Cancer

Question 1

Why are malignant tumours hard to eradicate?

Answer 1

Malignant tumors typically give rise to metastases

Question 2

Benign tumors

Answer 2

enclosed by a connective tissue capsule

Question 3

malignant tumors

Answer 3

invasive cancerous gland tubules

Question 4

the five most common cancers

Answer 4

Lung, stomach, breast, colon/ rectum, and uterine cervix

Question 5

The growth of a typical human tumor

such as a tumor of the breast

Answer 5

May take years for the tumor to become noticeable

The doubling time of a typical breast tumor, for example, is about 100 days

Question 6

What cancer arises from the translocation between chromosomes 9 and 22

Answer 6

chronic myelogenous leukemia

Question 7

Philadephia chromosome

Answer 7

The translocation between chromosomes 9 and 22 produces small chromosome

Question 8

Cancer incidence as a function of age

Answer 8

The incidence of cancer rises steeply as a function of age.

Due to it requiring multiple mutations

Question 9

Cancer following exposure to a carcinogen

Answer 9

Delayed

Question 10

In the normal stratified squamous epithelium, where are dividing cells

Answer 10

dividing cells are confined to the basal layer

Question 11

In low-grade intraepithelial neoplasia, where are dividing cells

Answer 11

dividing cells can be found throughout the lower third of the epithelium

Question 12

In high-grade intraepithelial neoplasia, where are dividing cells

Answer 12

cells in all the epithelial layers are proliferating and show no sign of differentiation

Question 13

When does true malignancy begin?

Answer 13

cells move through or destroy the basal lamina and invade the underlying connective tissue.

Question 14

How does a tumour develop

Answer 14

through repeated rounds of mutation and proliferation, giving rise eventually to a clone of fully malignant cancer cells

Question 15

How does each mutation affect cell proliferation

Answer 15

enhances

Question 16

Genetic instability compared to tumours

Answer 16

Normal cells have little instability

cells with too much instability genetic result in failure to survive

cells with optimum genetic instability cause cancerous cells

Question 17

Two types of derangement that can give rise to the unbridled proliferation characteristic of cancer

Answer 17

Stem cell fails to produce one non stem cell daughter in each divsion and thereby proliferates to form a tumour

daughter cells fail to differeciate normallly and instead proliferate to form a tumour

Question 18

Steps in the process of metastasis

Answer 18

Cell growth as benign tumour in epithelium

break through basal lamina

invade capillary

escape to blood vessel and proliferate

Tumor cells may enter the bloodstream directly by crossing the wall of a blood vessel, as diagrammed here, or, more commonly perhaps, by crossing the wall of a lymphatic vessel that ultimately discharges its contents (lymph) into the bloodstream

Question 19

The Ames test

Answer 19

for mutagenicity

see if carinogen is mutagenic and results in colonies formed in independent culture

Question 20

Metabolic activation of a carcinogen

Answer 20

many chemical carcinogens have to be activated by a metabolic transformation before they will cause mutations by reacting with DNA

Question 21

Which cancer has increased/ decreases over the years from 1930-2000

Answer 21

lung increased due to smoking. Females more recently due to advertising

stomach has decreased

breast and prostate same

Question 22

Effects of childbearing on the risk of breast cancer.

Answer 22

Having children earlier decreased the likelyhood of having breast cancer

Question 23

Oncogenes genes mutation act

Answer 23

dominantly

a gain-of- function mutation in a single copy of the cancer-critical gene can drive a cell toward cancer

Question 24

tumour supressor genes mutation act

Answer 24

recessive

the function of both alleles of the cancer-critical gene must be lost to drive a cell toward cancer

Question 25

What do mutations of tumour supressor genes and oncogenes result in?

Answer 25

cells that proliferate abnormally

Question 26

Hereditary retinoblastoma

Answer 26

Inherit mutant Rb gene

In the hereditary form, all cells in the body lack one of the normal two functional copies of the Rb tumor suppressor gene, and tumors occur where the remaining copy is lost or inactivated by a somatic mutation

Question 27

nonhereditary retinoblastoma

Answer 27

all cells initially contain two functional copies of the gene, and the tumor arises because both copies are lost or inactivated through the coincidence of two somatic mutations in one line of cells

Question 28

Ways proto-oncogenes can be made overactive

Answer 28

deletion or point mutation

gene amplifaction

chromosome rearrangement

Question 29

overactive proto-oncogenes convert to

Answer 29

oncogenes

Question 30

A cell that is defective in only one of its two copies of a tumor suppressor gene, the Rb gene —usually behaves as a normal, healthy cell;

how may it come to lose the function of the other gene copy as well

Answer 30

non disjunction, duplicaiton, recombination, conversion, deletion, point mutation

Question 31

Having two fused oncogenes can result in?

Answer 31

decreased tumor free cells

Question 32

Rb protein affect on cell cycle

what phase?

Answer 32

inhibits E2F preventing entry to S phase

Question 33

What does phosphorylated Rb result in

Answer 33

inactive Rb and active E2F

leads to expression of S phase genes

Question 34

Damaged DNA pathway

Answer 34

Chk2 activated –> rapid G1/S block

P53 stabilized and causes apoptosis, g1/g2 arrest, and DNA repaire

Question 35

Papillomaviruses give rise to

Answer 35

cancer of uterine cerix by E6 and E7 which inhibit Rb and p53

causes cell prolliferation

Question 36

How shortened telomeres may lead to

Answer 36

chromosomal instability and cancer.

Question 37

The barriers to metastasis

Answer 37

difficult for the cells to enter in blood steam

Question 38

Each tumor will generally contain a different set of

Answer 38

genetic lesions

Question 39

Effects of ionizing radiation on normal cells and tumour cells

Answer 39

Cancer cells tend to be more susceptible than normal cells to the damaging effects of ionizing radiation because they lack an ability to arrest the cell cycle and make the necessary repairs

Question 40

The conversion of the Abl proto- oncogene into an oncogene

Answer 40

The chromosome translocation responsible joins the Bcr gene on chromosome 22 to the Abl gene from chromosome 9 in chronic myelogenous leukemia

Question 41

Gleevec

Answer 41

blocks the activity of Bcr-Abl protein and halts chronic myeloid leukemia.

Gleevec sits in the ATP-binding pocket of the tyrosine kinase domain of Bcr-Abl and thereby prevents Bcr-Abl from transferring a phosphate group from ATP onto a tyrosine residue in a substrate protein. This blocks onward transmission of a signal for cell proliferation and survival.

Question 42

angiogenesis

Answer 42

A new blood capillary forms by the sprouting of an endothelial cell from the wall of an existing small vessel.

Question 43

What stimulates angiogenesis

Answer 43

Lack of oxygen

Question 44

Von Hippel-Lindau disease

Answer 44

VHL hereditary cancer syndrome

• Germ-line mutation of tumor suppressor gene (VHL)

Question 45

VHL

Answer 45

tumor suppressor gene

Question 46

Somatic VHL mutations common in

Answer 46

in sporadic CNS hemangioblastoma & kidney cancer
– Kidney cancer
• 3% of all malignancies
• Incidence: 4500 new cases/year (Canada) • Mortality: 1500 death/year (Canada)

Question 47

Reintroduction of wild-type VHL in VHL-/- RCC cells

Answer 47

restores their dependency on specific growth factors to proliferate

Question 48

VHL mutants found in patients fail to

Answer 48

ubiquitinate p220 and p100