Molecular Basis of Cancer: Genetic Alterations

Cancer development is a complex process where normal cells transform into cancer cells. It involves multiple genetic alterations that accumulate over time and lead to the development of cancer's characteristics.

Tumors originate from a single progenitor cell, unlike normal tissues that are made up of various cell types.

Cancer development is a result of several genetic changes happening in the cells over a significant period.

Cancer cells within a tumor are genetically diverse, accumulating different mutations as they multiply, leading to varied growth patterns and responses to treatments.

Continued mutation in cancer cells can lead to more aggressive behavior, increased growth, and spread to other parts of the body.

Cancer arises from either abnormal genes or normal genes with irregular expression. These abnormalities can be inherited or induced by carcinogens like chemicals, viruses, or radiation.

Certain genes control the cell cycle, preventing uncontrolled growth. Damage or abnormalities in these genes can contribute directly to cancer development.

The idea that two genetic hits are required for a cell to become cancerous. For example, a person might inherit one copy of a mutated gene and a second mutation in the other copy might be acquired during their lifetime, leading to cancer development.

Genes that normally promote cell growth and division. They encode proteins involved in various stages of the cell cycle, including signal transduction and transcription.

Mutated or overexpressed versions of proto-oncogenes. They contribute to uncontrolled cell growth and proliferation.

Genes that normally act as brakes to control cell growth and division. They prevent uncontrolled proliferation by halting the cell cycle, repairing DNA damage, and triggering programmed cell death.

A crucial tumor suppressor gene involved in preventing genome mutations. It plays a role in regulating cell cycle progression and promoting DNA repair.

Another important tumor suppressor gene involved in regulating cell cycle progression and preventing uncontrolled proliferation.

A type of programmed cell death that eliminates damaged or unwanted cells. It's a critical process for maintaining healthy tissues and preventing cancer.

Genes that regulate the process of apoptosis.

A proto-oncogene that encodes a signal transduction protein involved in cell growth pathways. When mutated, it can cause uncontrolled cell growth.

A gene that encodes a protein receptor involved in cell growth and division in breast tissue. Mutation or overexpression of this gene can contribute to breast cancer.

A gene associated with lymphoma and other types of cancer. It plays a role in cell growth and proliferation.

Tumors are able to grow without relying on external stimuli, often due to the activation of oncogenes.

Tumors may not respond to signals that normally inhibit cell growth, often due to the inactivation of tumor suppressor genes.

Tumors resist programmed cell death (apoptosis), allowing them to survive and proliferate.

Tumor cells possess an unlimited ability to divide, similar to stem cells, preventing them from aging and dying.

Tumors induce the formation of new blood vessels to supply them with nutrients and oxygen for their growth.

Tumors have the ability to invade surrounding tissues and spread to distant sites, a major cause of cancer deaths.

Cancer cells evade the immune system, allowing them to avoid detection and destruction.

Cancer cells switch to a different energy-producing process called aerobic glycolysis, enabling rapid growth.

A single base change in the DNA sequence can lead to gene alterations.

Mutations in proto-oncogenes can lead to uncontrolled cell growth, while mutations in tumor suppressor genes can hinder cell growth regulation.

They turn proto-oncogenes into oncogenes, leading to uncontrolled cell growth. An example is the RAS gene mutation.

These mutations reduce or completely disable the function of the tumor suppressor gene, leading to uncontrolled cell growth. An example is the TP53 gene mutation.

A piece of chromosome 9 with the ABL gene and a piece of chromosome 22 with the BCR gene swap places. This creates a new tyrosine kinase with powerful transforming activity, leading to chronic myeloid leukemia.

The MYC gene on chromosome 8 is moved next to a very active regulatory gene on chromosome 14. This causes the MYC gene to be overexpressed, leading to Burkitt lymphoma.