Journals / Bozok Tıp Dergisi / 2016 / Cilt: 6 - Sayı: 4

The Current State of MET Gene in Non-Small Cell Lung Cancer

KÜÇÜK HÜCRELİ DIŞI AKCİĞER KANSERİNDE MET GENİNİN GÜNCEL DURUMU

Pages
57–60
Publication Date
2022-10-11
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)

In this review, the role of the MET gene in NSCLC will be evaluated.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Lung cancer is the most common cause of cancer mortality all over the world.
📊
Key Findings & Data:NSCLC accounts for approximately 85% of all cases of lung cancer.
💡
Conclusion & Impact:In this review, the role of the MET gene in NSCLC will be evaluated.
🔬Design:Review & Systematic Survey
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Lung cancer is the most common cause of cancer mortality all over the world. Despite the fact that there has been a progress in lung cancer, it still has a poor prognosis. Lung cancer is classified into two major histological types; small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC). NSCLC accounts for approximately 85% of all cases of lung cancer. MET proto-oncogene is a tyrosine kinase receptor that plays a role in various cellular events and it is overexpressed in NSCLC. MET kinase inhibitors are currently used in the treatment of NSCLC. The resistance emerges upon the initiation of the treatment with tyrosine kinase inhibitors (TKI) against EGFR mutations frequently seen in NSCLC. One of the reasons for this resistance is MET amplifications. In this review, the role of the MET gene in NSCLC will be evaluated.

Özet

Akciğer kanseri tüm dünyada kansere bağlı ölüm sebepleri içinde ilk sırada yer alır. Tedavi alanında tüm gelişmelere rağmen hala kötü prognoza sahiptir. Akciğer kanseri histolojik tipine göre küçük hücreli akciğer kanseri (KHAK) ve küçük hücreli dışı akciğer kanseri (KHDAK) olarak iki ana tipe ayrılır. KHDAK tüm vakaların yaklaşık %85'ni oluşturur. MET proto-onkogeni birçok hücresel olayda rol oynayan tirozin kinaz reseptörüdür ve KHDAK'inde overeksprese olur. Güncel KHDAK tedavisinde MET inhibitörleri kullanılmaktadır. KHDAK'de sık görülen epidermal büyüme faktör reseptör (EBFR) mutasyonlarına karşı kullanılan tirozin kinaz inhibitörleri (TKI) tedavisinin başlangıcından bir süre sonra direnç ortaya çıkmaktadır. Bunun oluşmasındaki faktörlerden biri MET amplifikasyonlarıdır. Bu derlemede MET geninin KHDAK'indeki rolü gözden geçirilecektir.

🔖

Cite This Article

NURSAL, A. F. (2022). The Current State of MET Gene in Non-Small Cell Lung Cancer. Bozok Tıp Dergisi, Cilt: 6 - Sayı: 4, 57–60. https://ajindex.com/articles/468801

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (16)

  1. Korpanty GJ, Graham DM, Vincent MD, Leighl NB. Biomarkers That Currently Affect Clinical Practice in Lung Cancer: EGFR, ALK, MET, ROS-1, and KRAS. Front Oncol. 2014; 4: 204
  2. Petersen I. The morphological and molecular diagnosis of lung cancer. Dtsch Arztebl Int 2011; 108(31-32): 525-531
  3. Robinson KW, Sandler AB. The role of MET receptor tyrosine kinase in non-small cell lung cancer and clinical development of targeted anti-MET agents. Oncologist. 2013; 18(2): 115-122
  4. Pikor LA, Ramnarine VR, Lam S, Lam WL. Genetic alterations defining NSCLC subtypes and their therapeutic implications. Lung Cancer. 2013; 82(2): 179-189
  5. Koudelakova V, Kneblova M, Trojanec R, Drabec J, Hajduch M. Non-small cell lung cancer--genetic predictors. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2013; 157(2): 125-136
  6. Sattler M, Reddy MM, Hasina R, Gangadhar T, Salgia R. The role of the c-Met pathway in lung cancer and the potential for targeted therapy. Ther Adv Med Oncol. 2011; 3(4):171-184
  7. Yano S, Nakagawa T. The current state of molecularly targeted drugs targeting HGF/Met. Jpn J Clin Oncol 2014; 44(1): 9-12
  8. Sierra JR, Tsao MS. c-MET as a potential therapeutic target and biomarker in cancer.Ther Adv Med Oncol. 2011; 3(1): 21- 35
  9. Jung KH, Park BH, Hong SS. Progress in cancer therapy targeting c-Met signaling pathway. Arch Pharm Res. 2012; 35(4): 595-604
  10. Smyth EC, Sclafani F, Cunningham D. Emerging molecular targets in oncology: clinical potential of MET/hepatocyte growth-factor inhibitors. Onco Targets Ther. 2014;7: 1001- 1014
  11. Bladt F, Friese-Hamim M, Ihling C, Wilm C, Blaukat A. The c-Met Inhibitor MSC2156119J Effectively Inhibits Tumor Growth in Liver Cancer Models. Cancers. 2014; 6 (3): 1736- 1752
  12. Gelsomino F, Facchinetti F, Haspinger ER, Garassino MC, Trusolino L, De Braud F, et al. Targeting the MET gene for the treatment of non-small-cell lung cancer. Crit Rev Oncol Hematol. 2014; 89(2): 284-299
  13. Cipriani NA, Abidoye OO, Vokes E, Salgia R. MET as a target for treatment of chest tumors. Lung Cancer. 2009; 63(2): 169-179
  14. Takeuchi K, Ito F. Receptor tyrosine kinases and targeted cancer therapeutics. Biol Pharm Bull. 2011; 34(12): 1774- 1780
  15. Fong JT, Jacobs RJ, Moravec DN, Uppada SB, Botting GM, Nlend M, et al. Alternative signaling pathways as potential therapeutic targets for overcoming EGFR and c-Met inhibitor resistance in non-small cell lung cancer. PLoS One. 2013; 8(11):78398
  16. Turke AB, Zejnul