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Definition: How can apoptosis be dysregulated in cancer?

There are several ways in which apoptosis can be dysregulated in cancer:

1. Inactivation of pro-apoptotic proteins: Cancer cells often acquire mutations or alterations in genes encoding pro-apoptotic proteins, such as p53, Bax, or Bak. These mutations can lead to the loss of function of these proteins, impairing their ability to induce apoptosis in response to cellular stress or DNA damage.

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2. Overexpression of anti-apoptotic proteins: Cancer cells can also upregulate the expression of anti-apoptotic proteins, such as Bcl-2 or Bcl-xL. These proteins inhibit the activation of pro-apoptotic proteins and promote cell survival, allowing cancer cells to evade apoptosis and continue proliferating.

3. Dysregulation of apoptotic signaling pathways: Apoptosis is regulated by a complex network of signaling pathways, including the extrinsic pathway (activated by death receptors) and the intrinsic pathway (activated by cellular stress). In cancer, these signaling pathways can be disrupted, leading to aberrant activation or inhibition of apoptotic signals.

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4. Impaired clearance of apoptotic cells: In normal tissues, apoptotic cells are efficiently cleared by phagocytic cells, preventing the release of potentially harmful cellular contents. However, in cancer, the clearance of apoptotic cells can be impaired, leading to the accumulation of apoptotic debris and the release of pro-inflammatory signals that promote tumor growth and metastasis.

Understanding the dysregulation of apoptosis in cancer is crucial for the development of targeted therapies that can restore apoptosis in cancer cells and promote their elimination.

Keywords: apoptotic, apoptosis, proteins, dysregulation, cellular, promote, signaling, pathways, dysregulated