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Related Concept Videos

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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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...
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Mitogens and the Cell Cycle02:38

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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...
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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Inhibition of Cdk Activity02:34

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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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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.
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Related Experiment Video

Updated: Jun 29, 2025

Obtaining Cancer Stem Cell Spheres from Gynecological and Breast Cancer Tumors
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Obtaining Cancer Stem Cell Spheres from Gynecological and Breast Cancer Tumors

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CD133 expression is associated with less DNA repair, better response to chemotherapy and survival in

Takumi Sato1, Masanori Oshi2, Jing Li Huang3

  • 1University of Tokyo Hospital.

Research Square
|April 8, 2024
PubMed
Summary
This summary is machine-generated.

CD133 expression in ER+/HER2- breast cancer (BC) is linked to a cancer stem cell (CSC) phenotype. CD133-high BC shows enhanced inflammation and better response to chemotherapy, indicating improved prognosis.

Keywords:
CD133HR positive breast cancercancer stem cellcell surface marker

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Area of Science:

  • Oncology
  • Genomics
  • Molecular Biology

Background:

  • CD133 is a cancer stem cell (CSC) marker associated with treatment resistance in triple-negative breast cancer (BC).
  • The clinical significance of CD133 in ER-positive/HER2-negative (ER+/HER2-) BC, the most prevalent subtype, remains unclear.

Approach:

  • Utilized gene expression data from large BC cohorts (METABRIC and TCGA).
  • Analyzed biological variables and gene expression patterns associated with CD133 levels in ER+/HER2- BC.

Key Points:

  • CD133-high ER+/HER2- BC exhibits CSC-like characteristics (e.g., reduced proliferation, DNA repair) alongside increased inflammation and immune cell activity.
  • CD133-low BC is associated with cell proliferation and DNA repair gene sets.
  • CD133-high tumors demonstrated better pathological complete response to neoadjuvant chemotherapy and improved survival outcomes.

Conclusions:

  • CD133 expression in ER+/HER2- BC correlates with a distinct CSC phenotype, inflammatory microenvironment, and favorable clinical outcomes.
  • CD133 serves as a potential prognostic biomarker in ER+/HER2- breast cancer.