Chemotherapy Flashcards
A term to descripe the potential of cancer cells to spread to other parts of the body or one cell continues to divide without stopping
Metastasis
How does a normal cell and a cancer cell respond to faulty/unifxable DNA?
A normal cell will undergo apoptosis (programmed cell death) to stop the spread of abnormal DNA
A cancer cell will continue to divide
List all phases of the cell cycle
G1 phase
S phase
G2 phase
M phase
G0 phase
A phase in the cell cycle that is the checkpoint to ensure that the cell is ready for DNA synthesis
Options:
G1 phase
S phase
G2 phase
M phase
G0 phase
Q1 phase
The phase in which DNA synthesis occurs
S phase
Point in the cell cycle where it is a checkpoint to ensure that the cell is ready for mitosis
G2 phase
Phase in which cells divide into two daughter cells (mitotic phase)
M phase
The resting phase of the cell or the quiescent phase
G0 phas
Why are tumor supressor genes and protooncogenes are important in regulating the cell cycle?
Tumor suppressor genes and proto-oncogenes are essential regulators of the cell cycle because they maintain the balance between cell proliferation and cell death. They ensure that cells divide only when necessary and prevent uncontrolled growth that could lead to cancer.
Which of the following best describes the role of tumor suppressor genes in cancer prevention?
A) They promote uncontrolled cell growth and proliferation.
B) They encode proteins that repair DNA and initiate apoptosis.
C) They function as oncogenes when mutated, driving cancer progression.
D) They are only active during the S phase of the cell cycle.
They encode proteins that repair DNA and initiate apoptosis repress the cell cyle
What are the 3 ways that tumor supressor genes promote apoptosis?
- They inhibit cell division
- Initiate apoptosis after damaged DNA
- They use DNA repair proteins (BRCA)
What is the role of p53
It s tumor supressor protein that regulates the cell cycle
Why are cancer cells more susceptible to anti-cancer drugs that target the S and M phases of the cell cycle?
A) Cancer cells spend more time in the G0 phase, making them sensitive to these drugs.
B) Cancer cells have a higher percentage of actively dividing cells, increasing vulnerability in these phases.
C) Most cancer cells are permanently in the G1 phase, making DNA synthesis inhibitors ineffective.
D) Anti-cancer drugs can only act on cells undergoing apoptosis, which is most common in S and M phases.
Cancer cells have a higher percentage of actively dividing cells, increasing vulnerability in these phases.
S-phase is for DNA synthesis
M phase is the cell division phase
How does an oncogene differentiate from a proto-oncogene?
Oncogenes are mutated forms of proto-oncogenes that drive uncontrolled cell growth and cancer development.
Proto-onco genes are the genes that normally control how often a cell divides and how much it differentiates
When a mutated proto-oncogene turn into an oncogene what happens?
The oncogene becomes permanently activated when its not suppose to be, causing rapid cell division, increasing the risks of cancer
What are the major classes of oncogenes?
- Growth factors and their receptors
- Signal transducers
- Transcription factors/nuclear tranducers
- Programmed cell death regulators
which is false about the multiple hit hypothesis?
A) It suggests that multiple genetic mutations are required for cancer to develop.
B) Hereditary cancers require fewer “hits” compared to non-hereditary cancers.
C) A single mutation in a proto-oncogene is sufficient to cause cancer.
D) Tumor suppressor genes must be inactivated in both alleles for cancer to arise.
false: A single mutation in a proto-oncogene is sufficient to cause cancer.
what does the multiple hit hypothesis state?
states that multiple genetic mutations are required for a normal cell to become a cancer cell
Is the Multiple-Hit Hypothesis Related to Oncogenes?
Yes, but oncogenes follow a different pattern:
Oncogenes require just one mutation (“one hit”) to become cancer-promoting.
Tumor suppressor genes require two mutations (“two hits”) to lose function and contribute to cancer
Why do anti-cancer drugs have a narrow therapeutic index?
A) They selectively target only cancer cells, leaving normal cells unharmed.
B) They only act on non-dividing cells, leading to accumulation in healthy tissues.
C) They often damage normal rapidly dividing cells, leading to severe side effects.
D) They require high doses to be effective, but cancer cells quickly develop resistance.
They often damage normal rapidly dividing cells, leading to severe side effects.
How does resistance to chemotherapy commonly arise in cancer cells?
A) Increased expression of drug uptake transporters leading to intracellular accumulation.
B) Activation of tumor suppressor genes that enhance drug sensitivity.
C) Mutations in drug target proteins, leading to decreased drug efficacy.
D) Permanent arrest of the cell cycle in the G0 phase, preventing drug action.
Mutations in drug target proteins, leading to decreased drug efficacy.
also comes from resistance prior to drug intake or resistance is aquired through mutations or adaptation of tumor cells
Cancer is often diagnosed when the tumor is already large or has metastasized. What is the primary reason for this delayed detection?
A) Cancer cells divide at a slower rate initially, making them harder to detect.
B) Tumors only start causing symptoms once they reach approximately 10⁹ (1 billion) cells, making early stages undetectable.
C) The immune system completely eliminates small clusters of cancer cells before they grow.
D) Cancer cells remain dormant for most of their lifespan and only grow rapidly at a later stage.
Tumors only start causing symptoms once they reach approximately 10⁹ (1 billion) cells, making early stages undetectable.
In conclusion, you need to see a lot of cells in order to detect cancer
Why is it fundamental that you CANNot leave any cancer cells behind after treatment?
Any cancer cell left behind will just grow and rapidly divide again, bringing back the affects of cancer
how to alkylating agents work?
alkylating agents are chemotherapeutic drugs. they are electrophillic intermediates and bind covalently to DNA, forcing cell cycle arrest. they mostly cross link DNA strands to promote apoptosis
