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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 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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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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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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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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Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
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Harnessing Apoptosis in AML.

Kapil Saxena1, Courtney DiNardo2, Naval Daver2

  • 1Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Houston, Texas, 77030, United States.

Clinical Lymphoma, Myeloma & Leukemia
|September 1, 2020
PubMed
Summary
This summary is machine-generated.

The treatment for acute myeloid leukemia (AML) has advanced with new targeted therapies. Venetoclax, a BCL-2 inhibitor, shows efficacy in frontline AML treatment when combined with hypomethylating agents or low-dose cytarabine.

Keywords:
AMLBCL2MCL1synergyvenetoclax

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Area of Science:

  • Hematology
  • Oncology
  • Molecular Biology

Background:

  • The acute myeloid leukemia (AML) treatment landscape has rapidly evolved with new small molecule therapies.
  • Targeted therapies like FLT3 and IDH inhibitors are mutation-specific.
  • Venetoclax, a selective BCL-2 inhibitor, offers a broader efficacy in heterogeneous AML patient groups.

Purpose of the Study:

  • To review the recent advancements in AML treatment.
  • To highlight the role of venetoclax in combination therapies for AML.
  • To discuss the ongoing exploration of the intrinsic apoptotic pathway in AML.

Main Methods:

  • Review of recent clinical trial data and therapeutic approvals for AML.
  • Analysis of the efficacy of venetoclax in combination with hypomethylating agents (HMA) or low-dose cytarabine (LDAC).
  • Exploration of the scientific rationale behind targeting the intrinsic apoptotic pathway in AML.

Main Results:

  • Several new therapeutic small molecules have been approved for AML treatment in the last five years.
  • Venetoclax in combination with HMA or LDAC has demonstrated frontline efficacy in a diverse AML patient population.
  • Venetoclax is currently being investigated in novel combinations, underscoring its therapeutic potential.

Conclusions:

  • The combination of venetoclax with HMA or LDAC represents a significant advancement in frontline AML therapy.
  • Targeting the intrinsic apoptotic pathway, particularly via BCL-2 inhibition, is a promising strategy in AML.
  • Further research into novel venetoclax combinations is warranted to optimize AML treatment outcomes.