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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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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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B Cell Activation and Differentiation01:24

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The adaptive immune response, a sophisticated defense mechanism, relies on the activation and differentiation of B lymphocytes, or B cells. These processes enable our bodies to mount a tailored response against specific pathogens such as bacteria, free virus particles, toxins, and parasites.
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Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
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Modulating apoptosis pathways in low-grade B-cell malignancies using biological response modifiers.

John C Reed1, Shinichi Kitada, Youngsoo Kim

  • 1Burnham Institute, La-Jolla, CA; and The Ohio State University School of Medicine, Columbus, OH.

Seminars in Oncology
|February 1, 2017
PubMed
Summary
This summary is machine-generated.

Low-grade B-cell malignancies like chronic lymphocytic leukemia (CLL) and follicular lymphoma (FL) often result from apoptosis defects, leading to chemoresistance. Understanding how apoptosis modulators affect these cancer cells may improve therapies.

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Area of Science:

  • Oncology
  • Cell Biology
  • Immunology

Background:

  • Low-grade B-cell malignancies, including chronic lymphocytic leukemia (CLL) and follicular lymphoma (FL), are common and potentially lethal cancers.
  • These cancers are characterized by defects in programmed cell death (apoptosis), leading to prolonged survival of malignant B lymphocytes.
  • Apoptosis defects contribute to chemoresistance and immune evasion in neoplastic cells.

Purpose of the Study:

  • To explore the role of apoptosis defects in the pathogenesis of low-grade B-cell malignancies.
  • To review potential therapeutic strategies involving apoptosis modulators for treating CLL and FL.
  • To understand how novel agents can overcome chemoresistance by influencing apoptosis pathways.

Main Methods:

  • Review of existing literature on apoptosis pathways in B-cell malignancies.
  • Analysis of the mechanisms of action for various biological agents and small-molecule compounds.
  • Discussion of how these agents can be used to induce apoptosis in cancer cells.

Main Results:

  • Malignant B cells in CLL and FL accumulate due to impaired apoptosis, not increased proliferation.
  • Defective apoptosis pathways confer resistance to conventional chemotherapy and cellular immune responses.
  • Several agents, including rituximab, TRAIL, and kinase inhibitors, show promise in modulating apoptosis.

Conclusions:

  • Targeting apoptosis pathways offers a promising strategy for treating CLL, FL, and other malignancies.
  • Apoptosis modulators have the potential to re-sensitize cancer cells to therapy or induce cell death.
  • Further research into the mechanisms of these agents may lead to more effective and less toxic cancer treatments.