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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.
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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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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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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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Establishing Cell Lines Overexpressing DR3 to Assess the Apoptotic Response to Anti-mitotic Therapeutics
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Targeting apoptosis for anticancer therapy.

Simone Fulda1

  • 1Institute for Experimental Cancer Research in Pediatrics, Goethe-University, Komturstr. 3a, 60528 Frankfurt, Germany.

Seminars in Cancer Biology
|May 27, 2014
PubMed
Summary
This summary is machine-generated.

Cancer cells evade programmed cell death (apoptosis), driving tumor growth and treatment resistance. Reactivating these natural cell death pathways offers a promising strategy for developing more effective and less toxic cancer therapies.

Keywords:
ApoptosisCancerCell deathDeath receptorMitochondria

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Programmed cell death, or apoptosis, is frequently disrupted in human cancers.
  • This disruption promotes tumor formation, progression, and resistance to cancer treatments.
  • Many current cancer therapies depend on functional apoptosis pathways for efficacy.

Purpose of the Study:

  • To investigate the regulatory mechanisms controlling cell death signaling pathways.
  • To explore the potential of reactivating apoptosis in cancer cells as an anticancer strategy.
  • To identify new therapeutic approaches for overcoming treatment resistance in cancer.

Main Methods:

  • Analysis of cell death signaling pathways in cancer cells.
  • Investigation of regulatory mechanisms governing apoptosis.
  • Exploration of strategies to re-induce apoptosis in malignant cells.

Main Results:

  • Disturbed apoptosis is a hallmark of human cancers, contributing to disease progression and therapeutic challenges.
  • Understanding apoptosis regulation is crucial for overcoming treatment resistance.
  • Reactivating apoptosis pathways presents a potential avenue for novel anticancer treatments.

Conclusions:

  • Reactivating programmed cell death in cancer cells could lead to more effective and tumor-selective therapies.
  • Targeting apoptosis pathways may offer a less toxic alternative to current treatments.
  • Further research into apoptosis regulation is critical for advancing cancer therapy.