Lecture 31

Question 1

List the characteristics of cancer cells

Answer 1

Cells growing out of control

The become self sustaining (dont need signals to grow bc they secrete their own via autocrine secretion of growth factors)

ignore anti-growth signals and apoptosis signals

angiogenesis in order to feed the rapidly dividing cells that make up the tumor

gets help from stromal cells

do not show replicative-senescence (immortal)

Question 2

Compare benign tumors to malignant tumors

Answer 2

Benign tumors: a group of cells that exhibits abnormal growth, yet is NOT invasive

Malignant tumors: a group of cells that exhibits abnormal growth but IS invasive (usually bloodstream invasion)

Question 3

Describe Metastases

Answer 3

metastases exhibit the “invasiveness” characteristic of cancer by traveling to new areas of the body and forming secondary tumors

this is the major reason people die from cancer (not easy for the cells to do however)

Question 4

Describe tumor development and progression

Answer 4

All tumors come from a single ancestor cell that became abnormal due to a mutation

tumors begin as benign, and then slowly develop the ability to successfully metastasize

Question 5

List and describe the environmental causes of cancers

Answer 5

Tobacco: leads to lung, kidney, and bladder cancer

Diet high in fat and low in fiber: leads to bowel, pancreatic, prostate, and breast cancer

Chemicals/UV light/X-Rays: cause a variety of cancers

Question 6

List and describe an example of viral cause of cancer

Answer 6

AIDs, which causes Kaposi’s sarcoma

Question 7

Compare oncogenes and tumor suppressor genes

Answer 7

oncogenes: are “gain of function” genes formed by a single mutation event that occurs to a proto-oncogene
oncogenes cause exaggerated proliferation, and is a dominant allele

Tumor suppressor genes: are “loss of function” genes formed by 2 mutation events
Tumor suppressor genes only lead to cancer when both alleles are mutated (recessive) and tumors can no longer be suppressed

Question 8

describe the process by which oncogenes are activated by a virus

Answer 8

Retroviruses inject their RNA information into the host where it is reverse transcribed into the host DNA

viral oncogenes (v-src) are very similar to normal cellular genes (c-src) which code for proto-oncogenes

v-src hijack the c-src and activate proto-oncogenes into oncogenes by either over expression or mutation

oncogenes then drive cell over-proliferation

Question 9

What is the difference between oncogenes vs. tumor suppressor genes

Answer 9

oncogenes are “gain of function genes”

tumor suppressor genes are “loss of function genes”

both can lead to cancer via a different method

Question 10

Name and describe the 4 mechanisms in which proto-oncogenes are activated into oncogenes

Answer 10

Deletion/point mutation: creates a hyperactive protein

Regulatory mutation: a promoter mutation that causes an abnormally excessive expression/production of the normal protein

Gene amplification: several copies of genes are created instead of one. This causes an overproduction of normal protein

Chromosomal rearrangement: brings in a new regulatory sequence that causes over production OR creates overactive fusion protein

Question 11

Give an example of the deletion/point mutation mechanism for oncogene activation

Answer 11

Ras codon 12 Gly to Val

this keeps the Ras protein in the active state bc it can no longer be hydrolyzed from it’s GTP form to it’s GDP form (which would normally inactivate it)

Question 12

List the 3 stages (omit normal epithelium) of cervical cancer) and state the most effect weapon against cervical cancer

Answer 12

low-grade intraepithelial neoplasia

high-grade intraepithelial neoplasia

invasive carcinoma

early detection (via pap smear) is the best weapon

Question 13

List the 3 stages (omit normal epithelium) of cervical cancer) and state the most effect weapon against cervical cancer

Answer 13

low-grade intraepithelial neoplasia

high-grade intraepithelial neoplasia

invasive carcinoma

early detection (via pap smear) is the best weapon

Question 14

Compare neovascularization and angiogenesis. which of these is more associated with cancer?

Answer 14

neovascularization: the formation of new blood vessels from scratch
angiogenesis: sprouting new/more blood vessel branches from pre-existing blood vessels

angiogenesis is more associated with cancer

Question 15

Compare neovascularization and angiogenesis. which of these is more associated with cancer?

Answer 15

neovascularization: the formation of new blood vessels from scratch
angiogenesis: sprouting new/more blood vessel branches from pre-existing blood vessels

angiogenesis is more associated with cancer

Question 16

What is the Ames test, and how is it conducted?

Answer 16

it tests a cell sample for DNA-mutation (cause of cancer)

histidine dependent salmonella, the sample, and liver extract are all mixed into the same agar

after culturing this mix, the higher the colony count of salmonella, the more mutagens were present in the sample

(this is bc mutagens produce histidine, which salmonella feeds off of)

Question 17

What is the Philadelphia chromosome? what does it cause?

Answer 17

Philadelphia chromosomes are formed from a translocation even between Chr 9 and 22

this yields a small, mutate version of the 22nd chromosome that causes chronic myelogenous leukemia

Question 18

DNA maintenance genes are a subset of ____ ____ ____, and involve the inactivation of caretaker genes that promote genomic stability. list 2 examples of these type of genes

Answer 18

tumor suppressor genes

DNA repair genes

Checkpoint genes

Question 19

define “transformed cells”

Answer 19

small colonies of abnormally proliferating cells caused by an oncogene

(related to oncogenes formed by viral infections)

Question 20

What occurs in a “truncated EGF receptor” as opposed to a normal EGF receptor? what is this issue associated with?

Answer 20

Truncated EGF receptors lose their extracellular domain and become active without the binding of it’s ligand

this signals for a constant signal for the cell to divide and is associated with glioblastoma (brain tumor)

Question 21

What occurs in a “truncated EGF receptor” as opposed to a normal EGF receptor? what is this issue associated with?

Answer 21

Truncated EGF receptors lose their extracellular domain and become active without the binding of it’s ligand

this signals for a constant signal for the cell to divide and is associated with glioblastoma (brain tumor)

Question 22

In B cell lymphoma, Bcl2 genes on chromosome 18 undergo a ____ translocation with chromosome ____. This causes the _____ of Bcl2 in B cells and prevents ____ of damaged cells

Answer 22

reciprocal

14

over-expression

apoptosis

Question 23

In B cell lymphoma, Bcl2 genes on chromosome 18 undergo a ____ translocation with chromosome ____. This causes the _____ of Bcl2 in B cells and prevents ____ of damaged cells

Answer 23

reciprocal

14

over-expression

apoptosis

Question 24

Describe methods that oncogenes can manipulate/over stimulate cell growth pathways that require a ligand to signal for cell proliferation

Answer 24

the can produce ligands constitutively (ligand-autocrine signaling)

RTKs (receptor tyrosine kinases) can be constitutively produced in such a way that they no longer require a ligand to signal for cell proliferation