Genetic Basis of Cancer Quiz

A disease characterized by uncontrolled cell division; a genetic disease at the cellular level.

Cancer originates from a single cell, which divides to form a mass of identical cancer cells.

Cancer develops in stages, starting with a benign growth that progresses to cancerous growth through genetic changes.

Cancer that invades surrounding tissues. This type is highly aggressive.

Cancer that has spread to different parts of the body.

Genes that promote cell division and uncontrolled cell growth.

Genes that prevent uncontrolled cell growth and regulate cell division.

Substances, like radiation and certain chemicals, that damage DNA and increase the risk of mutation leading to cancer.

Normal genes that can mutate and become oncogenes, driving cancer.

A key tumor suppressor gene, often mutated in cancers.

Crucial tumor suppressor gene that triggers cell death if DNA is damaged.

The process where a normal cell becomes a cancer cell.

Changes in the genetic code of oncogenes that cause them to become overactive.

Oncogenes found in viruses and involved in cancer.

A change in a single DNA base pair that results in a different amino acid being incorporated into a protein.

An increase in the number of copies of a gene.

A rearrangement of genetic material between non-homologous chromosomes.

The insertion of viral DNA into the host cell's genome.

A gene whose normal function is to prevent the uncontrolled growth of cells. They act as brakes on cell division.

The Rb protein binds to a transcription factor called E2F, preventing E2F from activating genes needed for cell cycle progression.

Programmed cell death. It's a controlled process of cell self-destruction.

The p53 protein detects DNA damage and initiates repair mechanisms. If repair fails, it triggers cell cycle arrest or apoptosis.

When tumor suppressor genes are inactivated, cell division control is lost, leading to uncontrolled cell growth and cancer development.

They regulate cell division and apoptosis. They act as "gatekeepers" protecting the genome from mutations that can lead to cancer.

A crucial checkpoint in the cell cycle, ensuring proper cell growth and DNA integrity before entering S phase (DNA replication).

A tumor suppressor protein that inhibits progression through the restriction point, preventing uncontrolled cell division.

A protein complex that promotes passage through the restriction point by phosphorylating and inactivating Rb.

A tumor suppressor protein that inhibits the activity of Cdk4/6-Cyclin D complex, preventing uncontrolled cell division.

A tumor suppressor protein that plays a crucial role in cell cycle arrest and apoptosis (programmed cell death) in response to DNA damage.

A Cdk inhibitor protein that is induced by p53, leading to cell cycle arrest in response to DNA damage.

Pro-apoptotic proteins induced by p53, triggering apoptosis (controlled cell death) in response to severe DNA damage.

Mutations in proto-oncogenes can lead to increased protein production, altered protein activity, or expression in inappropriate cell types, all contributing to uncontrolled growth.

A GTPase involved in signaling pathways that regulate cell growth. Mutations in the Ras gene can lead to the formation of an oncogene.

E2F inhibition prevents the transcription of genes crucial for DNA replication and cell division.

The protein kinase p16 acts as a negative regulator of cyclin-dependent kinases, controlling the transition from the G1 phase to the S phase of the cell cycle.

NF1 protein stimulates Ras to hydrolyze GTP to GDP, essentially turning off Ras.

A loss of NF1 function leads to overactive Ras, which promotes cell division and can contribute to cancer development.

APC acts as a negative regulator of a pathway that activates genes promoting cell division.

Maintaining genome integrity refers to cellular mechanisms that prevent mutations or stop mutant cells from dividing or surviving.

Checkpoint proteins detect genetic abnormalities and prevent cell division, while DNA repair enzymes fix errors in the genetic code.

p53 acts as a sensor of DNA damage, regulating genes to control cell cycle progression and promote apoptosis if necessary.

Changes in gene expression without altering the DNA sequence. Think of it like adding sticky notes to your DNA to change how genes are read.

Alterations in gene expression due to epigenetics can contribute to disease development through direct involvement, subsequent changes, or indirect associations via a third factor.

Cancer cells often exhibit abnormal epigenetic modifications, including DNA methylation, histone modifications, and chromatin remodeling, contributing to uncontrolled cell growth.

Mutations in genes that encode chromatin-modifying proteins can lead to either inhibition or increased function of these proteins, ultimately affecting gene expression patterns.

Mutations in genes that encode DNA methyltransferases, the enzymes responsible for attaching methyl groups to DNA, can contribute to abnormal methylation patterns in cancer.

Mutations in histone-modifying enzymes, such as histone acetyltransferases, methyltransferases, demethylases, and kinases, can lead to aberrant histone modifications, altering gene expression in cancer.

Alterations in chromatin remodeling complexes, such as SWI/SNF, can disrupt chromatin structure and affect gene expression, contributing to cancer development.

Certain environmental factors, such as pollutants and toxic substances, can directly alter the functions of chromatin-modifying proteins, potentially influencing the development of cancer.

Inhibition of DNA methylation and histone modifications is a promising approach to target cancer cells. Drugs like 5-azacytidine and decitabine are examples of DNA methyltransferase inhibitors showing potential in leukemia treatment.

Epigenetic changes can lead to inappropriate gene expression, promoting uncontrolled cell growth, invasion, and metastasis. It is also important to note that epigenetic alterations can be influenced by environmental factors, which may contribute to cancer development.

Three major categories of epigenetic modifications are commonly affected in cancer: DNA methylation, histone modifications, and chromatin remodeling. Each type alters the accessibility and expression of genes.

Mutations in genes encoding enzymes that modify chromatin can alter the function of these enzymes, leading to inappropriate epigenetic modifications. This can either enhance or suppress gene expression, potentially causing cancer development.

Environmental factors like pollutants, tobacco smoke, endocrine disruptors, and heavy metals can directly influence the function of chromatin-modifying proteins, leading to epigenetic changes that may contribute to cancer development.

Drugs aimed at inhibiting DNA methylation and histone modifications, like 5-azacytidine and decitabine, are being investigated for their potential as cancer treatments. These drugs try to restore normal gene expression patterns to control cancer cell growth.