Genetic Basis of Cancer

Uncontrolled cell division, originating from a single cell, progressing through benign to malignant stages and potentially metastasizing.

Most cancers arise from one single cell, forming a clonal growth through cell division, becoming cancerous from benign growth through genetic alterations.

A cancerous growth that invades surrounding tissue.

Malignant cancer cells that move to other parts of the body.

Oncogenes promote cell growth and division. Tumor suppressor genes inhibit uncontrolled cell division and growth. Alterations in either can lead to cancer.

Radiation, chemical carcinogens, and viruses can damage DNA, inducing mutations and promoting cell proliferation, leading to cancer development.

Specific viruses that directly cause cancer in animals and/or humans by affecting cell divisions

Cancers are categorized by the type of cell that becomes cancerous, with over 100 identified types.

Genes capable of inducing cell transformation, leading to cancer development.

Normal genes that can become oncogenes through mutation.

Genes that normally stop tumor development by inhibiting cell growth.

A classic tumor suppressor gene, important for regulating cell growth.

A crucial tumor suppressor gene involved in cell cycle control and apoptosis.

The process where normal cells become cancerous.

Viruses that convert RNA to DNA, which can cause cancer.

A change in a gene's DNA sequence that alters gene function.

Rb inhibits cell cycle progression past a specific point (G1 restriction point)

This complex activates cell cycle progression by inactivating Rb.

p16 blocks Cdk4/6-cyclin D activity thus inhibiting Rb inactivation.

A GTPase protein, involved in cell signaling – a proto-oncogene.

Mutations in Ras often lead to uncontrolled cell division.

Mediates cell cycle arrest and apoptosis in response to DNA damage.

Cell cycle arrest prevents cell division, while apoptosis is programmed cell death.

The process where E2F, a transcription factor, is prevented from activating genes essential for DNA replication and cell division.

p16 protein acts as a brake on the cell cycle, preventing the transition from G1 to S phase, where DNA replication occurs, by inhibiting cyclin-dependent kinases (CDKs).

NF1 protein controls Ras, a key signaling protein, by helping it switch off. When NF1 is defective, Ras stays active, promoting cell division.

APC (Anaphase-Promoting Complex) acts as a negative regulator, limiting the activation of genes that drive cell division.

p53 acts as a guardian of the genome, monitoring DNA damage. It can stop cell division or trigger cell death (apoptosis) if damage is unrepaired.

These proteins function as DNA repair specialists, fixing damaged DNA. They can also activate cell death if repair is impossible.

Maintaining the integrity of genetic information by preventing mutations and ensuring proper functioning of mechanisms that detect and fix DNA mistakes.

Epigenetics explores how cellular function can change through mechanisms beyond alterations in DNA sequence. These changes can be inherited.

The first human tumor suppressor gene discovered, responsible for suppressing cancer growth in the retina. Mutations in this gene lead to retinoblastoma, a type of eye cancer.

A theory explaining how retinoblastoma develops. It requires two separate mutations in the Rb gene for cancer to occur. One hit can be inherited, the other acquired later.

The Rb protein regulates the cell cycle by controlling the activity of a transcription factor called E2F. Rb essentially acts as a 'brake' on cell division, preventing uncontrolled growth.

The p53 protein, when activated, initiates various responses to DNA damage, including DNA repair, cell cycle arrest, and programmed cell death (apoptosis). It prevents damaged cells from replicating and spreading mutations.

A programmed cell death process where damaged or mutated cells are eliminated in a controlled manner, preventing them from becoming cancerous.

A family of proteases (enzymes that break down proteins) involved in triggering and executing apoptosis. They play a critical role in 'executing' damaged or cancerous cells.

Mutations, deletions, or inactivation of tumor suppressor genes can lead to cancer. The loss of function of these genes allows uncontrolled cell growth and division.

When tumor suppressor genes are inactivated, the cellular safeguards against uncontrolled growth are removed. This allows cells with mutations to proliferate, eventually leading to tumor formation.

Changes in gene expression that affect disease development in three primary ways: directly contributing to disease symptoms, stemming from disease symptoms, or linked indirectly by a third factor.

Abnormal alterations in chromatin structure are prevalent in cancer cells, involving DNA methylation, histone modification, and chromatin remodeling.

Mutations in genes that encode chromatin-modifying proteins or environmental agents that alter the functions of these proteins can lead to abnormal chromatin modifications in cancer.

Changes in genes that encode chromatin-modifying proteins can have significant consequences for gene expression, potentially leading to cancer.

Exposure to certain environmental agents can directly alter the functions of chromatin-modifying proteins, potentially leading to cancer development.

Researchers are exploring drugs that inhibit cancer cells by influencing DNA methylation or histone modifications, aiming to restore normal gene expression.

Drugs that block the activity of DNA methyltransferase enzymes, which add methyl groups to DNA, have shown promise in leukemia treatment.

Two DNA methyltransferase inhibitors that have demonstrated some effectiveness in leukemia treatment, although their precise mechanisms of action are not fully understood.

Epigenetic changes, particularly DNA methylation and histone modifications, play a significant role in the development and progression of cancer by altering gene expression.

Cancer cells often exhibit abnormal chromatin modifications, leading to changes in gene expression that promote uncontrolled cell growth and division.

Exposure to certain environmental agents can directly alter chromatin-modifying proteins, leading to epigenetic changes that can contribute to cancer development.

Epigenetic mechanisms are becoming increasingly important targets for cancer therapy, with drugs that modify DNA methylation and histone modifications showing promising results.

Epigenetic modifications, such as DNA methylation and histone modifications, directly influence gene expression, potentially leading to disease.