Biology 318 Midterm Exam Study Guide

Loss of signals from supporting cells, potentially altering stem cell function.

Different cell fates arise from a single cell division due to distinct protein activity.

Cancer stem cells originate from either mutated normal stem cells or transformed progenitors gaining self-renewal.

Separating cells by virtue of surface proteins, helpful in identifying particular stem cells or cancer cells.

Purify tumor cells based on high CD44 expression and low CD24 levels for possible tumorigenicity in mice

Cancer stem cells differ from normal ones by having acquired partial transformed character or gained self-renewal ability.

A programmed cell death, crucial in the body's natural cleanup.

Unregulated cell death caused by damage or injury.

Apoptosis triggered by death receptors.

Cell surface proteins that initiate apoptosis.

Death receptor activated by Fas ligand.

Inhibits the extrinsic apoptosis pathway.

Transcription factor opposing apoptosis.

Mutant p53 proteins retain some structure but lose their function. They act as dominant negatives, mimicking activated oncogenes.

Complete loss-of-function mutations that result in no p53 protein production.

p53 regulates genes like p21, GADD45, and IGF-BP3, triggering cell cycle arrest or apoptosis in response to DNA damage.

p53 protein levels are tightly regulated, primarily through its rapid degradation. Stress activates p53 by inhibiting its degradation.

The movement of p53 into and out of the nucleus regulates its access to genes.

E1, E2, and E3 enzymes work together to add ubiquitin to target proteins, marking them for degradation.

p53's activity can be regulated by its stability, nuclear location, and post-translational modifications.

Low, because p53 is rapidly broken down in normal cells to prevent uncontrolled activity.

c-Myc is a gene that, when abnormally activated through translocation or amplification, is linked to various cancers, including Burkitt's lymphoma, neuroblastomas, and others.

Myc can either activate the expression of genes (like cyclins) or repress others (like p21). This activity plays a role in controlling the cell cycle.

Specific genes that are activated or deactivated by the protein Myc. Activation/deactivation is often cell type-dependent.

Loss of one copy of a gene or part of a chromosome.

Involves two mutations for a tumor suppressor gene to lose its function and contribute to cancer development. The first hit could happen early, in many cells, and lead to loss of the tumor suppressor gene function.

Inherited Rb is less severe and happens in a certain # of cells, while spontaneous Rb is more common and severe. This is explained by Knudson's two-hit hypothesis.

Ras activation is important in several cancers, and targeting Ras can be part of cancer treatment strategies.

FTIs are therapies that inhibit the activity of Ras, keeping it inactive from the membrane and subsequently having reduced effects on cancer growth.

High levels of p53 protein can trigger apoptosis. p53 can bind to regulatory sites in genes promoting cell cycle arrest and apoptosis. However, its affinity for arrest genes is higher, leading to cell cycle arrest first. Only with extremely high levels of p53, apoptosis is activated.

p53 relies on other proteins to specifically target genes for apoptosis. These partners can distinguish between arrest and apoptotic targets.

The apoptosome is a complex that activates caspases, triggering the execution phase of apoptosis. It forms when cytochrome c, released from mitochondria, binds to Apaf-1.

The Bcl-2 family of proteins controls the release of cytochrome c from mitochondria. Pro-survival proteins like Bcl-2 and Bcl-XL prevent release, while pro-apoptotic proteins like Bax and Bak promote release.

Bax and Bak proteins form oligomers (clusters) in the mitochondrial outer membrane. These oligomers create pores that allow cytochrome c to leak out.

Apoptosis triggered by mitochondrial dysfunction and release of cytochrome c, leading to caspase activation. It involves proteins like Bcl-2, Bax, Bak, and BH3-only proteins.

A group of proteins that regulate the mitochondrial pathway of apoptosis. Pro-survival Bcl proteins (like Bcl-2) prevent apoptosis, while pro-apoptotic proteins (like Bax and Bak) promote it.

A subfamily of Bcl-2 proteins that bind to pro-survival Bcl-2 proteins, triggering the release of cytochrome c and apoptosis.

Growth factors are essential for cell survival and metabolism. Loss of growth factor signaling can trigger apoptosis.

Cancer cells exhibit increased glycolysis and lactate production even in the presence of oxygen, despite having high metabolic activity.

New cancer therapies focus on manipulating apoptosis pathways. This includes inhibiting pro-survival Bcl proteins, activating BH3-only proteins, and engaging death receptors on tumor cells.

p53 is a tumor suppressor gene that can induce cell cycle arrest or apoptosis depending on the severity of the cellular damage.