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Related Concept Videos

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...
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

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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Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down
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Does lapatinib work against HER2-negative breast cancers?

Ingrid A Mayer1, Carlos L Arteaga

  • 1Departments of Medicine, Vanderbilt-Ingram Comprehensive Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|February 25, 2010
PubMed
Summary

Aberrant growth factor receptor signaling affects estrogen receptor (ER) function in breast cancer, leading to resistance to anti-estrogen therapies. Combining HER2 inhibition with endocrine therapy may restore sensitivity in ER+/HER2-negative breast cancers.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Endocrinology

Background:

  • Aberrant growth factor receptor signaling pathways can modulate estrogen receptor (ER) activity in hormone-dependent breast cancer.
  • This signaling crosstalk can lead to therapeutic resistance, particularly to anti-estrogen treatments.

Purpose of the Study:

  • To investigate the potential of interrupting HER2/ER signaling crosstalk to overcome endocrine resistance.
  • To evaluate the efficacy of combining lapatinib with endocrine therapy in ER+/HER2-negative breast cancers.

Main Methods:

  • Utilizing preclinical models of hormone-dependent breast cancer.
  • Assessing the impact of lapatinib on HER2/ER signaling pathways.
  • Evaluating the combination therapy's effect on tumor growth and sensitivity to anti-estrogens.

Main Results:

  • Interruption of HER2/ER cross-talk with lapatinib demonstrated potential in restoring sensitivity to anti-estrogen therapies.
  • Preliminary findings suggest that combination therapy warrants further investigation.

Conclusions:

  • Targeting HER2/ER signaling crosstalk represents a viable strategy to overcome endocrine resistance in breast cancer.
  • Combination of lapatinib with endocrine therapy should be explored in clinical trials for ER+/HER2-negative breast cancer patients.