Chemo drugs + treatment plans Flashcards

1
Q

Identify three commonly used alkylating agents and discuss their mechanism of action.

A

—alkylating agents
chlorambucil,
melphalan, and
cyclophosphamide.

covalently bind to DNA, causing cross-linking
preventing the DNA from unzipping
for replication, leading to cell death.

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

Explain how platinum compounds such as cisplatin function in cancer treatment.

Include the type of DNA binding and the phase of the cell cycle they target.

A

cisplatin,
carboplatin, and
oxaliplatin,

covalent bonds with DNA, leading to intra- and inter-strand cross-links.
disrupts DNA structure and replication
targeting the S phase

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

Describe how antimetabolites interfere with DNA and RNA synthesis.

Provide examples of folic acid, purine, and pyrimidine antagonists.

A

Antimetabolites interfere with DNA and RNA synthesis. specific to S phase

Folic acid antagonists (e.g., methotrexate) inhibit nucleotide synthesis by blocking folic acid.

Purine antagonists (e.g., mercaptopurine) interfere with purine bases needed for DNA.

Pyrimidine antagonists (e.g., 5-fluorouracil) disrupt pyrimidine synthesis.

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

What are the key toxicities associated with cisplatin, and how do they compare with those of carboplatin and oxaliplatin?

A

Cisplatin is known for its effectiveness in treating testicular cancer but causes severe nausea, vomiting, and kidney toxicity.
Carboplatin has a similar activity spectrum with reduced kidney toxicity, while oxaliplatin has mild kidney toxicity but can cause nerve damage (neuropathy).

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

Name the function, three vinca alkaloids and their target cancer types.

A

targeting microtubules to disrupt mitosis.

vincristine, vinblastine, and vinorelbine, which treat cancers like leukemia, lymphoma, and lung cancer.

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

What are taxanes, and how do they impact microtubule function during cell division? List some cancers commonly treated with taxanes.

A

Taxanes prevent microtubule disassembly
blocking mitosis
to treat breast, lung, and prostate cancers

Examples include paclitaxel and docetaxel.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Treatment that targets angiogenesis
+ name 2 VEGF inhibitors

A
  • SOFAFENIB + BEVACIZUMAB - VEGF inhibitors
  • angiopoetin inhibitors + combination approach
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

treatment that targets the cell cycle

A

CDK inhibitors
- CDK4/6 - ribociclib / palbociclib
- block transition to S phase
- used in HER2-neg breast cancer

Checkpoint kinase inhibitors
- CHK1 - prexasertib

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

Sofafenib

A

VEGF inhibitor

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

Bevacizumab

A

VEGF inhibitor

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

Ribociclib

A

CDK4/6 inhibitor

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

Palbociclib

A

CDK4/6 inhibitor

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

Prexasertib

A

CHK1 inhibitor

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

what are chlorambucil,
melphalan, and
cyclophosphamide.

A

alkylating agents

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

what are cisplatin,
carboplatin, and
oxaliplatin,

A

platinum compounds

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

treating breast cancer

A

Treatment: HER2-targeted therapies (e.g., trastuzumab, pertuzumab, and lapatinib).

Mechanism: HER2, a receptor tyrosine kinase, drives uncontrolled proliferation. These therapies block HER2 signaling, inhibiting growth in HER2-positive breast cancers.

Treatment: CDK4/6 inhibitors (e.g., palbociclib, ribociclib, and abemaciclib).

Mechanism: These drugs halt the cell cycle by inhibiting cyclin-dependent kinases required for the G1-S phase transition.

Treatment: PI3K/AKT/mTOR inhibitors (e.g., alpelisib, everolimus).
Mechanism: Dysregulation of the PI3K pathway can bypass tumor suppressors like PTEN. Inhibiting this pathway reduces cell survival and proliferation.

17
Q

what are the mechanisms and treatments of them that can be universally applied to all cancer?

A

cell cycle dysregulation - cyclins and CDKs
treatment:

PI3K/AKT/mTOR Pathway
treatment:

RAS/RAF/MEK/ERK (MAPK) Pathway
treatment:

VEGF/VEGFR Pathway (Angiogenesis)
treatment:

p53
treatment: