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Dundee uni med > FOM- week 9 > Flashcards

FOM- week 9 Flashcards

1
Q

What is cancer?

A

Cancer is uncontrolled cell growth that invades other tissues and can spread to distant organs.

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2
Q

What are tumors?

A

Tumors are swellings that can be benign (non-cancerous) or malignant (cancerous).

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3
Q

What is neoplasia?

A

Neoplasia is abnormal, uncontrolled growth of cells without a stimulus. It can be benign, premalignant, or malignant.

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4
Q

What is metaplasia?

A

Metaplasia is a reversible change in cell type, often due to stress (e.g., smoking).

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5
Q

What is dysplasia?

A

Dysplasia is abnormal cell growth that may lead to cancer.

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6
Q

What is malignancy?

A

Malignant cells invade surrounding tissues and can metastasize (spread) to distant sites.

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7
Q

What are the hallmarks of cancer?

A
  1. Evading growth suppression
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8
Q
A
  1. Avoiding immune destruction
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9
Q
A
  1. Sustaining proliferative signals
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10
Q
A
  1. Inducing angiogenesis
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11
Q
A
  1. Genome instability (mutations)
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12
Q

What are oncogenes?

A

Oncogenes (e.g., MYc, BRAF, RAS) promote cancer by accelerating the cell cycle.

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13
Q

What are tumor suppressor genes?

A

Tumor suppressor genes (e.g., p53) inhibit cell cycle progression and promote apoptosis. Loss of these genes can lead to cancer.

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14
Q

What causes cancer?

A

Cancer is a genetic disease arising from somatic cell mutations, driven by mosaicism and post-zygotic mutations, leading to a genetically diverse population of cells within an individual.

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15
Q

What are somatic mutations?

A

Somatic mutations occur in non-reproductive cells and cannot be inherited.

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16
Q

What is mosaicism?

A

Mosaicism refers to the presence of multiple genetically distinct cell lines within an individual due to mutations occurring during development.

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17
Q

What are driver mutations vs passenger mutations?

A

Driver mutations drive cancer development by altering critical genes (oncogenes and tumor suppressors). Passenger mutations are incidental and do not directly cause cancer.

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18
Q

What is epigenetics and its role in cancer?

A

Epigenetic changes alter gene expression without changing the DNA sequence, potentially turning genes on or off, contributing to cancer.

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19
Q

What is DNA methylation?

A

DNA methylation involves adding a methyl group to DNA, usually silencing gene expression. In cancer, tumor suppressor genes may be hypermethylated and silenced.

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20
Q

What is histone modification?

A

Histone modifications affect the proteins around which DNA is wrapped, influencing gene expression and potentially contributing to cancer.

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21
Q

What is methylation in cancer?

A

Methylation typically occurs at CpG sites, and hypermethylation of tumor suppressor genes can silence these genes, contributing to cancer development.

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22
Q

What are oncogenes?

A

Oncogenes are mutated or overexpressed proto-oncogenes that promote cancer cell growth. They can produce their own growth factors, overexpress receptors, or have constitutively active proteins.

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23
Q

How are oncogenes activated?

A

Oncogenes can be activated through: Point mutations (e.g., BRAF), Amplification (e.g., HER2), Translocation (e.g., Philadelphia Chromosome BCR-ABL).

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24
Q

What is the role of the BRAF gene in cancer?

A

A point mutation in the BRAF gene causes constitutive activation of the MAP-Kinase signaling pathway, leading to constant cell growth signals.

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25
Q

What is HER2 amplification?

A

HER2 gene amplification results in excessive HER2 receptors on the cell surface, promoting uncontrolled cell proliferation.

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26
Q

What is the Philadelphia Chromosome?

A

A translocation between chromosomes 9 and 22 creates a BCR-ABL fusion protein, which has enhanced kinase activity, promoting cancer cell growth.

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27
Q

What is the role of tumor suppressor genes?

A

Tumor suppressor genes inhibit cancerous growth by regulating the cell cycle and initiating apoptosis. Mutations in these genes can lead to cancer.

28
Q

What is the RB gene and its role in cancer?

A

The RB gene encodes pRB, a protein that controls the G1 checkpoint in the cell cycle. Mutations in this gene lead to uncontrolled cell division and retinoblastoma.

29
Q

What is the Two-Hit Hypothesis?

A

The Two-Hit Hypothesis suggests that both alleles of a tumor suppressor gene must be mutated or deleted for cancer to develop. This explains cancer’s increasing frequency with age.

30
Q

What is mismatch repair and its role in cancer?

A

Mismatch repair fixes DNA replication errors. Failure in this system (e.g., in Lynch Syndrome) leads to an increased mutation rate and higher cancer risk.

31
Q

What is Lynch Syndrome?

A

Lynch Syndrome is a hereditary form of colon cancer caused by mutations in mismatch repair genes, leading to failure in correcting replication errors.

32
Q

What is an oncogenic signature?

A

Cancer cells exhibit an oncogenic signature, a combination of driver mutations that define the cancer and contribute to tumor heterogeneity and rapid evolution.

33
Q

What causes cancer?

A

Cancer is a genetic disease that arises from somatic mutations and mosaicism, caused by post-zygotic mutations that result in genetically diverse cells.

34
Q

What are somatic mutations?

A

Somatic mutations occur in non-reproductive cells and are not inherited.

35
Q

What is mosaicism?

A

Mosaicism is the presence of more than one genetically distinct cell line within an individual due to mutations occurring during development.

36
Q

What are driver mutations vs passenger mutations?

A

Driver mutations directly contribute to cancer development by altering critical genes, while passenger mutations are incidental and do not cause cancer.

37
Q

What is epigenetics and its role in cancer?

A

Epigenetics involves changes in gene expression without altering the DNA sequence. These changes, like DNA methylation, can drive cancer by turning important genes on or off.

38
Q

What is DNA methylation?

A

DNA methylation adds a methyl group to DNA, silencing gene expression. Hypermethylation of tumor suppressor genes can contribute to cancer.

39
Q

What is histone modification?

A

Histone modification refers to changes in the proteins around which DNA is wrapped, influencing gene expression and potentially driving cancer.

40
Q

What are oncogenes?

A

Oncogenes are mutated or overexpressed proto-oncogenes that drive cancer cell growth by producing growth factors, overexpressing receptors, or having constitutively active proteins.

41
Q

How are oncogenes activated?

A

Oncogenes can be activated by point mutations (e.g., BRAF), gene amplification (e.g., HER2), or chromosomal translocations (e.g., Philadelphia Chromosome BCR-ABL).

42
Q

What is BRAF’s role in cancer?

A

A point mutation in BRAF causes constant activation of the MAP-Kinase pathway, promoting cell growth.

43
Q

What is HER2 amplification?

A

HER2 gene amplification leads to excessive HER2 receptors on the cell surface, resulting in uncontrolled cell proliferation.

44
Q

What is the Philadelphia Chromosome?

A

A translocation between chromosomes 9 and 22 creates a BCR-ABL fusion protein, enhancing kinase activity and promoting uncontrolled cell growth.

45
Q

What are tumor suppressor genes?

A

Tumor suppressor genes inhibit cancerous growth by regulating the cell cycle and initiating apoptosis. Mutations in these genes can lead to cancer.

46
Q

What is the RB gene and its role in cancer?

A

The RB gene encodes pRB, a protein that prevents uncontrolled cell division at the G1 checkpoint. Mutations cause retinoblastoma and other cancers.

47
Q

What is the Two-Hit Hypothesis?

A

The Two-Hit Hypothesis states that both alleles of a tumor suppressor gene must be mutated for cancer to develop, explaining why cancer occurs more frequently with age.

48
Q

What is mismatch repair and its role in cancer?

A

Mismatch repair corrects DNA replication errors. Failure in mismatch repair (e.g., Lynch Syndrome) leads to increased mutations and higher cancer risk.

49
Q

What is Lynch Syndrome?

A

Lynch Syndrome is a hereditary condition caused by mutations in mismatch repair genes, leading to an increased risk of colon cancer.

50
Q

What is an oncogenic signature?

A

An oncogenic signature is a combination of driver mutations that characterize a cancer and contribute to tumor heterogeneity and rapid evolution.

51
Q

What factors contribute to cancer risk?

A

Cancer risk is multifactorial, influenced by genetic predisposition, lifestyle factors, and environmental exposures.

52
Q

What are indicators of inherited cancer susceptibility?

A

Indicators include multiple affected family members, early onset of cancer, bilateral tumors, and multiple cancers in a single individual.

53
Q

How is cancer risk multifactorial?

A

Cancer risk is influenced by a combination of genetic factors and environmental/lifestyle factors, not just by genetics alone.

54
Q

What is the role of DNA repair in cancer?

A

DNA repair mechanisms like mismatch repair are critical in preventing cancer. Defects in these systems can lead to increased mutation rates and higher cancer risk.

55
Q

What is the Warburg Effect?

A

Cancer cells use anaerobic glycolysis (even in the presence of oxygen) for rapid energy production, supporting fast cell growth but producing inefficient ATP and lactate.

56
Q

What is glycolysis and where does it occur?

A

Glycolysis is the process that converts glucose to pyruvate and occurs in the cytoplasm, yielding 2 ATP per glucose molecule.

57
Q

What is the role of glucose in metabolism?

A

Glucose is used for ATP production and as a building block for synthetic reactions, such as nucleotide synthesis via the pentose phosphate pathway.

58
Q

How does glucose enter cells?

A

Glucose enters cells through Na+/glucose symporters or GLUTs (glucose transporters), regulated by tissue type.

59
Q

What are the key enzymes in glycolysis?

A

Key enzymes include hexokinase, phosphofructokinase, aldolase, and pyruvate kinase, which regulate the flow of glucose to pyruvate.

60
Q

What is the role of phosphofructokinase in glycolysis?

A

Phosphofructokinase is the rate-limiting enzyme in glycolysis, activated by AMP and inhibited by ATP and citrate.

61
Q

What happens in anaerobic metabolism?

A

In the absence of oxygen, pyruvate is converted to lactate, regenerating NAD+ for continued glycolysis.

62
Q

What is the fate of pyruvate in metabolism?

A

Pyruvate is converted to acetyl-CoA for the TCA cycle, where it undergoes further oxidation to produce ATP, NADH, and FADH2.

63
Q

What is the TCA Cycle?

A

The TCA cycle occurs in the mitochondrial matrix and oxidizes acetyl-CoA to produce ATP, NADH, FADH2, and CO2.

64
Q

What is the overall ATP yield from glucose metabolism?

A

One molecule of glucose yields 30-32 ATP through glycolysis, the TCA cycle, and oxidative phosphorylation.

65
Q

What is oxidative phosphorylation?

A

Oxidative phosphorylation is the process by which ATP is generated using the electron transport chain and a proton gradient in the inner mitochondrial membrane.

66
Q

What is the role of NADH and FADH2 in oxidative phosphorylation?

A

NADH and FADH2 carry high-energy electrons to the electron transport chain, which transfers electrons to oxygen, generating a proton gradient used for ATP synthesis.

67
Q

What inhibits oxidative phosphorylation?

A

Cyanide, azide, and CO inhibit electron transfer to O2, preventing the proton gradient formation and halting ATP synthesis.

Dundee uni med (9 decks)

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