Advances in Clinical and Experimental Medicine

Title abbreviation: Adv Clin Exp Med
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Advances in Clinical and Experimental Medicine

2013, vol. 22, nr 6, November-December, p. 861–864

Publication type: review article

Language: English

Will Therapies that Target Tumour Suppressor Genes be Useful in Cancer Treatment?

Czy terapia celowana prowadząca do utraty funkcji genów supresorowych będzie miała zastosowanie w leczeniu nowotworów?

Elwira Szychot1,A,B,C,D,E,F, Andrzej Brodkiewicz2,E,F, Jarosław Peregud-Pogorzelski3,E,F

1 Hematology and Oncology Department, Great Ormond Street Hospital for Children NHS Foundation Trust, London, UK

2 Department of Pediatrics, Nephrology with Dializotherapy and Management of Acute Poisoning, Pomeranian Medical University, Szczecin, Poland

3 Department of Pediatrics, Hematology and Pediatric Oncology, Pomeranian Medical University, Szczecin, Poland

Abstract

Human cancers represent one of the biggest challenges for modern societies. By 2020, cancer deaths worldwide could reach 10 million. Therefore, one of the important aims of science research is the improvement of antimalignant treatment options to mitigate cancer-related morbidity and mortality. This essay summarises current trends and future directions of target tumour suppressor genes therapies based on an example of one of the most promising targets, p53

Streszczenie

Choroby nowotworowe stanowią coraz większy społeczny problem. Uważa się, że do 2020 r. mogą być odpowiedzialne za śmierć nawet 10 milionów osób na świecie. Dlatego tak ważne jest poprawienie skuteczności leczenia przeciwnowotworowego, co w następstwie może znacznie zmniejszyć śmiertelność. Praca przedstawia aktualne trendy oraz przyszłe kierunki terapii celowanej genów supresorowych na przykładzie białka p53, rozpatrywanego jako najbardziej obiecujący cel terapii antynowotworowej

Key words

children, cancer, leukaemia, genes, targeted therapy.

Słowa kluczowe

dzieci, nowotwór, białaczka, geny, terapia celowana.

References (14)

  1. http://www.cancerresearchuk.org/cancer-info/cancerstats/incidence/all-cancers-combined/
  2. Hanahan D, Weinberg RA: The hallmarks of cancer. Cell 2000, 100, 57–70.
  3. Passioura T, Symonds G: Cancer gene suppression strategies: issues and potential. Curr Issues Mol Biol 2004, 6, 89–101.
  4. Brummelkamp TR, Bernards R, Agami R: A system for stable expression of short interfering RNAs in mammalian cells. Science 2002, 296, 550–553.
  5. Frezza C, Martins CP: From tumor prevention to therapy: Empowering p53 to fight back. Drug Resist Updat 2012, 15, 258–267.
  6. Wang Z, Sun Y: Targeting p53 for novel anticancer therapy. Transl Oncol 2010, 3, 1–12.
  7. Wade M, Wang YV, Wahl GM: The p53 orchestra: Mdm2 and Mdmx set the tone. Trends Cell Biol 2010, 20, 299–309.
  8. Hermeking H: MicroRNAs in the p53 network: micromanagement of tumour suppression. Nat Rev Cancer 2012, 12, 613–626.
  9. Lambert JM, Gorzov P, Veprintsev DB, Söderqvist M, Segerbäck D, Bergman J, Fersht AR, Hainaut P, Wiman KG, Bykov VJ: PRIMA-1 reactivates mutant p53 by covalent binding to the core domain. Cancer Cell 2009, 15, 376–388.
  10. Vogelstein B, Lane D, Levine AJ: Surfing the p53 network. Nature 2000, 408, 307–310.
  11. Fujiwara T, Grimm EA, Mukhopadhyay T, Cai DW, Owen-Schaub LB, Roth JA: A retroviral wild-type p53 expression vector penetrates human lung cancer spheroids and inhibits growth by inducing apoptosis. Cancer Res 1993, 53, 4129–4133.
  12. Secchiero P, Bosco R, Celeghini C, Zauli G: Recent advances in the therapeutic perspectives of Nutlin-3. Curr Pharm Des 2011, 17, 569–577.
  13. Lowe SW, Sherr CJ: Tumor suppression by Ink4a-Arf: progress and puzzles. Curr Opin Genet Dev 2003, 13, 77–83.
  14. Ringshausen I, O’Shea CC, Finch AJ, Swigart LB, Evan GI: Mdm2 is critically and continuously required to suppress lethal p53 activity in vivo. Cancer Cell 2006, 10, 501–514.
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