Chapter 11 Biology Of Cancer

Front 1

Benign or Malignant?

-Well defined capsule?

Back 1

Benign

Front 2

Benign or Malignant?

- high mitotic index

Back 2

Malignant

Front 3

What are Adenocarcinoma?

Back 3

from ductal or glandular structures

Front 4

What are Sarcomas?

Back 4

malignant connective tissues tumors

Front 5

What is pleomorphic?

Back 5

variety of size and shape


(Difference between pleiomorphic and anaplasia?
Anaplasia = not well differentiated)

Front 6

Anaplasia?

Back 6

Not well differentiated

Front 7

What is a lymphoma?

Back 7

Cancer of the lympthatic tissue

Front 8

What does in situ mean?

Back 8

Hasnt broken through the basement membrane

(if it has, its invasive)

Front 9

What is the correct order of cell differentiation after a egg is fertilized?

Back 9

Totipotent, multipotent, pluripotent and unipotent

TMPI

Front 10

Benign tuors often resemble their cell of __________.

Back 10

Benign tuors often resemble their cell of ORIGIN.
(well differentiated)

Front 11

What is p53

Back 11

Tumor suppressor gene

Front 12

What are the 5 possible tumor markers that can be secreted by a cancer?

Back 12

- Hormones
- Enzymes
- Genes
- Antigens
- Antibodies

Front 13

What are tumor makers used for?

Back 13

To screen and identify individuals at high risk for cancer
Diagnose specific types of tumors
Observe clinical course of cancer

Front 14

What is selective advantage?

Back 14

The mutated cell acquires characteristics that give it an advantage over its neighbor

Front 15

How can a cancer grow based on the hormone Growth factor?

Back 15

secretion of growth factors
increase growth factor receptors

Front 16

What does a cancer do to the cell-surface receptor?

Back 16

Mutates it in the "on" position

Front 17

What does a cancer do to the Ras intracellular signaling protein?

Back 17

Mutates it
(A proto-oncogene that turns into an oncogene

Front 18

What does a cancer do to the Rb ?

Back 18

Inactivates it

(this a tumor suppressor

Front 19

What are the two tumor suppressor genes?

Back 19

RB and p53

Front 20

50% of all cancers are suspected to have a mutation of which tumor supressor gene?

Back 20

p53 gene

Front 21

What does protein kinase do?

Back 21

Drives the cell cycle, it gets activated when leading to cancer

Front 22

What gets activated or turned on to make something cancerous?

Back 22

Secretion of GF
Cell surface receptor is turned on
Protein Kinase is activated to drive the cell cycle

Front 23

What is clonal proliferation

Back 23

Mutant cell has selective advantage over its neighbors.

Front 24

What are telomeres?

Back 24

Protective ends on each chromosome and are maintained by an enzyme called telomerase

Front 25

What does cancer to with with an enzyme telemerase?

Back 25

It activates it, making the cell able to divide over and over again.

Front 26

A gene in its normal state it is nonmutant. What is this gene called?

Back 26

Proto-oncogene
(a normal nonmutant gene that codes for cellular growth)

Front 27

What would oppose an oncogene that is directing proliferation?

Back 27

Tumor-suppressor gene

Front 28

What is gene amplification?

Back 28

Duplication of a small piece of chromosome over and over

Front 29

What is loss of heterozygosity?

Back 29

Both chromosomes copies of a gene are inactivated (required to knock out a tumor supprssor gene

Front 30

What is gene silencing?

Back 30

Whole regions of chromosomes are shut off while the same regions in other cells remain active

Front 31

What is the main concern behind chromosome instability?

Back 31

Results in lose of heterozygosity and likely will have a tumor suppressor gene knocked out.

Front 32

What are caretaker genes?

Back 32

genes responsible for the maintenance of genomic integrity. They protect and repaire the genome after compromising cell cycle procedures.

Front 33

What do inflammatory cells do that will develope a high risk of cancer?

Back 33

Release cytokines

(inflammation also causes free radicals, mutation promotion and less caretaker work on damaged DNA)

Front 34

Where does a mutation have to occur for it to be passed to future generations?

Back 34

In the germline cells

(wont be passed if its in the somatic cells)

Front 35

How is kaposi sarcoma or epstein Barr related to cancer

Back 35

They are viruses that can induce cancer

Front 36

Which of the following tumor suppressors requires a lost of heterozygosity to be cancerous?

Back 36

p53!

Not Ras! because Ras is a proto-oncogene that can be turned on

Front 37

How is helicobacter pylori related to cancer

Back 37

A bacteria that can induce cancer through chronic infection of the stomach and lymphnoid tissues.

Front 38

How is tabboco a possible inducer of cancer

Back 38

it has plenty of carcinogens

Front 39

Chronic Inflammation induces the risk of _______

Back 39

Cancer!!

Front 40

What is the Bystander Effect?

Back 40

If mutations causes chromosomal instability (nondisjuction, deletion) You will see some effected individuals in the 2nd and 3rd generations.

Front 41

Whys is Ultraviolent radation a cause of cancer?

Back 41

It promotes skin inflmmation and the release of free radicals

Front 42

What effect does exercise have on insulin?

Back 42

Decreases insulin and insulin-like growth factors

Front 43

What effect does exercise have on inflammatory mediators?

Back 43

It decreases inflammatory mediators

Front 44

How does asbestos cause cancer?

Back 44

Causes chronic inflammation

Front 45

What are xenobiotics

Back 45

foreign life that are toxic, mutogenic and carginogenic in our food