Exam 3 pt 4 Flashcards

1
Q

contact inhibition

A

normal cells stop moving when reach contact each other, cancer cells dont do this and keep growing
* cancer cells dont need survival factors/signals
* selective advantage because proliferate when normal cells would stop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

cancer cells alterred sugar metabolism

A
  • tumor cells have increased rate of glucose uptake
  • small amount of oxidative phosphorylation
  • cancer cells instead form lactate at high levels, promoting cell growth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

tumors grow within

A

a framework of supporting connective tissue stroma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

metastasis

A
  • EMT for carcinomas allows decreased adhesion and escape from parent tissue
  • enter blood through aid of angiogenesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

metastasis

A
  • EMT for carcinomas allows decreased adhesion and escape from parent tissue
  • enter blood through aid of angiogenesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

cancer critical gene

A

genes whose alteration frequenctly contributes to the causation of cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

oncogenes

A
  • gain of function mutations
  • dominant
  • non mutated forms are called proto oncogenes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

tumor supressor genes

A
  • loss of function mutations
  • often recessive
  • cant add to tester strain to find
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

_ can act as vectors for oncogenes

A

retroviruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Ras oncogene

A

First identified and one of the most important cancer critical genes, it codes for a monomeric GTPase involved in control of cell proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

chromosomal rearrangements

A

The breaking and rejoining of DNA segments which can lead to the expression of a hyperactive or overexpressed fusion protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

EGF receptor in cancer

A

deltion that deletes extracellular domain of EGF receptor, causing it to always stay active and promote growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

excessive quantities of myc protein

A

causes cells to proliferate when they usually would not

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Burkitt’s lymphoma

A

Type of lymphoma in which a translocation brings the Myc gene under the control of regulatory sequences which normally control the production of antibodies in B lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

individuals with heriditary form of retinoblastoma

A

have a deletion in one copy of the Rb gene in every somatic cell
* retinal cells become transformed when an event eliminates the good copy of a gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

loss of Rb gene

A

allows cells to enter the cell cycle when they otherwise would not

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Rb gene

A

A universal regulator of the cell cycle in almost all cells in the body, its loss allows cells to enter the cell cycle when they otherwise would not

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

_ of tumor supressor genes causes cancer

A

inactivation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

ways to see tumor supressor genes

A
  • sequencing of cancer cell genomes
  • analysis of methylation patterns
  • karyotype analysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

drivers of cancer

A

Group of mutations present in a tumor that play a role in the development of the cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

drivers of cancer

A

Group of mutations present in a tumor that play a role in the development of the cancer

21
Q

passenger mutations

A

Group of mutations present in a tumor that arise due to the genetic instability of the cancer, but are irrelevant to the development of the disease

22
Q

mutations found at _ are candidates for drivers

A

high frequencies

23
Q

uncontrolled proliferation of cancer cells requires the loss of restraints on

A

cell cycle progression and also regulate cell growth

24
Q

Warburg effect

A

The excessive rate of glycolysis that is observed in tumor cells
* result of PI3/AKt/mTOR pathway being activated abnormally

25
Q

loss of p53 promotes cancer in four ways

A
  • allows DNA damage to continue throughout cell cycle
  • allows damaged cells to escape apoptosis
  • allows continues division of damages cells
  • cells become relatively resistant to anticancer drugs
26
Q

_ copy/s of p53 has to be mutated

A

one copy only

27
Q

cancer stem cells

A

Small subset of tumor cells which maintain the tumor cell population and are less sensitive to many types of anti-cancer therapies; they undergo self-renew without limit and give rise to transit amplifying cancer cells

28
Q

carcinogens

A

Any agent (i.e. chemicals or radiation) that causes increased cancer rates

29
Q

Ames test

A

A quick and accurate test for mutagenicity using bacteria defective in histidine synthesis and DNA repair
* if colony grow, then mutation has corrected his synthe
* means it is a mutagen

30
Q

the most potent carcinogens are intially

A

initally chemically inert and only become damaging when altered by ctochrome p-450 oxidases in the liver

31
Q

Hep A and B causes

A

liver cancer

32
Q

HPV

A

Virus which causes warts, and is implicated in most cases of cervical cancer

33
Q

products of viral oncogenes bind

A

Rb and p53

34
Q

binding of Rb by _ allows _

A

E7 and E3 allows incontrolled entry into S phase

35
Q

binding of p53 by _ allows _

A

E6 allows continued proliferation of abnormal cells

36
Q

Brca 1 and 2 are

A

needed for homologous recombination, repair double stranded breaks

37
Q

PARP

A

repairs single stranded breaks

38
Q

Brac1 and 2 tumor supressor genes

A

Mutations in these tumor suppressor genes predispose humans to breast and ovarian cancers

39
Q

drugs that block PARP

A

kill cells that dnt have Brac but spare normal cells
* good treatment

40
Q

philadelphia translocation results in

A

formation of a hyperactive tyrosine kinase

41
Q

imatinib (gleeve)

A
  • binds and inhibits the activity of Bcr-Abl protein
  • cells with philadelphia chromosome are yeeted
  • relapse when cancer cells develop resistance to the drug
42
Q

The process by which an initial mildly disordered cell behavior gradually accumulates more mutations and evolves into a full-blown cancer.

A

tumor progression

43
Q

Human cancer cells display _____________________ which causes them to accumulate genetic changes at an abnormally rapid rate.

A

genetic instability

44
Q

Loss-of-function mutations in these genes can promote the formation of cancer

A

tumor suppressor genes

45
Q

A cancer arising from connective tissue or muscle cells.

A

sarcoma

46
Q

Tumors whose cells have acquired the ability to invade other tissues are referred to as ______________________

A

malignant

47
Q

Hepatitis-B and C cause

A

chronic inflammation of the liver (hepatitis) and are implicated in the development of liver cancer.

48
Q

T or F: Oncogenes directly promote cancer by causing unregulated cell proliferation, while tumor suppressor mutations only promote cancer indirectly by causing genetic instability.

A

False

49
Q

Most carcinogens are also .

A

mutagens

50
Q

The activity of cytochrome P-450 oxidases in the liver may

A

sometimes convert chemically inert substances into potent carcinogens.