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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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Plk1-targeted therapies in TP53- or RAS-mutated cancer.

Hyungshin Yim1, Raymond L Erikson2

  • 1Department of Pharmacy, College of Pharmacy, Institute of Pharmaceutical Science and Technology, Hanyang University, Ansan, Gyeonggi-do 426-791, Republic of Korea.

Mutation Research. Reviews in Mutation Research
|March 18, 2014
PubMed
Summary

Polo-like kinase 1 (Plk1) is a promising target for cancer treatment and a prognostic marker in carcinomas. Inhibiting Plk1 shows potential, especially in p53-deficient or KRAS-mutant cancers, guiding new drug development.

Keywords:
KRASPolo-like kinase 1PrognosisStructureTissue distributionp53

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Prognosis for many carcinomas remains poor despite treatment advances.
  • Polo-like kinase 1 (Plk1) is a key mitotic kinase involved in cell division and DNA damage response.
  • Plk1 is highly expressed in several carcinomas and correlates with reduced patient survival.

Purpose of the Study:

  • To present evidence for Plk1 as a prognostic marker and potential therapeutic target in carcinomas.
  • To discuss the clinical implications of Plk1 inhibition in p53- or KRAS-mutated cancers.
  • To review strategies for developing Plk1-specific anticancer drugs.

Main Methods:

  • Review of existing literature on Plk1 function, expression, and therapeutic targeting in carcinomas.
  • Analysis of Plk1's role in relation to p53 and KRAS mutations.
  • Discussion of structural aspects and inhibitor development strategies for Plk1.

Main Results:

  • Plk1 expression is inversely correlated with survival in non-small cell lung, head and neck, and esophageal cancers.
  • Plk1 inhibitors may be particularly effective in p53-deficient tumors.
  • Plk1's essential role in KRAS-mutant cancers warrants further investigation for targeted therapies.

Conclusions:

  • Plk1 is a validated prognostic marker and a promising therapeutic target for various carcinomas, especially solid tumors.
  • Targeting Plk1 offers potential treatment avenues for specific patient populations based on p53 and KRAS mutation status.
  • Development of Plk1 inhibitors targeting the ATP binding site or polo-box domain is crucial for advancing cancer therapy.