Related Experiment Video

Updated: Oct 14, 2026

Repression of Multiple Myeloma Cell Growth In Vivo by Single-wall Carbon Nanotube (SWCNT)-delivered MALAT1 Antisense Oligos
07:24

Repression of Multiple Myeloma Cell Growth In Vivo by Single-wall Carbon Nanotube (SWCNT)-delivered MALAT1 Antisense Oligos

Published on: December 13, 2018

The use of topoisomerase I inhibitors in multiple myeloma

E H Kraut1, R Ju, M Muller

  • 1Division of Hematology-Oncology and Arthur G. James Cancer Hospital and Research Institute, Ohio State University, Columbus 43210-1240, USA.

Seminars in Hematology
|October 21, 1998
PubMed

Insights

New anticancer agents called topoisomerase I (topo I) inhibitors show promise for treating multiple myeloma. Topotecan, a topo I inhibitor, demonstrated activity in advanced cases, suggesting potential for this drug class in future myeloma therapies.

Area of Science:

  • Oncology
  • Pharmacology

Background:

  • Standard treatment for multiple myeloma relies on systemic chemotherapy.
  • Despite decades of research, no new drug regimens have significantly surpassed melphalan and prednisone.
  • Previous phase II studies of novel drugs in multiple myeloma yielded disappointing results, with low response rates and no survival benefit.

Purpose of the Study:

  • To explore the potential of topoisomerase I (topo I) inhibitors as a new therapeutic class for multiple myeloma.
  • To investigate the demonstrated activity of topotecan, a topo I inhibitor, in advanced multiple myeloma.
  • To propose further research into resistance mechanisms, combination therapies, and other topo I inhibitors for multiple myeloma treatment.

Main Methods:

  • Review of existing literature on systemic chemotherapy for multiple myeloma.
  • Analysis of phase II study outcomes for new drugs in multiple myeloma.
  • Evaluation of recent studies on topoisomerase I (topo I) inhibitors, including topotecan, in advanced multiple myeloma.

Main Results:

  • Current chemotherapy regimens for multiple myeloma have not been significantly improved upon.
  • New drug development in myeloma has historically shown limited efficacy and survival benefits.
  • Topotecan, a topoisomerase I (topo I) inhibitor, has shown activity in advanced multiple myeloma.

Conclusions:

  • Topoisomerase I (topo I) inhibitors represent a promising new class of anticancer agents for multiple myeloma.
  • Topotecan's demonstrated activity suggests a potential role in the treatment of advanced multiple myeloma.
  • Further research is warranted to explore resistance mechanisms, combination therapies, and other topo I inhibitors for multiple myeloma.

More Related Videos

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs10:44

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs

Published on: May 15, 2019

Simple and Fast Rolling Circle Amplification-Based Detection of Topoisomerase 1 Activity in Crude Biological Samples10:13

Simple and Fast Rolling Circle Amplification-Based Detection of Topoisomerase 1 Activity in Crude Biological Samples

Published on: December 2, 2022

Related Concept Videos

DNA Topoisomerases02:02

DNA Topoisomerases

Topoisomerases are enzymes that relax overwound DNA molecules during various cell processes, including DNA replication and transcription. These enzymes regulate positive and negative DNA supercoiling without changing the nucleotide sequence. DNA overwinding in a clockwise direction results in positively supercoiled DNA, whereas underwinding in a counterclockwise direction produces negatively supercoiled DNA.
Types and Mechanism of action
Topoisomerases are divided into two main types.  Type I...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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.
There are several types of targeted therapies against specific...
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
Drugs that Destabilize Microtubules01:10

Drugs that Destabilize Microtubules

Microtubules are dynamic structures and can be regulated by microtubule targeting agents (MTAs). Microtubule destabilizing drugs are a class of MTAs that destabilize and prevent microtubules' polymerization. Both natural and synthetic chemicals can be found under this class of drugs. Vincristine and vinblastine, two vinca alkaloids, and colchicine were among the first to be discovered. These drugs can affect cells in various ways, either by inducing a change in cell morphology, preventing...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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.
There are several types of targeted therapies against specific...
Inhibitors of Bacterial DNA Synthesis01:28

Inhibitors of Bacterial DNA Synthesis

Bacterial pathogens depend on precise and efficient DNA replication to sustain infection. Two type II topoisomerases—DNA gyrase and topoisomerase IV—are critical to this process, as they resolve DNA supercoiling and unlink chromosomes during replication. Fluoroquinolones, synthetic derivatives of quinolones, exploit this mechanism by stabilizing the transient DNA–enzyme cleavage complex, preventing strand religation, and causing lethal double-strand breaks. These antibiotics are selectively...