Chapter 8 Bio

Front 1

28. How are cancerous cells different from normal cells

Back 1

1.Immortal - will not stop dividing
2.Altered cell membranes means they can’t anchor & so they metastasize: spread into other tissues
3.Have lost the genetic ability to stop dividing
4.Cancer is heritable: Cancer cells give rise to cancer cells
5.Are dedifferentiated - less specialized than the cell it came from
6.No contact inhibition
7.If not treated will eventually cause death

Front 2

29. How do you get cancer? i.e. What genes need to mutate for normal cells to become cancerous cells?

Back 2

The most common way that people get cancer is by a mutations in tumor-supressor genes like p53 or by mutations in proto-oncogenes

Front 3

Proto-oncogenes

Back 3

These are genes that code for growth factors (growth factors are protein messengers that stimulate cell division). When mutated, these genes become oncogenes (cancer-causing genes).

Front 4

Oncogenes

Back 4

These arise from mutated proto-oncogenes. An oncogene causes cancer by unregulated production of growth factors. (In other words, they produce way too much gowth factor!)

Front 5

Tumor suppresser genes

Back 5

In their normal state these genes code for proteins that turn off mitosis (i.e. prevent cell division). When mutated these genes cause cancer (unregulated cell division)

Front 6

p53 gene

Back 6

A tumor suppressor gene that holds the cell cycle in the G1 phase. When mutated, this gene causes cancer (unregulated cell division).

Front 7

Why doesn’t one mutant Tumor Suppresser Gene (e.g. one mutant p53 gene) cause cancer?

Back 7

We need multiple mutations in several cell-cycle genes to cause cancer

Front 8

What kind of gene is the BRCA 1 gene?

Back 8

tumor-supressor gene

Front 9

Why do women that inherit a mutant BRCA 1 gene have a very high chance (80-90% chance) of getting breast cancer

Back 9

This is because these women have inherited a mutant (recessive) form of the gene from either Mom or dad. They only need to acquire a mutation in the other allele (on the other homologue) to get a mutant BRCA1 gene

Front 10

Why are the percentages much lower for the average woman?

Back 10

Because most women inherit the non-mutated (dominant) form of the gene. Thus they need the genes on BOTH homologues to mutate in order to get cancer.

Front 11

25. List three different factors that can cause genes (e.g. p53 gene, BRCA 1 gene, etc.) to mutate

Back 11

a.)viruses
b.)toxins
c.)radiation

Front 12

a.) How could you prevent the cells from entering mitosis?

Back 12

Block growth factor receptors on cell membrane with antibody (e.g. Herceptin)

Front 13

Once started, how can you stop the chromosomes from completing mitosis?

Back 13

Taxol: interferes with the movement of the chromosomes along spindle fibers

Front 14

How could you block the S phase?

Back 14

Methotrexate and other chemotherapeutic drugs block DNA synthesis

Front 15

What is cancer?

Back 15

Cancer is a genetically dictated loss of cell cycle control

Front 16

1. a. What is the function of meiosis?

Back 16

to produce gametes, cells with half the number of chromosomes as their parent cells. Gametes function in sexual reporduction

Front 17

What kinds of cells are produced by meiosis?

Back 17

sex cells (gametes)

Front 18

Are these cells haploid or diploid?

Back 18

haploid

Front 19

What would be the genetic consequences to a species (i.e. to the number of chromosomes) if mitosis, rather than meiosis, produced these cells?

Back 19

The gametes would each have a diploid number of chromosomes, and so when the gametes fuse the zygote would be tetraploid. All animal zygotes would die in this situation (but not plants – they can have multiple ploidies).

Front 20

a. How do the chromosomes align at metaphase I of meiosis?

Back 20

with their homologous pairs

Front 21

b. What separates during anaphase I of meiosis?

Back 21

homologous pairs

Front 22

c. How do the chromosomes align at metaphase II of meiosis?

Back 22

individually, randomly

Front 23

d. What separates during anaphase II of meiosis?

Back 23

sister chromatids

Front 24

e. How do the daughter cells compare genetically?

Back 24

all four are genetically different

Front 25

f. Are the daughter cells haploid or diploid?

Back 25

haploid

Front 26

(v.) The two cells at end of meiosis I. Are these cells haploid or diploid? ¬¬-

Back 26

haploid They each have 4 chromosomes (replicated) instead of 8.

Front 27

Explain why the age of the mother and not that of the father is correlated with the probability of having a child with Down syndrome.

Back 27

Because mom’s pre-egg cells are arrested in metaphase I until ovulation. In metaphase I, the chromosome are attached to the spindle fibers. Spindle fibers degenerate with age, leading to nondisjunction.

Front 28

Explain how nondisjunction of chromosomes during anaphase I of meiosis can lead to Down syndrome

Back 28

The homologous pair #21 is misaligned at Metaphase I. Thus the homologues don’t separate at Anaphase I, and one cell gets both homologues and the other cell gets none. Thus one of the gametes has two copies of chromosome 21. When this gamete is fertilized, the zygote now has three copies of chromosome 21.