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Related Concept Videos

Treatment Resistant Cancers02:56

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
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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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Related Experiment Video

Updated: Jun 15, 2026

Amide Coupling Reaction for the Synthesis of Bispyridine-based Ligands and Their Complexation to Platinum as Dinuclear Anticancer Agents
07:20

Amide Coupling Reaction for the Synthesis of Bispyridine-based Ligands and Their Complexation to Platinum as Dinuclear Anticancer Agents

Published on: May 28, 2014

Platinum-DNA interactions and subsequent cellular processes controlling sensitivity to anticancer platinum complexes.

Saeed Ahmad1

  • 1Department of Chemistry, University of Engineering and Technology, Lahore 54890, Pakistan. saeed_a786@hotmail.com

Chemistry & Biodiversity
|March 17, 2010
PubMed
Summary

Platinum drugs like cisplatin fight cancer by interacting with DNA, triggering cell death pathways. Resistance develops through drug deactivation, DNA repair, and apoptosis defects, influencing treatment effectiveness.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Platinum-based compounds are crucial chemotherapeutics for various cancers.
  • Their anticancer activity stems from interactions with cellular DNA.
  • Cellular responses include DNA repair, translesion synthesis, and apoptosis induction.

Purpose of the Study:

  • To review the formation and cellular interactions of platinum-DNA adducts.
  • To elucidate the biological effects of these interactions.
  • To understand mechanisms of platinum drug resistance and differential cytotoxicity.

Main Methods:

  • Review of existing literature on platinum-DNA adducts and cellular responses.
  • Analysis of molecular mechanisms underlying platinum drug action and resistance.
  • Comparison of DNA adducts and cellular processing of cisplatin and oxaliplatin.

Main Results:

  • Platinum-DNA adducts activate cellular pathways like DNA repair and apoptosis.
  • Resistance mechanisms include drug deactivation, enhanced DNA repair, and impaired apoptosis.
  • Oxaliplatin exhibits greater activity than cisplatin, especially in resistant cells, due to differential adduct recognition.

Conclusions:

  • Cellular processing of platinum-DNA adducts dictates drug efficacy and resistance.
  • Understanding these interactions is key to optimizing platinum-based cancer therapy.
  • Differential recognition of adducts by cellular proteins influences drug response.