Journals / Mersin Üniversitesi Sağlık Bilimleri Dergisi / 2019 / Cilt: 12 - Sayı: 3

Microsatellite instability screening and clinical efficacy in tumor tissue in patients with colorectal cancer

Kolorektal kanserli hastalarda tümör dokusunda mikrosatellit instabilite taranması ve klinik üzerine etkinliği

Pages
469–477
Publication Date
2019-12-31
DOI
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AI Summary & Key Takeaways

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

Further studies with more cases are needed.

📌 3 Key Takeaways

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Objective & Hypothesis:Aim: Microsatellite instability is a genetic pathway responsible for approximately 15% of sporadic colon cancers.
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Key Findings & Data:Microsatellite instability occurs in people with a damaged DNA mismatch repair system and the risk of mutation increases.
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Conclusion & Impact:Further studies with more cases are needed.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Kolorektal Kanser · Mikrosatellit İnstabilite · Prognoz

Abstract

Aim: Microsatellite instability is a genetic pathway responsible for approximately 15% of sporadic colon cancers. It is caused by defects in the DNA mismatch repair system. Microsatellite instability occurs in people with a damaged DNA mismatch repair system and the risk of mutation increases. These mutations in tumor suppressor genes cause colorectal cancer development. Microsatellite instability is most commonly detected in proximal colon cancers. Microsatellite instability in cancer tissues can be determined by PCR method. In our group of patients with colorectal cancer, we planned a study to investigate the effect of microsatellite instability on the clinicopathological features and prognosis. Methods: In this study, microsatellite instability was investigated in 50 patients who were diagnosed to have colorectal cancer in Çukurova University Medical Faculty Hospital. Results: Paraffin-embedded specimens were examined by PCR method and 20 (40%) of them were ‘’microsatellite instable’’ and 30 (60%) were ‘’microsatellite stable’’. In cases with microsatellite instability, tumors were found to be more proximal in the proximal colon than in microsatellite stable cases (40% to 13.3%, respectively, p <0.05). The age at the time of diagnosis was found younger in the microsatellite instable group compared to the microsatellite stable group (52.2 versus 61.97 years, respectively). Conclusion: The fact that microsatellite instable colorectal tumors are different from those of microsatellite stable in terms of clinicopathological and prognostic aspects suggests that this feature can be used as a prognostic marker in the future. Further studies with more cases are needed.

Özet

Amaç: Mikrosatellit instabilite, sporadik kolon kanserlerinin yaklaşık %15’inden sorumlu bir genetik yolaktır. DNA mismatch (hatalı eşleşme) onarım sistemindeki defektlerden dolayı oluşmaktadır. DNA mismatch onarım sistemi hatalı olan kişilerde mikrosatellit instabilite oluşmakta ve mutasyon riski artmaktadır. Tümör süpresör genlerde oluşan bu mutasyonlar başta kolorektal kanser olmak üzere, endometrium kanseri, gastrik kanser vb malignansilerin gelişimine yol açmaktadır. Mikrosatellit instabilite en sık proksimal kolon kanserlerinde saptanmaktadır. Kanser dokularında mikrosatellit instabilite, PCR yöntemi ile saptanabilmektedir. Kliniğimizde tanı koyulan kolorektal kanserli hasta grubumuzda, Mikrosatellit İnstabilitenin klinikopatolojik özellikleri ve prognoz üzerine etkisini araştırmak üzere bir çalışma planladık. Yöntem: Bu çalışmada Çukurova Üniversitesi Tıp Fakültesi Hastanesi’nde tanı almış kolorektal kanserli 50 hastadan elde edilen kanserli parafin doku örneklerinde mikrosatellit instabilite aranmıştır. Bulgular: Parafine gömülü örneklerin PCR yöntemiyle incelenmesi sonucunda hastaların 20’si (%40) mikrosatellit instabil, 30’u (%60) mikrosatellit stabil olarak saptandı. Mikrosatellit instabil olan olgularda, mikrosatellit stabil olgulara göre daha sık oranda tümörlerin proksimal kolonda yerleştiği saptandı (sırasıyla %40’a karşılık %13.3, p<0.05). Mikrosatellit instabil grupla mikrosatelit stabil grup, tanı sırasındaki yaş açısından karşılaştırıldığında, instabil olanlarda tanı sırasındaki yaşın daha küçük olduğu saptandı (sırasıyla 52.2’ye karşılık 61.97 yaş). Sonuç: Mikrosatellit instabil kolorektal tümörlerin klinikopatolojik ve prognostik açıdan mikrosatellit stabil olanlardan farklı olması, ileride bu özelliğin prognostik bir belirteç olarak kullanılabileceğini düşündürmektedir. Konuyla ilgili daha fazla olgu sayılarıyla yeni çalışmalara ihtiyaç vardır.

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Cite This Article

YARAŞ, S., AKKIZ, H. (2019). Microsatellite instability screening and clinical efficacy in tumor tissue in patients with colorectal cancer. Mersin Üniversitesi Sağlık Bilimleri Dergisi, Cilt: 12 - Sayı: 3, 469–477. https://ajindex.com/articles/43978

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References (16)

  1. Gill, S., R.R. Thomas, and R.M. Goldberg, Review article: colorectal cancer chemotherapy. Aliment Pharmacol Ther, 2003. 18(7): p. 683-92
  2. Compton, C.C. and F.L. Greene, The staging of colorectal cancer: 2004 and beyond. CA Cancer J Clin, 2004. 54(6): p. 295-308
  3. Gryfe, R., et al., Tumor microsatellite instability and clinical outcome in young patients with colorectal cancer. N Engl J Med, 2000. 342(2): p. 69-77
  4. Narayan, S. and D. Roy, Role of APC and DNA mismatch repair genes in the development of colorectal cancers. Mol Cancer, 2003. 2: p. 41
  5. Bisgaard, M.L., et al., Familial adenomatous polyposis patients without an identified APC germline mutation have a severe phenotype. Gut, 2004. 53(2): p. 266-70.6. Lindblom, A., Different mechanisms in the tumorigenesis of proximal and distal colon cancers. Curr Opin Oncol, 2001. 13(1): p. 63-9
  6. Tejpar, S. and E. Van Cutsem, Molecular and genetic defects in colorectal tumorigenesis. Best Pract Res Clin Gastroenterol, 2002. 16(2): p. 171-85
  7. Sevignani, C., et al., Tumorigenic conversion of p53-deficient colon epithelial cells by an activated Ki-ras gene. J Clin Invest, 1998. 101(8): p. 1572-80
  8. Carethers, J.M., et al., Use of 5-fluorouracil and survival in patients with microsatellite-unstable colorectal cancer. Gastroenterology, 2004. 126(2): p. 394-401
  9. De' Angelis, G.L., et al., Microsatellite instability in colorectal cancer. Acta Biomed, 2018. 89(9-s): p. 97-101
  10. Lawes, D.A., S. SenGupta, and P.B. Boulos, The clinical importance and prognostic implications of microsatellite instability in sporadic cancer. Eur J Surg Oncol, 2003. 29(3): p. 201-12
  11. Wheeler, J.M., W.F. Bodmer, and N.J. Mortensen, DNA mismatch repair genes and colorectal cancer. Gut, 2000. 47(1): p. 148-53
  12. Wynter, C.V., et al., Methylation patterns define two types of hyperplastic polyp associated with colorectal cancer. Gut, 2004. 53(4): p. 573-80
  13. Umar, A., et al., Revised Bethesda Guidelines for hereditary nonpolyposis colorectal cancer (Lynch syndrome) and microsatellite instability. J Natl Cancer Inst, 2004. 96(4): p. 261-8
  14. Jass, J.R., HNPCC and sporadic MSI-H colorectal cancer: a review of the morphological similarities and differences. Fam Cancer, 2004. 3(2): p. 93-100
  15. Ribic, C.M., et al., Tumor microsatellite-instability status as a predictor of benefit from fluorouracil-based adjuvant chemotherapy for colon cancer. N Engl J Med, 2003. 349(3): p. 247-57
  16. Parc, Y., et al., Prognostic