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Related Concept Videos

The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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Cancer-Critical Genes II: Tumor Suppressor Genes01:05

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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
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The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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Loss of Tumor Suppressor Gene Functions01:12

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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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Apoptosis01:30

Apoptosis

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Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
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Tumor Progression02:07

Tumor Progression

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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.
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Genes Associated with Apoptosis in an Experimental Breast Cancer Model.

Gloria M Calaf1, Leodan A Crispin1

  • 1Instituto de Alta Investigación, Universidad de Tarapacá, Arica 1000000, Chile.

International Journal of Molecular Sciences
|October 16, 2025
PubMed
Summary

Breast cancer progression involves altered apoptosis-related gene expression, impacting treatment resistance. Targeting these genes may offer new therapeutic strategies and prognostic biomarkers for personalized breast cancer care.

Keywords:
ERTP63apoptosisbreast cancerp53

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Breast cancer remains a significant cause of mortality globally.
  • Metastasis and drug resistance are primary challenges in breast cancer treatment.
  • Understanding apoptosis regulation is crucial for overcoming therapeutic evasion.

Purpose of the Study:

  • To investigate the modulation of apoptosis-related genes in breast cancer cells.
  • To analyze gene expression changes in response to ionizing radiation and estrogen.
  • To identify potential molecular targets and biomarkers for breast cancer therapy.

Main Methods:

  • Utilized a human breast epithelial cell model (MCF-10F and variants).
  • Treated cells with high linear energy transfer alpha particles and 17β-estradiol.
  • Performed gene expression profiling using microarrays and bioinformatic analyses.

Main Results:

  • Identified distinct gene expression patterns across cell lines and tumor subtypes.
  • Found correlations between specific genes (e.g., TP53, TP63, BCLAF1, PHLDA2) and tumor characteristics.
  • Observed associations between elevated BCLAF1 and PHLDA2 expression and poorer patient survival in specific subtypes.

Conclusions:

  • Apoptosis resistance is a key mechanism in breast cancer progression and therapeutic evasion.
  • Breast tumors selectively alter apoptosis-related gene expression to promote growth and resistance.
  • These genes represent potential targets for personalized therapies and prognostic biomarkers.