda etkili bu genetik lezyonlar; hücre ölümü, farklılaşma ya da bölünmenin düzenlenme mekanizmalarında hasara yol açarak lösemi gelişimine neden olabilirler. Henüz belirlenmemiş genetik anomalilerin bilinmesi bu basamaklara etki eden tedavi seçeneklerinin bulunması ve bu sayede kemoterapiye dirençli ve nüks gösteren lösemilerin tedavi edilmesine, kişiselleştirilmiş tedavi yöntemlerinin geliştirilmesine olanak sağlamaktadır. Bu derlemede kanser gelişiminde önemli olduğu yapılan çalışmalar neticesinde ortaya konulan RAS/RAF/MEK/ERK yolağının pediatrik lösemi alt türü olan Akut Lenfoblastik Lösemi’de (ALL) incelenme yaklaşımını ortaya koyabilmek amaçlanmıştır.

🔖

Cite This Article

AKIN, D. F., SÜT, B. B. (2019). A MOLECULAR VIEW OF RAS /RAF/MEK /ERK IN PEDIATRIC ALL. Zeynep Kamil Tıp Bülteni, Cilt: 50 - Sayı: 3, 162–166. https://ajindex.com/articles/725416

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (18)

  1. Golub E, Arceci RJ. Acute myelogenous leukemia. 4 ed. Philadelphia: Lippincott Williams and Wilkins Company; 2002
  2. Margolin JF, Steuber CP, Poplack DG. Acute Lymphoblastic Leukemia. In: Pizzo PA, editor. Principles and Practice of Pediatric Oncology. 4 ed. Philadelphia: Lippincott Williams & Wilkins; 2002
  3. Williams WJ, Beutler E, Litchman MA, Coler BS, Kipps TJ, Mauner AM. William’s Hematology. New York: McGraw Hill Company; 1991
  4. Franks LM, Teich NM. Introduction to the Cellular and Molecular Biology of Cancer. New York: Oxford University Pres; 2001
  5. Apak H. Çocukluk çağı lösemileri. Türk Pediatri Arşivi. 2006;41:189-96
  6. Lowell C. Fundamentals of blood cell biology. In: Stites DP, Terr AI, Parslow TG, editors. Medical Immunology. 9 ed; 1997. p. 9-25
  7. Oláh E. Basic Concepts of Cancer: Genomic Determination. The Journal of The International Federation of Clinical Chemistry and Laboratory Medicine 2005;16(2)
  8. Martinez JD, Parker MD, Fultz KE, Ignatenko NA, Gerner EW. Molecular Biology of Cancer. Arizona: John Wiley&Sons; 2003
  9. Kleinsmith LJ. Principles of Cancer Biology. Michigan: Benjamin Cummings; 2006
  10. Mullighan CG, Downing JR. Genome-wide profiling of genetic alterations in acute lymphoblastic leukemia: recent insights and future directions. Leukemia. 2009 Jul;23(7):1209-18
  11. Durmaz ÖE. B hücre aktivasyonu ve antikor üretimi B cell activation and antibody. Türkderm. 2013;47(1):24-7
  12. Look AT. Oncogenic transcription factors in the human acute leukemias. Science. 1997 Nov 7;278(5340):1059-64
  13. Greaves M. Molecular genetics, natural history and the demise of childhood leukaemia. European journal of cancer. 1999 Dec;35(14):1941-53
  14. Takai Y, Sasaki T, ve Matozaki T. Small GTP binding proteins. Physiol. Rev.2001; 81: 153-208
  15. Hancock JF. Ras proteins: different signals from different locations. Nat. Rev. Mol. Cell. Biol. 2003; 4: 373-384
  16. Knight T, Irving JA. Ras/Raf/MEK/ERK Pathway Activation in Childhood Acute Lymphoblastic Leukemia and Its Therapeutic Targeting. Front Oncol. 2014 Jun 24;4:160
  17. Al-Kzayer LF, Sakashita K, Al-Jadiry MF, Al-Hadad SA, Ghali HH, Uyen le TN, Liu T, Matsuda K, Abdulkadhim JM, Al-Shujairi TA, Matti ZI, Sughayer MA, Rihani R, Madanat FF, Inoshita T, Kamata M, Koike K. Analysis of KRAS and NRAS Gene Mutations in Arab Asian Children With Acute Leukemia: High Frequency of RAS Mutations in Acute Lymphoblastic Leukemia. Pediatr Blood Cancer. 2015 Dec;62(12):2157-61
  18. Perentesis J