Cell Biology Quiz: Apoptosis and Cell Cycle

A protein complex that controls the transition from G2 phase to M phase (mitosis) in the cell cycle by activating key events like chromosome condensation and spindle assembly. It's nicknamed the 'maturation-promoting factor.'

The stage of the cell cycle where the cell grows and prepares for division. Consists of three phases: G1 (growth and development), S (DNA replication), and G2 (preparing for mitosis).

A resting state outside the active cell cycle where cells perform their specialized functions, but do not divide. Most adult cells are in this state.

Proteins that regulate transitions between different phases of the cell cycle by activating cyclin-dependent kinases (CDKs).

Enzymes that are essential for the regulation of the cell cycle. They are activated by cyclins and control the progression through different stages.

A specific type of cyclin that activates CDK4/6 and is crucial for the transition through the restriction point in G1 phase. This point marks the commitment to cell division.

A point in the G1 phase where the cell commits to the cell cycle and no longer needs external mitogenic signals to continue. It's controlled by the activity of D-type cyclins and CDK4/6.

A family of proteins that act as transcriptional repressors, controlling the expression of genes involved in cell proliferation. They bind to and inhibit E2F which is the key transcription factor for cell cycle progression.

A protein family that regulates progression through the cell cycle by controlling the activity of cyclin-dependent kinases (CDKs).

The process by which proteins are tagged with ubiquitin, marking them for degradation by the proteasome. This process is crucial for regulating the cell cycle, ensuring proper timing of events.

A protein that can activate or inhibit the cell cycle, depending on its phosphorylation state.

A protein that can activate or inhibit the cell cycle, depending on its phosphorylation state.

A protein that can inhibit the activity of cyclin-dependent kinases (CDKs), acting as a brake on the cell cycle.

A gene that inhibits apoptosis. It is classified as an oncogene because it can promote cancer development by preventing the death of damaged cells.

Proteins that block apoptosis by inhibiting the activity of caspases, the enzymes responsible for executing cell death.

A viral protein that inhibits apoptosis by blocking the activity of caspases 1 and 8, preventing the activation of inflammatory pathways.

The process by which normal cells undergo a series of changes, including alterations in morphology and function, to become cancerous.

The normal cell cycle is regulated by proteins called cyclins and cyclin-dependent kinases (CDKs). Cancer cells can bypass these regulatory mechanisms and continue to divide without external signals.

Cancerous cells have the ability to divide indefinitely without limitations, effectively bypassing the normal mechanisms that limit the number of cell divisions.

Cancer cells can maintain relatively efficient processes of DNA replication and mitosis, even though their DNA may be abnormal. This allows them to reproduce and spread.

Apoptosis and necrosis are two distinct ways cells can die. Apoptosis is a programmed, controlled process that is beneficial to the organism, while necrosis is an uncontrolled, damaging process that can lead to inflammation.

Cancer cells are able to grow and divide without the need for external signals called mitogens. They achieve this by deregulating signaling pathways involved in cell cycle progression.

Cancer cells can divide indefinitely due to the activity of telomerase, an enzyme that prevents telomeres from shortening. This allows for continuous cell division.

Telomeres are protective caps at the ends of chromosomes that shorten with each cell division, acting as a 'mitotic clock' to limit cell replication. When they become critically short, the cell enters senescence.

Telomerase is an enzyme responsible for adding nucleotides to telomeres, counteracting their shortening and enabling continued cell division. Unlike normal cells, cancer cells often express high levels of telomerase.

Dysfunctional telomeres in the absence of telomerase can trigger chromosomal instability. The cell attempts to repair the shortened telomeres, resulting in genetic abnormalities.

The activity of telomerase is often increased in cancer cells, leading to uncontrolled cell division. This is a key characteristic of cancer.

The RB and p53 pathways are crucial checkpoints in the cell cycle that prevent cells with damaged DNA or short telomeres from dividing. This is a critical mechanism for preventing cancer.

Deregulation of the cell cycle is a hallmark of cancer. This can occur due to defects in checkpoints, leading to uncontrolled proliferation and genomic instability.

Barrett's esophagus is a condition where the normal lining of the esophagus, made of squamous cells, is replaced by abnormal columnar cells, similar to those found in the intestines. This replacement is called metaplasia.

Metaplasia is the reversible replacement of one mature cell type by another mature cell type. It's a cellular adaptation to stress or injury.

Dysplasia is a disordered growth and differentiation of cells, leading to abnormal tissue architecture. It's often a precursor to cancer.

The main risk factor for Barrett's esophagus is a history of acid reflux, which is the backflow of stomach acid into the esophagus. This chronic irritation can lead to metaplasia.

While Barrett's esophagus increases the risk of esophageal cancer, it doesn't mean everyone with it will develop cancer. Only a small percentage of individuals with Barrett's esophagus actually develop cancer.

Barrett's esophagus is more common in men than women and in older individuals. Abdominal obesity is also a risk factor.

Barrett's esophagus often doesn't cause any specific symptoms. If symptoms are present, they are usually related to the underlying acid reflux, such as heartburn.

The abnormal columnar cells in Barrett's esophagus can eventually grow abnormally, leading to dysplasia. This dysplasia can display abnormal cellular characteristics under a microscope.

A process where a cell changes from one type to another, usually becoming more specialized. This occurs during development, transforming a simple zygote into a complex organism with diverse tissues and cell types.

When a fully differentiated cell type changes into another fully differentiated cell type. Often happens in response to harmful environmental factors.

A disruption in the normal maturation or differentiation of cells, commonly seen on epithelial surfaces. It represents abnormal growth and development, leading to pre-cancerous cells and potentially cancer.

The reactivation of telomerase, an enzyme that adds DNA repeats to chromosome ends (telomeres), can stabilize scrambled chromosomes in cancer cells. This allows for potential translocations of proto-oncogenes, activating cancer-causing genes and promoting tumor growth.

Mutations in the TERT gene's promoter, which regulates telomerase expression, lead to loss of negative regulation. This results in telomerase reactivation, observed in conditions like cervical cancer, contributing to cancer progression.

Damaged or disrupted chromosomes can be repaired through various mechanisms, but these repair processes can also lead to chromosomal re-arrangement and genomic instability, often harming the cell.

DNA sequences at the ends of chromosomes (telomeres) shorten with each cell division, eventually limiting the number of cell divisions. Telomerase can lengthen these sequences, potentially contributing to cancer cell immortality.

Changes in the genome, particularly in cancerous cells, can alter gene expression and lead to the development of a cancerous phenotype. This can be a result of mutations, amplifications, or deletions in genes.