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Targeted Cancer Therapies02:57

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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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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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Amide Coupling Reaction for the Synthesis of Bispyridine-based Ligands and Their Complexation to Platinum as Dinuclear Anticancer Agents
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Digoxin is a selective modifier increasing platinum drug anticancer activity.

T A Bogush1, V Yu Chernov2, E A Dudko3

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Cardiac glycoside digoxin significantly enhances cisplatin

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Area of Science:

  • Oncology
  • Pharmacology
  • Biochemistry

Background:

  • Ehrlich ascites tumor in mice is a model for breast cancer.
  • Cisplatin is a cytostatic drug used in cancer therapy.
  • Cardiac glycosides, like digoxin, have potential anticancer properties.

Purpose of the Study:

  • To investigate the effect of digoxin on cisplatin's anticancer efficacy.
  • To explore digoxin's mechanism of action in modifying cisplatin's effect.
  • To assess the potential of digoxin in clinical settings for ascites cancers.

Main Methods:

  • A single intraperitoneal injection of digoxin was administered 1 hour before cisplatin in a mouse model.
  • The anticancer effect was evaluated based on tumor growth inhibition.
  • Glycolysis inhibition in tumor cells was hypothesized as the mechanism.

Main Results:

  • Digoxin more than doubled the anticancer effect of cisplatin when administered beforehand.
  • The enhanced effect was observed when recalculated per dose.
  • Digoxin's action is presumed to involve direct inhibition of tumor cell glycolysis.

Conclusions:

  • Digoxin shows promise as a potentiator of cisplatin chemotherapy.
  • The study suggests digoxin could enhance cisplatin efficacy in treating ascites cancers.
  • Clinical evaluation of digoxin in intracavitary therapy for disseminated ascites cancers is warranted.