cancer

Question 1

Cancer

Answer 1

abnormal cells divide in accelerated/uncontrolled manner AND have potential to invade other tissues

Question 2

Benign

Answer 2

non-cancerous

lack ability to spread into neighboring tissues

Question 3

Malignant

Answer 3

cells divide uncontrollably and at abnormally fast and INVADE neighbors
aka cancerous tumors

Question 4

Metastasis

Answer 4

spread of CA from one tissues to another

Question 5

6 hallmarks of CA

Answer 5

Evading growth suppressors 
activating invasion and metastases
Enabling replicative immortality
inducing angiogenesis
resisting cell death 
sustaining proliferative signaling

Question 6

Evading apoptosis

Answer 6

Normal cells are signaled to die with damage
CA cell can evade this: allows damaged cells to continue replicating
genetic factors may be involved
p53 tumor suppressor gene

Question 7

Self0sufficiency in growth signals

Answer 7

normal cells require external growth factors in order to grow and proliferate
CA cell do NOT, they produce them on their own
can bypass check points

Question 8

Insensitivity to Anti-growth Signal

Answer 8

Normal cel proliferation is regulated and kept under control by antigrowth signal, no more basement membrane–stop growth.
CA are insensitive to antigrowth signals, will grow on top of each other
this is evident even in vitro

Question 9

tissue invasion and metastasis

Answer 9

cancer cells must be able to metastasize or invade new tissues
tumors send “pioneer cell” to invade adjacent tissue
pioneer cells must first interact normally with existing normal local cells
pioneer cells then recruit cells from local tissue to make mew tumors

Question 10

limitless replicative potential

Answer 10

normal cells can only divide a certain number of times before they die: telomere length determines the number of times a cell can divide, it shortens after each division until no more left and stops dividing
Telomearase maintain telomeres length: is UPREGULATED in CA
CA cells can divide infinitely, but the often pick up DNA errors due to increased in frequency of cell division
p53 tumor suppressor gene plays a role in limiting replication: TURNED OFF in CA

Question 11

Sustained Angiogenesis

Answer 11

the formation of new blood vessels
tumors need a blood supply to be able to grow in size and spread
angiogenesis also provides the tumors the o2 and nutrients it needs to grow

Question 12

tumor suppressor

Answer 12

a gene that protects a cell from becoming CA

generally loss-of-function nutation in these genes cause cells to become susceptible to becoming CA

Question 13

Oncogene

Answer 13

a gene that puts a cell on the path to becoming CA
begin as proto-oncogenes which have regular physiological function in the cell (mostly relating to proliferation and differentiation)
begin to over express, thereby becoming oncogenes
proto-oncogenes mutate and becomes oncogenes

Question 14

tumor suppressor p53

Answer 14

classic role: prevents cells with DNA damage from dividing and proliferating
know as “guardian of the genome”
about 50% of CA have p53 mutations
in CA p53 is permanently OFF

Question 15

two-hit hypothesis

Answer 15

for why tumor suppressor genes become insufficient to prevent CA
basically states that both alleles for a tumor suppressor gene must be mutated in order for the gene to lose function
not universally true but stands for the majority of tumor suppressor genes
*need 2 mutations

Question 16

interfering with DNA synthesis

Answer 16

folate must be taken up by the cell and reduced at FH2 then FH4 by dihydrofolate reductase in order to produce nucleosides

Question 17

Methotrexate

Answer 17

has a higher affinity for dihydrofolate reductase than does FH2, thereby preventing its reduction to FH4
bind to dihydrofolate so FH2 can’t make nucleosides

Question 18

Doxorubicin

Answer 18

Cytotoxic antibiotic
topoisomerase II opens ups DNA and this drug:
prevents the DNA strand from being put back together, thereby inhibiting DNA replication: therefore the cell can’t divide

Question 19

Topoisomerase II

Answer 19

relaxed the DNA supercoil and breaks the strand for replication

Question 20

Cyclophosphamide

Answer 20

Alkylating agents prevent 
replication of DNA
attach alkyl groups to guanines
causes guanines on the helix to crosslink, thereby making DNA "stuck" in its supercoil (covalent bond, so can straighten out and copy machinery can do its job and replicate)
if DNA cannot uncoil, it can't replicate

Question 21

Vincristine

Answer 21

interfering with mitosis
binds to microtubules dimers, preventing polymerization of dimers
arrest the cell in metaphase
can’t get into 2 cells

Question 22

New targeted therapies

Answer 22

hormone therapy
monoclonal antibodies
tyrosine kinase inhibitors

Question 23

tamoxifen

Answer 23

hormone therapy
for Tx estrogen receptor positive breast CA
antagonist at the estrogen receptor
in ER positive breast CA estrogen is necessary for cell proliferation
bind to receptor so estrogen can’t so then never get signal to divide

Question 24

monoclonal antibodies

Answer 24

block growth signals

stop new blood vessels from forming

Question 25

cetuximab

Answer 25

block growth signals
binds to mutated growth factor receptor and prevents its downstream signaling
but not all hyper-proliferation is caused by mutated EGFR (external), may be caused by nutated downstream effectors of EGFR–in this case cetuximab would NOT work, only effects GF receptor

Question 26

Bevacizumab

Answer 26

trade name: avastin
anti-angiogenic
monoclonal antibody that blocks angiogenesis
inhibits vascular endothelial growth factor-A
without vascularization, tumors cannot survive
binds to receptor prevents GF from binding and tumor won’t survive

Question 27

tyrosine kinase

Answer 27

tyrosine kinase an enzymes that removes a phosphate group from ATP and attaches it to a protein onto a tyrosine amino acid
the addition of a kinase to a protein generally starts a signaling cascade that can lead to cell proliferation

Question 28

tyrosine kinase inhibitors:

Answer 28

somehow prevent the phosphorylation of the tyrosine kinase target

Question 29

Philadelphia chromosome

Answer 29

also known as Philadelphia translocation
occurs when chromosome 22 has a specific translocation with chromosome 9 which results in a fusion gene known as BCR-Abl
associated with Chronic myelogenous leukemia

Question 30

BCR-Abl

Answer 30

contains a portion that codes for a tyrosine kinase
in the nutated form of the protein the tyrosine kinase is constitutively (or always) on
tx options include: Gleevec (imantinib) which is a tyrosine kinase inhibitor