GYOEDU questions Flashcards
In cancer cells, loss of function of which tumor suppressor gene can lead to uncontrolled cell growth and proliferation due to deregulation of the G1/S checkpoint?
A) BRCA1
B) TP53
C) PTEN
D) APC
TP53, also known as p53, is a key tumor suppressor gene that regulates the cell cycle, DNA repair, and apoptosis. Loss of p53 function disrupts the G1/S checkpoint, allowing cells with DNA damage to proceed through the cell cycle, leading to uncontrolled cell growth and proliferation.
In the context of cancer, how does hypoxia contribute to cell growth and proliferation?
A) By increasing oxidative stress
B) By activating the unfolded protein response
C) By stabilizing HIF-1α and promoting angiogenesis
D) By inducing autophagy
C) By stabilizing HIF-1α and promoting angiogenesis
Hypoxia, or low oxygen levels, is common in solid tumors. Under hypoxic conditions, the hypoxia-inducible factor-1α (HIF-1α) is stabilized under hypoxic conditions, leading to gene transcription that promotes angiogenesis, glycolysis, and cell survival. This adaptation enables cancer cells to maintain growth and proliferation despite the limited oxygen supply.
Dysregulation of which cellular process can lead to chromosomal instability and aneuploidy in cancer cells?
A) Telomere maintenance
B) Mitotic spindle assembly
C) Transcription
D) DNA replication
B) Mitotic spindle assembly
Explanation: Mitotic spindle assembly is critical for properly segregating chromosomes during cell division. Errors in this process can lead to chromosomal instability and aneuploidy, which are common features in cancer cells and contribute to their growth and proliferation.
Which protein activates the DNA damage response (DDR) pathway and plays a crucial role in maintaining genomic stability?
A) ATM
B) RET
C) JNK
D) MEK
A) ATM
Explanation: Ataxia-telangiectasia mutated (ATM) is a serine/threonine kinase activated upon DNA double-strand breaks. ATM phosphorylates and activates several downstream targets, including p53, leading to cell cycle arrest, DNA repair, or apoptosis. Loss of ATM function can result in genomic instability and contribute to cancer development.
Many proteins activate the DNA damage response (DDR) pathway, but one of the most important is ATM. ATM is a serine/threonine kinase activated in response to DNA damage. It phosphorylates a number of downstream targets, including checkpoint proteins, DNA repair proteins, and apoptosis-promoting proteins. ATM plays a crucial role in maintaining genomic stability by triggering the DNA repair process and preventing the accumulation of mutations.
Here are some other proteins involved in the DDR pathway:
ATR is another serine/threonine kinase activated in response to DNA damage.
CHK1 and CHK2: Checkpoint proteins that are involved in cell cycle arrest.
BRCA1 and BRCA2: DNA repair proteins involved in homologous recombination repair.
P53: A tumor suppressor protein that is involved in apoptosis.
The DDR pathway is a complex protein network that protects the genome from damage. Mutations in any of these proteins can lead to increased susceptibility to cancer.
Which of the following growth factors is commonly upregulated in various types of cancer and plays a key role in promoting tumor growth, angiogenesis, and metastasis?
A) Fibroblast growth factor (FGF)
B) Vascular endothelial growth factor (VEGF)
C) Insulin-like growth factor (IGF)
D) Platelet-derived growth factor (PDGF)
B) Vascular endothelial growth factor (VEGF)
Explanation: Vascular endothelial growth factor (VEGF) is a potent angiogenic factor that promotes the growth of new blood vessels. Overexpression of VEGF is commonly observed in various types of cancer and contributes to tumor growth, angiogenesis, and metastasis.
Which of the following proteins functions as an oncogene in the context of cancer?
A) MYC
B) BRCA1
C) TP53
D) RB1
C) MYC
An oncogene is a gene that can promote the development of cancer. MYC is a proto-oncogene, meaning it is a normal gene that can become an oncogene if it is mutated or amplified. MYC is involved in cell growth, proliferation, and apoptosis. When MYC is mutated or amplified, it can lead to uncontrolled cell growth and division, eventually leading to cancer.
BRCA1 and BRCA2 are tumor suppressor genes. They are involved in DNA repair. When BRCA1 or BRCA2 is mutated, it can increase the risk of developing breast and ovarian cancer.
TP53 is a tumor suppressor gene. It is involved in cell cycle regulation and apoptosis. When TP53 is mutated, it can increase the risk of developing various cancers, including lung, breast, and colon cancer.
RB1 is a tumor suppressor gene. It is involved in cell cycle regulation. When RB1 is mutated, it can increase the risk of developing retinoblastoma, a type of eye cancer.
In conclusion, MYC is the only option that is an oncogene.
Tumor suppressor genes
TP53
BRCA1
BRCA2
RB1
PTEN
APC
CDKN2A (p16, p14)
VHL
SMAD4
NF1
ATM
CDH1
STK11
Oncogenes
MYC
RAS (e.g., HRAS, KRAS, NRAS)
ABL1
ERBB2 (HER2/neu)
EGFR
BCL2
MYCN
PIK3CA
MET
MDM2
SRC
JAK2
ALK
What is the primary mechanism of action of methotrexate?
A. Inhibition of DNA synthesis
B. Induction of DNA damage through free radical formation
C. Inhibition of protein synthesis
D. Inhibition of DNA topoisomerase activity
(A) Methotrexate primarily inhibits DNA synthesis by inhibiting the enzyme dihydrofolate reductase, which is necessary for the synthesis of thymidine and purines. This leads to the depletion of nucleotides and impaired DNA synthesis, ultimately resulting in cell death.
What is the specific consequence of Topotecan’s inhibition of topoisomerase I?
A. Preventing DNA supercoil relaxation
B. Inducing DNA strand breaks
C. Stabilizing the cleavage complex
D. Preventing DNA replication
C. Stabilizing the cleavage complex
Explanation: Topotecan inhibits topoisomerase I by stabilizing the cleavage complex, which leads to DNA strand breaks and ultimately cell death.
Which of the following DNA lesions is the most common type induced by Cisplatin?
A. Single-strand breaks
B. DNA adducts
C. Double-strand breaks
D. Intrastrand crosslinks
D. Intrastrand crosslinks
Explanation: Cisplatin mainly induces intrastrand crosslinks, which distort the DNA helix structure and prevent DNA replication, transcription, and repair, leading to cell death.
Vincristine’s ability to inhibit microtubule assembly is primarily due to its interaction with which protein?
A. Tubulin
B. Actin
C. Myosin
D. Kinesin
A. Tubulin
Explanation: Vincristine binds to tubulin, preventing the assembly of microtubules, which are essential for mitosis. This disrupts cell division and results in cell death.
What is the primary mechanism of action of Doxorubicin in cardiotoxicity?
A. Induction of DNA damage
B. Formation of free radicals
C. Inhibition of topoisomerase II
D. Disruption of calcium homeostasis
B. Formation of free radicals
Explanation: Doxorubicin is known to cause cardiotoxicity primarily through the formation of free radicals, leading to oxidative stress, mitochondrial dysfunction, and cell death.
What is the primary reason for the increased cytotoxicity of gemcitabine compared to other nucleoside analogs?
A. Greater affinity for DNA polymerase
B. Intracellular activation by multiple phosphorylation steps
C. Resistance to deamination
D. Self-potentiation through inhibition of ribonucleotide reductase
D. Self-potentiation through inhibition of ribonucleotide reductase
Explanation: Gemcitabine is more cytotoxic than other nucleoside analogs due to its self-potentiation mechanism. Apart from acting as a nucleoside analog, it also inhibits ribonucleotide reductase, reducing the pool of competing deoxynucleotides and enhancing its own incorporation into DNA.
Which of the following cellular processes is specifically affected by Etoposide, leading to its anticancer activity?
A. DNA replication
B. Transcription
C. DNA repair
D. Decatenation
D. Decatenation
Explanation: Etoposide targets topoisomerase II, inhibiting the enzyme’s ability to decatenate (unlink) DNA strands, which is essential for chromosome segregation during cell division. This results in DNA breaks and ultimately cell death.
