Chapter 18: Beyond the Control of Individual Genes - Cancer and Cell Cycle Regulation

Vocabulary flashcards detailing cancer-critical genes, cell cycle checkpoints, oncogene activation mechanisms, and the multistep model of colorectal cancer development.

Apoptosis

Programmed cell death or "cell suicide" that is triggered when DNA damage cannot be repaired, characterized morphologically by membrane blebbing.

Proto-oncogenes

Normal genes located on various chromosomes that code for proteins that stimulate normal cell growth and division, acting as a "GO" signal or "accelerator" for the cell cycle.

Oncogenes

Cancer-causing genes that arise from mutated proto-oncogenes, becoming inappropriately active and overstimulating cell division ("mitosis gone crazy").

Tumor-suppressor genes

Genes that code for proteins that act like "brakes" to inhibit cell division by pausing the cell cycle, repairing damaged DNA, or initiating apoptosis.

$G_1$ Checkpoint

A regulatory checkpoint in interphase that assesses whether conditions are acceptable to begin DNA replication.

$G_2$ Checkpoint

A regulatory checkpoint following DNA synthesis that inspects for DNA replication errors and general DNA damage.

$M$ Checkpoint

A mitotic checkpoint that verifies whether chromosomes are properly aligned and ready to separate.

Gene Amplification

A genetic alteration where multiple copies of a proto-oncogene are produced, resulting in an excess of normal growth-stimulating protein.

Translocation or Transposition

A chromosomal alteration where a proto-oncogene is relocated adjacent to a new, highly active promoter, leading to normal growth-stimulating protein being produced in excess.

Point Mutation (in Proto-oncogenes)

A single-base change either within a control element (leading to excess normal protein) or within the protein-coding sequence itself (yielding a hyperactive or degradation-resistant protein).

$ras$ Gene

A cell cycle regulatory gene that acts as a proto-oncogene; mutations leading to an active oncogene are implicated in approximately $30\%$ of human cancers.

$p53$ Gene

A crucial tumor-suppressor gene coding for a protein that stops division and facilitates apoptosis following DNA damage; mutated or lost in approximately $50\%$ of human cancers.

$BRCA$ Gene

A tumor-suppressor gene whose functional protein repairs damaged DNA; mutations prevent repair and allow damaged cells to divide uncontrollably and accumulate additional mutations.

Polyp

A small benign epithelial growth on the colon wall, commonly initiated by the loss of the tumor-suppressor gene $APC$.

Adenoma

A larger benign colon growth that forms when cells of a polyp accumulate further genetic changes, such as the activation of the $ras$ oncogene and the loss of the $DCC$ tumor-suppressor gene.

Carcinoma (Colorectal)

A malignant tumor of the colon that develops after successive mutations, including the loss of the $p53$ tumor-suppressor gene alongside other accumulated genetic changes.

Multistep Model of Cancer Formation

The paradigm describing cancer development as a gradual process typically requiring about $\frac{1}{2}$ dozen ($6$) DNA alterations, including the activation of at least one oncogene and the loss of tumor-suppressor genes.