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Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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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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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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Targeting the DNA Damage Response for Cancer Therapy by Inhibiting the Kinase Wee1.

Amirali B Bukhari1, Gordon K Chan1, Armin M Gamper1

  • 1Department of Oncology, Cross Cancer Institute, University of Alberta, Edmonton, AB, Canada.

Frontiers in Oncology
|March 7, 2022
PubMed
Summary
This summary is machine-generated.

Targeting Wee1 kinase, a key regulator of the G2/M checkpoint, offers a promising cancer therapy. Inhibiting Wee1 triggers cancer cell death and can enhance anti-tumor immune responses.

Keywords:
DNA damage response (DDR)Wee1cancer therapycell cyclekinasesynthetic lethality

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Area of Science:

  • Cell Biology
  • Molecular Oncology
  • Cancer Therapeutics

Background:

  • Cancer cells depend on the G2/M checkpoint to manage DNA damage.
  • Cyclin-dependent kinase 1 (CDK1) is crucial for the G2/M checkpoint, regulated by Wee1 kinase and cdc25 phosphatase.
  • Wee1 activity controls CDK1 phosphorylation, enabling rapid cellular stress responses.

Purpose of the Study:

  • To review therapeutic strategies involving small molecule inhibitors of Wee1.
  • To explore combinations of Wee1 inhibition with genotoxic agents or synthetic lethality pathways.
  • To discuss the role of Wee1 inhibition in modulating anti-tumor immune responses.

Main Methods:

  • Review of existing literature on Wee1 inhibitors and combination therapies.
  • Analysis of mechanisms underlying Wee1 inhibition's effects on cell cycle and DNA repair.
  • Examination of Wee1's impact on intrinsic and systemic anti-tumor immunity.

Main Results:

  • Wee1 inhibition leads to premature mitosis with unrepaired DNA, causing mitotic catastrophe.
  • Combining Wee1 inhibitors with radiation or replication stress inducers shows therapeutic potential.
  • Wee1 inhibition can synergize with other targeted therapies via synthetic lethality.
  • Wee1 inhibition demonstrates immunomodulatory effects, enhancing anti-tumor immunity.

Conclusions:

  • Wee1 inhibitors represent a viable therapeutic strategy for various cancers.
  • Combination therapies involving Wee1 inhibition offer enhanced anti-tumor efficacy.
  • Wee1 inhibition has the potential to improve cancer treatment outcomes by modulating both cancer cells and the immune system.