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Scientist Otto Warburg, whose research activities led to the formulation of the Warburg hypothesis for explaining the root cause of cancer.. The Warburg hypothesis (/ ˈ v ɑːr b ʊər ɡ /), sometimes known as the Warburg theory of cancer, postulates that the driver of carcinogenesis (cancer formation) is insufficient cellular respiration caused by insult (damage) to mitochondria. [1]
Disseminating cancer cells can proliferate or become dormant depending on the microenvironment and factors such as the ERK/p38 ratio. Dormancy is a stage in cancer progression where the cells cease dividing but survive in a quiescent state while waiting for appropriate environmental conditions to begin proliferation again. [1]
Overview of signal transduction pathways involved in apoptosis. Cell death is the event of a biological cell ceasing to carry out its functions. This may be the result of the natural process of old cells dying and being replaced by new ones, as in programmed cell death, or may result from factors such as diseases, localized injury, or the death of the organism of which the cells are part.
For many years, neither "apoptosis" nor "programmed cell death" was a highly cited term. Two discoveries brought cell death from obscurity to a major field of research: identification of the first component of the cell death control and effector mechanisms, and linkage of abnormalities in cell death to human disease, in particular cancer.
In cancer cells, major changes in gene expression increase glucose uptake to support their rapid growth. Unlike normal cells, which produce lactate only when oxygen is low, cancer cells convert much of the glucose to lactate even in the presence of adequate oxygen. This is known as the “Warburg Effect.”
Apoptosis is the programmed cell death of superfluous or potentially harmful cells in the body. It is an energy-dependent process mediated by proteolytic enzymes called caspases, which trigger cell death through the cleaving of specific proteins in the cytoplasm and nucleus. [13] The dying cells shrink and condense into apoptotic bodies.
More specifically p16INK4a-pRb tumor suppressor and p53 are known effectors of senescence. Most cancer cells have a mutated p53 and p16INK4a-pRb, which allows the cancer cells to escape a senescent fate. [41] The p16 protein is a cyclin dependent kinase (CDK) inhibitor and it activates Rb tumor suppressor.
The evolutionary processes do not cease when a population of cancer stem cells arises in a tumor. Cancer treatment drugs pose a strong selective force on all types of cells in tumors, including cancer stem cells, which would be forced to evolve resistance to the treatment. Cancer stem cells do not always have to have the highest resistance ...