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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...
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
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.
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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.
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Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
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Related Experiment Video

Updated: Jul 15, 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

Pathways to tamoxifen resistance.

Rebecca B Riggins1, Randy S Schrecengost, Michael S Guerrero

  • 1Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20057, USA.

Cancer Letters
|May 4, 2007
PubMed
Summary

Estrogen-targeting therapies are crucial for breast cancer treatment but face resistance. Understanding resistance mechanisms helps predict patient response and design combination therapies to overcome this challenge.

Related Experiment Videos

Last Updated: Jul 15, 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

Area of Science:

  • Oncology
  • Endocrinology
  • Pharmacology

Background:

  • Estrogen-targeting therapies are standard treatments for estrogen receptor-positive breast cancer.
  • Resistance to these therapies (de novo and acquired) significantly limits treatment efficacy.
  • Understanding resistance mechanisms is key to improving patient outcomes.

Purpose of the Study:

  • To review common mechanisms of antiestrogen resistance in breast cancer.
  • To discuss how understanding these mechanisms can predict patient response.
  • To explore rational approaches for combinatorial treatments to overcome resistance.

Main Methods:

  • Literature review of molecular mechanisms underlying antiestrogen resistance.
  • Analysis of studies investigating prediction of response to endocrine therapies.
  • Synthesis of information on combination therapy strategies.

Main Results:

  • Identified common molecular mechanisms contributing to de novo and acquired antiestrogen resistance.
  • Highlighted the potential for predicting patient response based on resistance mechanisms.
  • Discussed the rationale for combining different therapeutic agents.

Conclusions:

  • Mechanistic insights into antiestrogen resistance are vital for personalized breast cancer treatment.
  • Predictive biomarkers and combination therapies are essential to circumvent resistance.
  • Further research is needed to optimize combinatorial strategies for resistant breast cancer.