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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...
Treatment Resistent Cancers02:56

Treatment Resistent 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...
Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
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...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...

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Related Experiment Video

Updated: Jul 10, 2026

Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down
08:59

Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down

Published on: December 11, 2017

What makes tumors multidrug resistant?

Piet Borst1, Jos Jonkers, Sven Rottenberg

  • 1The Netherlands Cancer Institute, Division of Molecular Biology, Amsterdam, The Netherlands. p.borst@nki.nl

Cell Cycle (Georgetown, Tex.)
|November 14, 2007
PubMed
Summary
This summary is machine-generated.

Genetically modified mouse models with spontaneous tumors offer new insights into drug resistance mechanisms. These models show resistance develops via drug transporters, not apoptosis interference, and can aid in developing new cancer treatments.

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Generation of Prostate Cancer Cell Models of Resistance to the Anti-mitotic Agent Docetaxel
06:44

Generation of Prostate Cancer Cell Models of Resistance to the Anti-mitotic Agent Docetaxel

Published on: September 8, 2017

Related Experiment Videos

Last Updated: Jul 10, 2026

Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down
08:59

Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down

Published on: December 11, 2017

Generation of Prostate Cancer Cell Models of Resistance to the Anti-mitotic Agent Docetaxel
06:44

Generation of Prostate Cancer Cell Models of Resistance to the Anti-mitotic Agent Docetaxel

Published on: September 8, 2017

Area of Science:

  • Oncology
  • Genetics
  • Pharmacology

Background:

  • Spontaneous tumors in genetically modified mice mimic human cancers.
  • Studying drug resistance mechanisms in these models is crucial for therapeutic development.

Purpose of the Study:

  • To investigate drug resistance mechanisms in mouse mammary tumors induced by Brca1 and p53 deletion.
  • To evaluate the potential of these models for drug development and treatment regimen improvement.

Main Methods:

  • Induction of mammary tumors via conditional deletion of Brca1 and p53 in mice.
  • Treatment of tumors with doxorubicin, docetaxel, and cisplatin to assess response and resistance development.
  • Analysis of resistance mechanisms, focusing on drug transporters and apoptosis/senescence pathways.

Main Results:

  • Tumors responded to doxorubicin and docetaxel but developed resistance, primarily through drug transporter upregulation.
  • Cisplatin treatment led to tumor response without resistance development, even after repeated doses.
  • Resistance mediated by interference with apoptosis or senescence pathways was not observed in these tumors.

Conclusions:

  • Drug resistance in these models is mainly mediated by drug transporters, not cell death pathway interference.
  • Spontaneous mouse tumor models are valuable tools for studying drug resistance and advancing cancer therapy.
  • The resistant remnant fraction in these models may serve as a platform for testing the tumor stem cell hypothesis.