Bio 93 Lecture 18: Cell Cycle Regulation and Cancer

Vocabulary practice flashcards covering cell cycle regulation checkpoints, cyclin-Cdk interactions, tumor suppressor genes, oncogenes, and cancer mechanisms from Bio 93 Lecture 18.

Checkpoints

Critical control points where stop and go signals regulate progression through the eukaryotic cell cycle.

$G_1$ Checkpoint

A primary cell cycle control point where a cell either receives a go-ahead signal to complete the cycle and divide or, lacking the signal, exits the cycle into $G_0$.

$G_0$ Phase

A non-dividing state that a cell enters when it fails to receive a go-ahead signal at the $G_1$ checkpoint.

Cyclin-Dependent Kinases (Cdks)

Protein kinases that give go-ahead signals at cell cycle checkpoints and must be bound to a cyclin protein to be enzymatically active.

Cyclin

A regulatory protein whose concentration fluctuates periodically during the cell cycle, accumulating to bind and activate cyclin-dependent kinases.

MPF (Maturation-Promoting Factor)

A protein complex consisting of a cyclin and a cyclin-dependent kinase ($\text{MPF} = \text{Cyclin} + \text{Cdk}$) that regulates the $G_2$ checkpoint and promotes entry into mitosis.

$G_2$ Checkpoint

A critical control point at the end of the $G_2$ phase where sufficient accumulation of active MPF triggers the transition into the mitotic phase.

M Checkpoint

A mitotic checkpoint that halts cell cycle progression at prometaphase if any chromosomes are unattached to the spindle, and issues a go-ahead signal when all chromosomes are attached at metaphase.

CDK4/6 - Cyclin D Complex

A signaling complex at the $G_1/S$ checkpoint that removes inhibition of gene expression so that genes necessary for DNA replication can be expressed.

Platelet-Derived Growth Factor (PDGF)

An external growth factor required by cultured fibroblasts to pass the $G_1$ checkpoint and proliferate.

Anchorage Dependence

The requirement observed in normal cells where cells must be attached to a solid substratum or surface in order to divide.

Density-Dependent Inhibition

A phenomenon in normal cells where crowded cells cease dividing once they form a single confluent layer or fill an open space.

93stop

An experimental inhibitor evaluated in human brain cancer cell cultures that stops cell cycle progression at the end of the $G_1$ phase.

Proto-oncogene

A normal cellular gene that codes for proteins stimulating normal cell growth and division, with the potential to cause cancer if altered or mutated.

Oncogene

A gene found in viruses or as an altered part of the normal genome that triggers cancerous characteristics and abnormal cell cycle stimulation.

Gene Amplification

A genetic change resulting in multiple copies of a proto-oncogene, producing an excess of normal growth-stimulating protein.

Translocation or Transposition

A chromosomal alteration where a proto-oncogene is moved to a new locus under the control of a different, highly active promoter, leading to excess protein production.

Epigenetic Changes (in Oncogenesis)

Mutations in genes encoding chromatin-modifying enzymes that cause chromatin loosening and inappropriate expression of an unaltered proto-oncogene.

Point Mutation within a Control Element

A nucleotide alteration within a promoter or enhancer region of a proto-oncogene that causes excess normal growth-stimulating protein production.

Point Mutation within a Gene

A nucleotide alteration within the coding sequence of a proto-oncogene that produces a hyperactive or degradation-resistant protein.

Ras Gene

A proto-oncogene encoding a G protein involved in growth factor signaling; mutations can generate a constitutively active Ras protein that stimulates division without growth factor.

Tumor-Suppressor Gene

A gene whose normal protein products inhibit cell division and prevent uncontrolled cell growth.

p53

A tumor-suppressor transcription factor known as the 'guardian of the genome' that is activated by DNA damage to halt the cell cycle and prevent replication of damaged DNA.

ATM

A protein kinase that responds to genomic DNA damage by initiating a phosphorylation cascade that activates p53.

Polyp

A small benign epithelial growth arising on the colon wall, associated with an initial mutation such as the loss of the tumor-suppressor gene APC.

Adenoma

A larger benign epithelial growth in colorectal cancer development that forms following subsequent genetic alterations, such as ras activation and loss of DCC.

Carcinoma

A malignant epithelial tumor that arises after multiple genetic hits, including the loss of the tumor-suppressor gene p53.

Metastasis

The spread of malignant cancer cells from a primary tumor site to other parts of the body via blood and lymph vessels.

Multistep Model of Colorectal Cancer

A paradigm demonstrating that the development of malignant colorectal cancer requires an accumulation of sequential mutations across both tumor-suppressor genes and oncogenes.

Peto’s Paradox

The observation that there is no correlation between an animal species' body size (or cell number) and its lifetime probability of developing cancer.