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The "Bcl2" gene was first identified in B cell lymphoma cancer cells, where a chromosome translocation causes excessive production of Bcl2 protein (which suppresses apoptosis). How does excess Bcl2 protein suppress apoptosis in B-cell lymphoma tumors?

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Final answer:

In B-cell lymphoma, excess Bcl2 protein suppresses apoptosis by inhibiting the activity of proteins that promote cell death, thereby contributing to tumor development and survival.

Step-by-step explanation:

How Excess Bcl2 Protein Suppresses Apoptosis In B-cell lymphoma, a chromosome translocation can cause excessive production of the Bcl2 protein. This protein plays a crucial role in the regulation of apoptosis, which is the programmed cell death process. Normally, proteins such as Bak and Bax form channels in the outer mitochondrial membrane and contribute to apoptosis by allowing the release of cytochrome C, which in turn triggers a cascade of molecular events leading to cell death. However, excess Bcl2 protein can suppress the activity of Bak and Bax, preventing this release and consequently the apoptosis pathway. This suppression leads to increased cell survival and proliferation, contributing to the development and persistence of tumors. Tumor suppressor genes like p53 also play a significant role in apoptosis. They are responsible for preventing the cell cycle progression in the presence of DNA damage. If p53 is mutated, which is common in various cancers, it may lead to diminished apoptosis and unregulated cell proliferation, characteristic of cancer cells.

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