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It is proposed that mutated cells are eliminated through apoptosis due to accumulated DNA damage.
The failure of apoptosis allows mutated cells to continue to enter the cell cycle, perpetuating the cycle of mutation and oncogenesis.
Moreover, we show that most cells do not undergo apoptosis after irradiation but rather cease proliferation and start a differentiation program.
Journal ArticleDOI
Daniel S. Marsman, J. Carl Barrett 
01 Jun 1994-Risk Analysis
23 Citations
While enhanced cell replication may contribute to an increased frequency of mutation, apoptosis within a tissue may counteract chemical carcinogenesis through loss of mutated cells.
Open accessJournal ArticleDOI
32 Citations
Abnormal cells are prone to destruction through spontaneous apoptosis or because of the immunosurveillance that needs to stay highly vigilant.
These results support the hypothesis that apoptosis plays a crucial role in maintaining genomic integrity by selectively eliminating highly mutated cells from the population.
Apoptosis was classically regarded as a silent form of cell death, but mounting evidence indicates that apoptotic cells “don't go silently” and leave a heritage to the local microenvironment.
Dysregulation of apoptosis can result in the persistence of mutated cells, leading to malformations, autoimmune disease, and cancer.
The inhibition of apoptosis prevents the elimination of mutation-affected cells which leads to an uncoordinated proliferation of a mutated cell clone.
However, if mutation generates relative resistance to apoptosis it may result in growth advantage for the mutated cells.

Related Questions

What are the most frequently mutated genes in cancer?5 answersThe most frequently mutated genes in cancer include MADCAM1, EIF1AX, NF1, PTPRS, NRAS, and TP53, with varying mutation frequencies. Among these, TP53 is a crucial tumor suppressor gene involved in various cellular processes like DNA repair, apoptosis, and cell cycle regulation. Additionally, driver mutation analysis across 20,066 primary tumors revealed that tumor suppressor genes are the most commonly mutated class, with TP53 mutations associated with poor disease outcomes. Furthermore, a meta-analysis focusing on leptomeningeal carcinomatosis identified TP53, PTEN, PIK3CA, IL7R, and KMT2D as commonly mutated genes in cancers leading to this condition, emphasizing their roles in cell communication, signaling, and proliferation. These genes play pivotal roles in cancer development and progression, highlighting their significance in oncology research.
What cause mutation in cancer cells?5 answersMutations in cancer cells can be caused by various factors. Environmental mutagens, such as chemotherapeutic drugs, genotoxic gut bacteria, ultraviolet exposure, and altered activity of error-prone polymerase, can induce mutations in the DNA of healthy cells. Additionally, endogenous processes associated with aging and DNA replication errors can also contribute to the accumulation of mutations in cancer cells. Specific bacterial strains, such as pks+ E. coli, can produce toxins that induce DNA damage and lead to mutations. The mutational processes triggered by these factors can dysregulate cancer signal transduction pathways and disrupt DNA repair mechanisms. Understanding the role of these mutational processes in carcinogenesis can help identify preventable causes of cancer and inform public health strategies.
Which mutations are responsible for cancer progression?5 answersMutations in genes such as B-raf proto-oncogene (BRAF), MYO5B, and mitochondrial DNA (mtDNA) have been identified as drivers of cancer progression. The V600E mutation in the BRAF gene is a common mutation that leads to continuous activation of the MAPK/ERK signaling pathway, promoting cell proliferation and invasion. In addition, mutations in MYO5B have been found to increase proliferation and migration in pheochromocytoma and paraganglioma (PPGL) tumors. Somatic mtDNA mutations can induce mitochondrial dysfunction, affecting energy production, oxidative stress, and cell survival, and have been implicated in aging and cancer progression. These mutations can lead to a metabolic shift from oxidative phosphorylation to glycolysis, facilitate adaptation to altered environments, and promote resistance to chemotherapy and metastasis. Overall, mutations in these genes play a critical role in the development and progression of cancer.
How do mutations increase cancer?3 answersMutations increase cancer by causing defects in genes that regulate cell proliferation, differentiation, and cell death. There are two types of mutations: gain-of-function mutations in oncogenes and loss-of-function mutations in tumor suppressor genes. Mutations can also affect gene expression through epigenetic mechanisms, leading to similar consequences as genetic mutations. Multiple gene defects often accumulate in a cancer cell during its development, with benign lesions having fewer defects than malignant ones. Clonal selection plays a role in determining the specific genetic and epigenetic defects present in a cancer cell, promoting the outgrowth of cells with mutations that confer proliferative and survival advantages. Cancer cells acquire certain traits that allow them to grow unchecked, including stem cell-like properties, enhanced response to growth signals, resistance to growth inhibitors, increased mutation rate, angiogenesis, immune evasion, limitless cell division, invasion, and adaptation to different microenvironments. Some gene defects may contribute to specific traits, but many exert pleiotropic effects on the cancer cell phenotype. Targeting key signaling pathways and proteins affected by gene defects could be useful in advanced cancers.
How do these genetic mutations affect the cell cycle?5 answersGenetic mutations can affect the cell cycle in various ways. Disturbances in the cell cycle can lead to delayed DNA synthesis, delayed mitosis, and blockage in anaphase. Mutations in genes such as ZDS1 and ZDS2 can cause defects in initiating DNA replication, resulting in plasmid loss. Mutations in genes like SIN4 can affect transcriptional regulation and chromatin structure, leading to growth defects and difficulties in completing S phase or entering mitosis. Mutations in genes that influence cellular proliferation, such as those affecting the restriction point, can result in neoplasia and predispose individuals to tumorigenesis. Mutations in the dna mutants of Saccharomyces cerevisiae can inhibit progress through the cell cycle, particularly DNA synthesis, indicating a connection between DNA and cell cycle regulation. Mutations in the p53 gene can disrupt the cell cycle and genetic integrity control, potentially contributing to tumor development.
Is mutant protein any good?10 answers