Exam III review cancer genetics chapter 19

Question 1

Phenotypic change causing uncontrolled growth of cancer cells. Cells divide even when surrounded by other cells. Transformed foci.

Answer 1

Contact inhibition

Question 2

Programmed cell death

Answer 2

Apoptosis

Question 3

State of permanent growth arrest

Answer 3

Senescence

Question 4

Autocrine stimulation, lose contact inhibition, apoptosis is avoided

Answer 4

Characteristics of cancer cells

Question 5

The chromosome abnormality that causes chronic myeloid leukemia (CML). Abbreviated as the Ph chromosome. The Ph chromosome is an abnormally short chromosome 22 that is one of the two chromosomes involved in a translocation (an exchange of material) with chromosome 9.

Answer 5

Translocation, (9;22 Philadelphia chromosome)

Question 6

Cancerous cells evade normal controls by making their own division simulating signals

Answer 6

Autocrine stimulation

Question 7

The chromosome abnormality that causes chronic myeloid leukemia (CML). Is an abnormally short chromosome 22 that is one of the two chromosomes involved in a translocation (an exchange of material) with chromosome 9.

Answer 7

Philadelphia chromosome

Question 8

Produce substances that promote blood vessel growth

Answer 8

Angiogenesis

Question 9

Cells that acquire the ability to break through membranes and travel to distant locations in the body

Answer 9

Metastasis

Question 10

Natural killer cells recognize their own cancers

Answer 10

Immune surveillance

Question 11

Successive mutations confer the properties of cancer to a clone of cells.
4 to 10 mutations in right type of jeans. First mutation may have a growth advantage. It may de couple from normal cell constraints. It may disrupt the DNA repair machinery to increase the rate of mutation in the cells Genome.

Answer 11

Genetic (clonal) basis of cancer

Question 12

Molecular signals that influence cell growth and division

Answer 12

Growth factors

Question 13

Growth factors that stimulate cell proliferation

Answer 13

Mitogens

Question 14

Proteins with signal binding site outside the cell, transmembrane segment, and and intracellular domain

Answer 14

Growth factor receptors

Question 15

Really the signal inside the cell

Answer 15

Signal transducers

Question 16

Proteins who’s levels fluctuate during the cell cycle. They specify which set of proteins are phosphorylated..

Answer 16

Cyclins

Question 17

A family of protein kinases that can phosphorylate other proteins when bound to a cyclin. Phosphorylation can inactivate or activate a protein.

Answer 17

Cyclin-dependent kinases

Question 18

Homogeneously staining regions, pieces of DNA lacking telomeres or centromeres. And increase from the normal two copies of a gene.

Answer 18

HSr double minutes/Jean amplification

Question 19

Mutated versions of Proto-oncogenes, act in a dominant manner. Proto oncogenes often and code proteins needed for cell cycle progression. Gain of function mutations result in increased cell proliferation. Green light.

Answer 19

Oncogenes

Question 20

Normal alleles of these often encode proteins that slow down the cell cycle or guard against genome instability. Loss of function mutations in both Jean copies result in increased cell proliferation or increased DNA damage. Red light.

Answer 20

Tumor suppressor genes

Question 21

Signal transducer. Usually active when bound to growth factor. Oncogenic point mutations cause this protein to be constituetively active without growth factor.

Answer 21

Ras

Question 22

Second copy of tumor suppressor genes becomes non-functional. Rb+/rb-. Two hit hypothesis – cancer requires loss of both alleles of a tumor suppressor gene. Retinoblastoma/chromosome 13.

Answer 22

Loss of heterozygosity/retinalblastoma gene

Question 23

Cancer requires loss of both alleles of a tumor suppressor gene.

Answer 23

Two hit hypothesis

Question 24

Enzymatic systems that repair DNA damage caused by external agents are often defective. Mismatch repair systems that correct mistakes in nucleotide incorporation during DNA replication fail. Many cancer cells have major chromosomal aberrations.

Answer 24

Genomic instability

Question 25

Elaborate mechanisms have evolved to give cells time to repair DNA damage or correct potential segregation errors. These check for the integrity of the genome before allowing the cell to continue to the next phase of the cell cycle.

Answer 25

Checkpoints

Question 26

A transcription factor that participates in the G1 to S checkpoint. Activated by DNA damage, it induces expression of CDK inhibitor P 21. Induces expression of DNA repair jeans. Induces expression of apoptosis jeans.

Answer 26

P 53

Question 27

proto-oncogene encodes a cytoplasmic and nuclear protein tyrosine kinase that has been implicated in processes of cell differentiation, cell division, cell adhesion, and stress response.

Answer 27

Abl

Question 28

Clonal basis of cancer

Answer 28

Growth advantage
normal cell constraints
DNA repair machinery