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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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Overview of Cell Death01:30

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Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
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The Extrinsic Apoptotic Pathway01:17

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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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The innate immune response is an immediate and non-specific response against pathogens, acting swiftly to prevent the spread of infections. The primary cells involved in this response are phagocytes and natural killer (NK) cells.
Phagocytes
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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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Regulation of Hematopoietic Stem Cells01:01

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All blood and immune cells are produced from the multipotent hematopoietic stem cells (HSCs) by the process of hematopoiesis. However, they all have a limited life span. In addition, many are depleted in immune surveillance or combatting an injury or infection. This makes blood one of the most regenerative tissues. Hematopoiesis helps replenish these blood and immune cells, restoring the body's normal functioning. However, overproduction of blood and immune cells can make them cancerous or...
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Methods to Assess Beta Cell Death Mediated by Cytotoxic T Lymphocytes
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Cell Death Pathways in Lymphoid Malignancies.

Luke Fletcher1, Edward Nabrinsky2, Tingting Liu1

  • 1Division of Hematology & Medical Oncology, Department of Medicine, Oregon Health & Science University, Portland, OR, USA.

Current Oncology Reports
|January 29, 2020
PubMed
Summary

Targeting Bcl-2 family proteins, crucial for lymphoma cell survival, offers new therapeutic strategies. BH3 mimetics like Venetoclax are approved, with novel agents targeting Mcl-1 and signaling pathways showing promise.

Keywords:
ApoptosisBcl-2Mcl-1Venetoclax

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Area of Science:

  • Molecular Biology
  • Cancer Therapeutics
  • Cell Death Regulation

Background:

  • Bcl-2 family proteins regulate mitochondrial outer membrane permeabilization (MOMP), a key event in apoptosis.
  • Dysregulation of these proteins contributes to lymphoma cell survival and therapeutic resistance.

Purpose of the Study:

  • To review the role of Bcl-2 family members in lymphoma.
  • To discuss therapeutic strategies targeting these proteins for lymphoma treatment.

Main Methods:

  • Review of scientific literature on Bcl-2 family proteins and lymphoma.
  • Analysis of current and emerging therapeutic approaches, including BH3 mimetics.

Main Results:

  • BH3 mimetics, such as Venetoclax, are effective in treating certain leukemias.
  • Preclinical studies show success in targeting Mcl-1 and other pro-survival proteins.
  • Indirect targeting of anti-apoptotic Bcl-2 members via signaling pathways is a viable strategy.

Conclusions:

  • Modulating Bcl-2 family proteins presents a promising avenue for lymphoma therapy.
  • Targeting both direct and indirect pathways offers diverse therapeutic options.
  • Further development of BH3 mimetics and combination therapies is warranted.