Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Bloc I - Reproduction > Sept13 M2-Hormonal Cancer Therapies > Flashcards

Sept13 M2-Hormonal Cancer Therapies Flashcards

1
Q

HCT used in what 4 cancers

A
  • testis
  • ovary
  • breast
  • prostate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

4 principles of use of HCT

A
  • effective singly
  • additive, synergistic
  • non cumulative toxicity
  • use at max tolerated dose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

testis cancer origin and initial signal

A
  • most probably dev in fetus

- initial signal is on germ cells

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

(imp) current tx for testis cancer

A

unilateral orchiectomy followed by chemo (BEP = 3 drugs given)

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

(important) 3 chemo drugs for testis cancer (note: all three are used at the same time**)

A
  • bleomycin
  • etoposide
  • cisplatin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

(imp) bleomycin MOA

A
  • Abx. glycoprotein
  • found to be antineoplastic
  • causes ssDNA and dsDNA breaks
  • inhibits DNA synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

topoisomerase function

A

enzyme that helps DNA not get overwound or underwound during replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

(imp) etoposide fct

A

topoisomerase II inhibitor

  • complexes with it
  • enhances dsDNA and ssDNA cleavage
  • inhibits religation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

(imp) cisplatin MOA

A
  • heavy metal complex
  • inoculating agent
  • alkylating agent that racts with DNA to form intra and interstrand crosslinks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

SEs of BEP in postsurgical chemo for testis cancer

A
  • SE on dividing tissues (GI, repro, immune)
  • sperm anomalies including aneuploidy
  • infertility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

2 most common types of ovarian cancers

A
  • epithelial

- germ cell tumor

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

first line drug combination for epithelial cell cancer in ovaries

A
  • CEP (is the same as BEP): cisplatin, etoposide, bleomycin + placlitaxel
  • alternatives if this doesn’t work
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

SEs of CEP (BEP) for ovarian cancer

A

like BEP for testis cancer. nausea, vomiting, hair and apetite loss, rashes, mouth sores, dividing organs

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

(imp?) taxane (paclitaxel, taxol) MOA (chemo for ovarian epith ca)

A

stabilizes microtubules

-can’t breakdown during cell division, stabilizes the spindle

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

ovarian germ cell tumor first line drug combination + SEs

A

BEP (CEP)

  • bleomycin
  • etiposide
  • cisplatin
  • SEs still the same
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

main thing to do before chemo tx of testicular cancer for fertility

A

bank sperm before the start of the chemo

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

two most common cancers in life

A

prostate and breast

18
Q

do androgens cause prostate cancer

A

no

19
Q

are androgens needed for prostate ca

A

yes. Rs for testo and estradiol in prostate
- for testo = in stroma
- for E = in epithelium

20
Q

mainstay of tx for prostate cancer

A

combination of:

  • GnRH agonist that causes an increase in LH and spike in testo but eventually if give enough, testo prod goes down
  • androgen R antagonist
21
Q

how androgen R antag works

A

binds a peripheral allosteric site on the receptors, changes its structure, prevents testo binding
problem - reversible

22
Q

other approaches to prostate tx

A
  • block enzymes making testo into active steroids (finasteride inhibits 5 alpha reductase and DHT prod)
  • block estrogen Rs (tamoxifen)
  • block estrogen prod (aromatase inhibitors)
23
Q

how tamoxifen works

A
  • blocks partially but not completely the ER activity
  • is a competitive partial agonist, antagonist at the estrogen R
  • activity depends on ERalpha to ERbeta ratio in the cells
  • supresses insulin-like GF (IGF-1)
  • upregulates transforming GF beta (TGF-b)
24
Q

management of ER+ breast cancer (chemo)

A
  • aromatase inhibitor (after menopause)

- tamoxifen (anti-estrogen R)

25
Q

management of ER- breast cancer (chemo)

A
  • toposiomerase II inhibitor (doxorubicin. is like etoposide)
  • taxane
  • alkylating agent (cyclophosphamide. is like cisplatin)
  • trastuzumab (Her-2+)
26
Q

management of ER+ HER+ breast ca (chemo)

A

combine tx

27
Q

other possibility for breast ca tx

A

PAPR inhibitors

28
Q

why removing ovaries doesn’t work in post menopausal women with breast ca

A

E still made from testo in other tissues

29
Q

how trastuzumab works

A
  • monoclonal Ab to the epidermal GF (EGF) receptor HER2, expressed sometimes on SURFACE of ca cells
  • prevents response to EGF so cells can’t divide
30
Q

how PARP inhibitors work

A
  • PARP is an enzyme that recognizes recognizes and repairs DNA damage
  • inhibit it so get more cell death
31
Q

(IMP) BPH vs prostate ca

A

BPH

  • does not evolve into ca
  • in the periurethral area
  • doesn’t kill you
32
Q

prostate ca management

A

tx if you can

33
Q

2 phases of prostate ca

A
  1. hormone dependent (can tx with GnRH agonist and testo R antagonist. + block testo synthesis, etc.
  2. hormone indep (ca comes back after several yrs, not responding to hormonal tx anymore
34
Q

examples of options of tx for recurrent prostate ca

A
  • enzalutamide (binds ARs)
  • abiraterone (steroid synthesis blocker)
  • sipuleucel-T (immunotherapy)
35
Q

how enzalutamide works

A
  • binds androgen Rs (still present in prostate) with very high affinity
  • blocks their translocation to the nucleus
  • if they get to nucleus, prevents their binding to DNA and to coactivator proteins
36
Q

abiraterone works how

A
  • blocks steroid synthesis in other tissues
  • blocks all sources of androgens
  • acts on cholesterol use in the cells making testo to block testo synthesis
37
Q

sipuleucel-T works how

A
  • active cellular immunotherapy

- stims patient T cells to recognize and attack prostate ca cells expressing prostatic acid phosphatase (PAP) antigen

38
Q

sipuleucel-T made how

A
  • isolate T cells
  • teach them to recognize PAP Ag
  • inject them back in individual
39
Q

new ideas for antica drugs

A

T cell reactivation with checkpoint inhibitors

  • in ca, T cells eventually become repressed and stop attacking cancer cells
  • currently trying PD-1 (on T cells) and PDL-1 (on APCs) inhibitors
  • remove break from ability of T cells to recognize foreign cells
40
Q

SEs of T cell reactivation by checkpoint inhibitors

A

more autoimmune disease bc more T cell activity

Bloc I - Reproduction (57 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions