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Cancer

Cancer

Cancers arise due to mutations in genes involved in the regulation of cell division, which leads to unrestricted cell proliferation. Modern science and medicine have made great strides in the understanding and treatment of cancer, including eradicating cancer in some patients. However, there is still no cure for cancer. This is largely due to the fact that cancer is a large group of many diseases.

Cancers Originate from Somatic Mutations in a Single Cell

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...

Adaptive Mechanisms in Cancer Cells

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...

Cancer Prevention

Cancer Prevention

Several factors can increase the risk of cancer in an individual. About 50% of cancer cases can be prevented by adopting a healthy lifestyle, regular exercise, eating healthy, and following a modest cancer prevention diet. Epidemiological studies have consistently shown that populations with vegetable and fruit-rich diets have reduced the incidence of cancer. On the other hand, populations who have a diet rich in animal fat, red meat, junk food, or high calories are predisposed to cancer.
Some...

Cancers Originate from Somatic Mutations in a Single Cell

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...

Cancer Prevention

Cancer Prevention

Several factors can increase the risk of cancer in an individual. About 50% of cancer cases can be prevented by adopting a healthy lifestyle, regular exercise, eating healthy, and following a modest cancer prevention diet. Epidemiological studies have consistently shown that populations with vegetable and fruit-rich diets have reduced the incidence of cancer. On the other hand, populations who have a diet rich in animal fat, red meat, junk food, or high calories are predisposed to cancer.
Some...

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Mosaic Zebrafish Transgenesis for Functional Genomic Analysis of Candidate Cooperative Genes in Tumor Pathogenesis

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Cancers beget mutations versus mutations beget cancers

¹Department of Pathology, University of Washington, Seattle 98195.

Cancer Research

|October 15, 1994

Summary

Cancer may not primarily stem from genetic mutations. Instead, aberrant gene expression due to epigenetic factors could cause cancer, with mutations being a consequence, not a cause.

Area of Science:

Oncology
Epigenetics
Genomics

Background:

The traditional view posits cancer arises from genetic mutations in oncogenes and tumor suppressor genes.
This perspective is challenged by evidence suggesting alternative mechanisms.
The role of epigenetic alterations in cancer development warrants further investigation.

Purpose of the Study:

To propose and examine the alternative hypothesis that cancer phenotypes result from aberrant gene expression patterns.
To explore the role of epigenetic mechanisms, rather than mutations, in driving cancer development.
To re-evaluate the causal relationship between mutations and cancer.

Main Methods:

Review and synthesis of existing evidence supporting epigenetic dysregulation in cancer.

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Theoretical examination of how epigenetic changes could lead to cancer phenotypes.

Analysis of the potential role of replicative errors in the cancer genome.

Main Results:

The study proposes that epigenetic dysregulation, not mutations, is the primary driver of cancer.
Mutations observed in cancer may arise as a consequence of epigenetic changes and slow repair mechanisms.
These mutations, occurring at inactivated genomic sites, may have limited biological significance.

Conclusions:

The hypothesis that cancer is primarily caused by mutations may be incorrect.
Aberrant gene expression patterns, driven by epigenetic mechanisms, are a more likely cause of cancer.
Cancers may actually 'beget' mutations, rather than the other way around.