Exam III review cancer genetics chapter 19 Flashcards Preview

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Flashcards in Exam III review cancer genetics chapter 19 Deck (28)
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1

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

Contact inhibition

2

Programmed cell death

Apoptosis

3

State of permanent growth arrest

Senescence

4

Autocrine stimulation, lose contact inhibition, apoptosis is avoided

Characteristics of cancer cells

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.

Translocation, (9;22 Philadelphia chromosome)

6

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

Autocrine stimulation

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.

Philadelphia chromosome

8

Produce substances that promote blood vessel growth

Angiogenesis

9

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

Metastasis

10

Natural killer cells recognize their own cancers

Immune surveillance

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.

Genetic (clonal) basis of cancer

12

Molecular signals that influence cell growth and division

Growth factors

13

Growth factors that stimulate cell proliferation

Mitogens

14

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

Growth factor receptors

15

Really the signal inside the cell

Signal transducers

16

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

Cyclins

17

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

Cyclin-dependent kinases

18

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

HSr double minutes/Jean amplification

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.

Oncogenes

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.

Tumor suppressor genes

21

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

Ras

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.

Loss of heterozygosity/retinalblastoma gene

23

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

Two hit hypothesis

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.

Genomic instability

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.

Checkpoints

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.

P 53

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.

Abl

28

Clonal basis of cancer

Growth advantage
normal cell constraints
DNA repair machinery