Lecture 1 Flashcards

1
Q

what term is used to describe new growths in tissues

A

Neoplasia

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2
Q

What role does the protein p53 play in cancer?

A) It promotes cell division
B) It suppresses apoptosis
C) It is a tumour suppressor gene
D) It causes mutations

A

C) It is a tumour suppressor gene

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3
Q

Which of the following is NOT a known carcinogen?

A) Tobacco smoke
B) Radon gas
C) Vitamin C
D) Benzene

A

C) Vitamin C

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4
Q

Which of the following is a significant risk factor for colorectal cancer?

A) Low fibre diet
B) High red meat consumption
C) High alcohol consumption
D) Regular exercise

A

A) Low fibre diet
B) High red meat consumption
C) High alcohol consumption

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5
Q

What is the function of the cyclin-dependent kinases (CDKs)?

A) They inhibit apoptosis
B) They regulate cell cycle progression
C) They promote genetic mutations
D) They repair DNA

A

B) They regulate cell cycle progression

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6
Q

What is the role of growth factors in the cell cycle?

A) They inhibit cell division
B) They stimulate cell division
C) They cause DNA damage
D) They induce apoptosis

A

B) They stimulate cell division

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7
Q

Which virus is associated with cervical cancer?

A) Hepatitis B virus
B) Epstein-Barr virus
C) Human Papillomavirus (HPV)
D) Human Immunodeficiency Virus (HIV)

A

C) Human Papillomavirus (HPV)

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8
Q

What is the most significant infectious agent contributing to gastric cancer?

A) Hepatitis C
B) Human Papillomavirus
C) Helicobacter pylori
D) Epstein-Barr virus

A

C) Helicobacter pylori

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9
Q

In which phase of the cell cycle is DNA replicated?

A) G1 phase
B) S phase
C) G2 phase
D) M phase

A

B) S phase

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10
Q

What is the function of p53 in response to DNA damage?

A) Promote cell cycle progression
B) Induce apoptosis
C) Cause further mutations
D) Repair DNA directly

A

B) Induce apoptosis

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11
Q

What percentage of lung cancers are associated with mutations in p53?

A) 30%
B) 50%
C) 70%
D) 90%

A

C) 70%

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12
Q

Which type of cancer is most associated with obesity?

A) Lung cancer
B) Cervical cancer
C) Colorectal cancer
D) Melanoma

A

C) Colorectal cancer

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13
Q

Which cancer is commonly linked to HPV?

A) Lung cancer
B) Breast cancer
C) Colorectal cancer
D) Cervical cancer

A

D) Cervical cancer

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14
Q

What is a significant factor in the increased incidence of colorectal cancer in developed countries?

A) Increased fibre intake
B) Decreased red meat consumption
C) Increased red meat consumption
D) Increased exercise

A

C) Increased red meat consumption

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15
Q

What is the term for the process by which cancer cells spread to other parts of the body?

A) Metaplasia
B) Carcinogenesis
C) Metastasis
D) Dysplasia

A

C) Metastasis

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16
Q

What is the role of apoptosis in cancer?

A) To promote cell survival
B) To prevent cell division
C) To eliminate damaged cells
D) To increase mutation rates

A

C) To eliminate damaged cells

17
Q

Which research finding connects diet to cancer risk?

A) Increased fruit and vegetable intake reduces cancer risk.
B) High sugar intake is the primary factor.
C) All fats are carcinogenic.
D) Meat consumption has no effect.

A

A) Increased fruit and vegetable intake reduces cancer risk.

18
Q

Which of the following statements best describes the role of p53 in the regulation of the cell cycle?

A) p53 primarily promotes cell cycle progression by inhibiting cyclin-dependent kinase inhibitors.
B) p53 functions as a transcription factor that can induce cell cycle arrest in response to DNA damage.
C) p53 is only activated during mitosis to prevent tumour formation.
D) p53 is solely responsible for DNA replication during the S phase of the cell cycle.

A

B) p53 functions as a transcription factor that can induce cell cycle arrest in response to DNA damage.

19
Q

A study finds that a specific carcinogen significantly increases the incidence of colorectal cancer when combined with a viral infection. Which of the following carcinogens is most likely being studied?

A) Aflatoxin B
B) Tobacco smoke
C) Nitrosamines
D) Benzopyrene

A

A) Aflatoxin B

20
Q

What is the primary mechanism by which ultraviolet (UV) radiation contributes to skin cancer development?

A) UV radiation directly stimulates DNA replication by activating cyclin-dependent kinases.
B) UV radiation causes the formation of pyrimidine dimers, leading to mutations during DNA replication.
C) UV radiation increases the production of reactive oxygen species that inhibit apoptosis.
D) UV radiation enhances the expression of oncogenes through chromosomal translocation.

A

B) UV radiation causes the formation of pyrimidine dimers, leading to mutations during DNA replication.

21
Q

Which of the following best explains the difference in cancer incidence between developed and developing countries?

A) Developed countries have a higher prevalence of hereditary cancers due to genetic factors.

B) Developing countries have better access to cancer treatment, leading to lower incidence rates.

C) Environmental exposures and lifestyle factors in developed nations contribute to higher cancer rates, while infectious agents play a larger role in developing nations.

D) The incidence of cancer is uniform across all countries due to global lifestyle homogenisation.

A

C) Environmental exposures and lifestyle factors in developed nations contribute to higher cancer rates, while infectious agents play a larger role in developing nations.

22
Q

Which of the following mutations is most commonly associated with breast and ovarian cancers?

A) Mutations in the RB gene
B) Mutations in the p53 gene
C) Mutations in the BRCA1 and BRCA2 genes
D) Mutations in the APC gene

A

C) Mutations in the BRCA1 and BRCA2 genes

23
Q

Which of the following statements regarding the role of growth factors in the cell cycle is TRUE?

A) Growth factors inhibit the activation of cyclin-dependent kinases, preventing cell cycle progression.

B) Growth factors bind to their receptors and stimulate downstream signalling pathways that promote cell cycle entry and progression.

C) Growth factors are not involved in the regulation of the cell cycle.

D) Growth factors only act during the G2 phase of the cell cycle.

A

B) Growth factors bind to their receptors and stimulate downstream signalling pathways that promote cell cycle entry and progression.

24
Q

Which of the following best illustrates a critical cellular mechanism underlying neoplasia, particularly involving cell cycle dysregulation and apoptosis bypass?

A) Overexpression of E-cadherin, leading to enhanced cell-cell adhesion and reduced motility

B) Loss-of-function mutations in RB1, allowing uncontrolled progression through the G1/S checkpoint

C) Activation of caspase pathways, ensuring effective clearance of damaged cells

D) Stabilisation of p53 protein, inducing cell cycle arrest and repair of damaged DNA

A

B) Loss-of-function mutations in RB1, allowing uncontrolled progression through the G1/S checkpoint

25
Q

Which of the following correctly matches a type of carcinogen with its associated mechanism of cancer development?

A) Physical carcinogen: Ionising radiation causing DNA strand breaks and mutations

B) Biological carcinogen: Asbestos inducing chronic inflammation and mesothelioma

C) Chemical carcinogen: Human Papillomavirus (HPV) disrupting tumour suppressor genes

D) Physical carcinogen: Aflatoxins binding to DNA, leading to mutations

A

A) Physical carcinogen: Ionising radiation causing DNA strand breaks and mutations

26
Q

Which of the following correctly describes the relationship between aflatoxin B1, Aspergillus flavus, and the development of liver cancer?

A) Aflatoxin B1, produced by Aspergillus flavus, is a biological carcinogen that primarily causes hepatocellular carcinoma after inhalation exposure to contaminated air.

B) Aflatoxin B1, produced by Aspergillus flavus, is a chemical carcinogen that binds to DNA and is strongly associated with the development of hepatocellular carcinoma after chronic ingestion of contaminated crops like peanuts and corn.

C) Aflatoxin B1, produced by Aspergillus flavus, induces lung cancer through its action on the respiratory tract after exposure to contaminated water.

D) Aflatoxin B1, produced by Aspergillus flavus, is a physical carcinogen that causes skin cancer upon direct contact with contaminated soil.

A

B) Aflatoxin B1, produced by Aspergillus flavus, is a chemical carcinogen that binds to DNA and is strongly associated with the development of hepatocellular carcinoma after chronic ingestion of contaminated crops like peanuts and corn.

27
Q

Which of the following best describes alcohol as a known carcinogen and its association with various types of cancer, including its genotoxic effects?

A) Alcohol is a genotoxic carcinogen that increases the risk of oral, pharyngeal, and laryngeal cancers by inducing DNA damage and disrupting DNA repair mechanisms.

B) Alcohol is a non-genotoxic carcinogen that promotes breast and colorectal cancers by enhancing cell differentiation and inhibiting apoptosis.

C) Alcohol is a genotoxic carcinogen that causes liver cancer primarily by inducing oxidative stress, but has little association with oral and pharyngeal cancers.

D) Alcohol is a genotoxic carcinogen that contributes to oral, pharyngeal, laryngeal, breast, and colorectal cancers through its effects on DNA repair, oxidative stress, and acetaldehyde metabolism.

A

D) Alcohol is a genotoxic carcinogen that contributes to oral, pharyngeal, laryngeal, breast, and colorectal cancers through its effects on DNA repair, oxidative stress, and acetaldehyde metabolism.

28
Q

Which of the following correctly describes the genotoxicity of acetaldehyde in alcohol metabolism and its role in carcinogenesis?

A) Ethanol is metabolised by alcohol dehydrogenase to acetate, which is a non-genotoxic by-product that contributes to cellular repair.

B) Ethanol is metabolised to acetaldehyde by alcohol dehydrogenase, which is a genotoxic agent that forms DNA adducts and contributes to cancer development, and then further metabolised to acetate.

C) Acetaldehyde is formed by the oxidation of acetate, and it acts as a genotoxic compound causing DNA repair mechanisms to activate and repair the damage.

D) Ethanol is metabolised to acetate directly, which binds to DNA and induces mutations leading to cancer, while acetaldehyde is non-genotoxic.

A

B) Ethanol is metabolised to acetaldehyde by alcohol dehydrogenase, which is a genotoxic agent that forms DNA adducts and contributes to cancer development, and then further metabolised to acetate.

29
Q

Which of the following best explains the mechanism by which radiation contributes to carcinogenesis?

A) Radiation directly ionises DNA strands, causing base loss and single-stranded DNA damage, while also creating reactive oxygen species (ROS) from the breakdown of water molecules, which can further damage DNA.

B) Radiation causes base loss in DNA by stripping electrons from water molecules, producing reactive oxygen species (ROS) that exclusively lead to double-stranded DNA breaks, without affecting single-stranded DNA.

C) Radiation directly ionises DNA without the involvement of water molecules, resulting only in base loss and no interaction with reactive oxygen species (ROS).

D) Radiation induces oxidative stress that leads to double-stranded DNA breaks, but does not affect base loss or single-stranded DNA damage.

A

A) Radiation directly ionises DNA strands, causing base loss and single-stranded DNA damage, while also creating reactive oxygen species (ROS) from the breakdown of water molecules, which can further damage DNA.

30
Q

Which of the following correctly describes the DNA damage caused by radiation?

A) Ionising radiation causes thymine cross-linking and pyrimidine dimerisation, leading to DNA strand breaks.

B) Ultraviolet (UV) radiation induces pyrimidine dimerisation through thymine cross-linking, resulting in DNA distortion and replication errors.

C) Ionising radiation forms pyrimidine dimers by creating cross-links between thymine and cytosine, leading to chromosomal breakage.

D) Ultraviolet (UV) radiation causes thymine cross-linking and pyrimidine dimerisation without leading to replication errors.

A

B) Ultraviolet (UV) radiation induces pyrimidine dimerisation through thymine cross-linking, resulting in DNA distortion and replication errors.

31
Q

Which of the following best explains how dysregulation of the cell cycle contributes to cancer development?

A) Cancer cells have an accelerated cell cycle, with uncontrolled progression through checkpoints, allowing them to divide excessively.

B) Cancer cells have a slower cell cycle, leading to reduced division rates and subsequent loss of tumorigenic potential.

C) Cancer cells arrest at the G1 checkpoint, preventing progression to the S phase, and thus avoiding uncontrolled proliferation.

D) Cancer cells lack DNA checkpoints, which leads to regulated cell division and prevents tumour formation.

A

A) Cancer cells have an accelerated cell cycle, with uncontrolled progression through checkpoints, allowing them to divide excessively.

32
Q

Which of the following is most closely associated with cancer development due to its dysregulation of the cell cycle?

A) Overexpression of cyclins and increased activity of cyclin-dependent kinases (CDKs) promote excessive progression through the cell cycle, bypassing normal checkpoints.

B) Reduced expression of cyclins and CDKs leads to cell cycle arrest, causing cell death and preventing tumour formation.

C) Mutations in retinoblastoma (Rb) protein prevent the G1 checkpoint from halting the cell cycle, thus inhibiting cancer cell proliferation.

D) Inhibition of cyclin-dependent kinases (CDKs) by tumour suppressor proteins results in rapid cell division and cancer development.

A

A) Overexpression of cyclins and increased activity of cyclin-dependent kinases (CDKs) promote excessive progression through the cell cycle, bypassing normal checkpoints.

33
Q

Which tumor suppressor gene is crucial for regulating the cell cycle and preventing cancer by inhibiting progression from G1 to S phase?

A) p53, which promotes cell cycle progression and inhibits apoptosis to allow cancer cell survival.

B) Rb (Retinoblastoma), which inhibits the G1 to S phase transition, preventing unregulated cell division.

C) Cyclin D, which activates CDKs to promote uncontrolled progression through the cell cycle.

D) Bcl-2, which prevents cell cycle arrest and promotes unregulated cell proliferation in cancer cells.

A

B) Rb (Retinoblastoma), which inhibits the G1 to S phase transition, preventing unregulated cell division.

34
Q

How is the Rb (Retinoblastoma) protein phosphorylated, and what is the consequence of this phosphorylation in the cell cycle?

A) Rb is phosphorylated by cyclin-dependent kinases (CDKs), which leads to its inactivation, allowing the cell to progress from G1 to S phase and promoting cell division.

B) Rb is phosphorylated by DNA polymerase, which prevents the G1 to S phase transition, thereby halting cell cycle progression and promoting apoptosis.

C) Rb is phosphorylated by mitogen-activated protein kinases (MAPKs), resulting in the activation of the G1 checkpoint, stopping cell division to prevent cancer.

D) Rb is phosphorylated by cyclin D alone, which causes it to bind to E2F, promoting the progression of the cell cycle from G1 to S phase.

A

A) Rb is phosphorylated by cyclin-dependent kinases (CDKs), which leads to its inactivation, allowing the cell to progress from G1 to S phase and promoting cell division.

35
Q
A