Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Patho > Hallmark > Flashcards

Hallmark Flashcards

1
Q

What are the hallmarks of cancer?

A

A1: The hallmarks of cancer refer to the molecular pathogenesis of cancer, considering the common phenotypic and biological properties of cancer cells.

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

What is the definition of proto-oncogenes?

A

Proto-oncogenes are normal cellular genes whose products promote cell proliferation.

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

How are oncogenes defined?

A

Oncogenes are mutant or overexpressed versions of proto-oncogenes that function autonomously without a requirement for normal growth-promoting signals.

And Oncogenes are genes that encode proteins called oncoproteins.

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

What are oncoproteins and what is their role?

A

Oncoproteins are proteins that promote uncontrolled cell proliferation. Oncoproteins promote cell growth, even in the absence of normal growth-promoting signals.

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

What are the 10 fundamental changes in cell physiology that are considered the hallmarks of cancer?

A

The 10 hallmarks of cancer are:
1. Self-sufficiency in growth signals
2. Insensitivity to growth-inhibitory signals
3. Altered cellular metabolism
4. Evasion of apoptosis
5. Limitless replicative potential (immortality)
6. Sustained angiogenesis
7. Invasion and metastasis
8. Evasion of immune surveillance
9. Genomic instability
10. Tumor-promoting inflammation

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

What is meant by self-sufficiency in growth signals in cancer cells?

A

Self-sufficiency in growth signals refers to gain-of-function mutations that convert proto-oncogenes to oncogenes.

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

Give me examples of Oncogenes ?

A

GROWTH FACTORS :
PGF-bata, fibroblast GF.

GROWTH FACTOR RECEPTORS:
EGF family R , PGF R

PROTEINS INVOLVED IN SIGNAL TRANSDUCTION:
GTP-binding ,RAS signal transduction.

NUCLEAR-REGULATORY PROTEINS:
Transcriptional activators (eg. MYC oncogenes).

CELL CYCLE REGULATORS:
Cyclins(D,E) ,Cyclin-dependent kinase(eg.CDK4).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How the Oncogenes can be activeted

A

Overexpression, Amplification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  1. What is the first step of cell proliferation under physiological conditions?
A

The first step is the binding of a growth factor to its specific receptor on the cell membrane.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
  1. What happens after the binding of the growth factor to its receptor?
A

After binding, there is transient activation of the growth factor receptor, which activates several signal transducing proteins on the inner surface of the plasma membrane.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
  1. How is the signal transmitted from the cell membrane to the nucleus?
A

The signal is transmitted across the cytosol to the nucleus by second messengers or a cascade of signal transduction molecules.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
  1. What happens after the signal reaches the nucleus?
A

Nuclear regulatory factors are activated, which initiate and regulate DNA transcription.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
  1. What is synthesized after DNA transcription is initiated?
A

Cellular components needed for cell division, such as ribosomes, are biosynthesized.

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

6 What happens after the biosynthesis of cellular components?

A

The cell enters and progresses into the cell cycle, ultimately leading to cell division.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
  1. How are these steps related to cancer cells?
A

Each of these steps is susceptible to corruption in cancer cells, which can lead to uncontrolled cell proliferation.

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

What role do growth factors play in cancer cells?

A

Cancer cells may secrete their own growth factors or induce stromal cells to produce growth factors in the tumor microenvironment.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do some cancer cells acquire growth self-sufficiency?

A

Some cancer cells acquire growth self-sufficiency by acquiring the ability to synthesize the same growth factors to which they are responsive.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Can you provide an example of cancer cells secreting growth factors and responding to them?

A

Glioblastomas secrete platelet-derived growth factor (PDGF) and express the PDGF receptor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is an example of a cancer cell using an autocrine loop for growth factor signaling?

A

Sarcomas make both transforming growth factor-α (TGF-α) and its receptor, creating an autocrine loop.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How do growth factor receptors function as oncoproteins?

A

Many growth factor receptors function as oncoproteins when they are mutated or overexpressed. The mutated receptors deliver signals to cells even in the absence of growth factors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the role of the Epidermal Growth Factor (EGF) receptor family in cancer?

A

The Epidermal Growth Factor (EGF) receptor family plays a role in cancer by contributing to tumorigenesis when mutated or overexpressed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the significance of ERBB1 in cancer?

A

ERBB1 is overexpressed in squamous cell carcinomas of the lung, glioblastomas, and epithelial tumors of the head and neck.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What cancers is HER2 (ERBB2) amplified in?

A

HER2 (ERBB2) is amplified in breast cancers, adenocarcinomas of the lung, ovary, stomach, and salivary glands.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How is tyrosine kinase activity stimulated in certain cancers?

A

Tyrosine kinase activity is stimulated by point mutations, which are commonly seen in leukemias, lymphomas, and some sarcomas.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How do cancer cells often acquire growth autonomy?

A

Cancer cells often acquire growth autonomy as a result of mutations in genes that encode components of signaling pathways downstream of growth factor receptors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How are signals transmitted to the nucleus in cancer cells?

A

Signals are transmitted to the nucleus through various signal transduction molecules.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are two important oncoproteins in the category of signaling molecules?

A

Two important oncoproteins in the category of signaling molecules are RAS and ABL.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is RAS, and why is it important in human tumors?

A

RAS is one of the most commonly mutated oncogenes in human tumors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Can you give an example of a tumor where RAS mutation is common?

A

pancreatic adenocarcinoma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What state is RAS in when it is inactive?

A

RAS is inactive when bound to GDP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What triggers the activation of RAS?

A

Stimulation of cells by growth factors such as EGF (Epidermal Growth Factor) and PDGF (Platelet-Derived Growth Factor) triggers the activation of RAS.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How does the activation of RAS occur?

A

Activation occurs through the exchange of GDP for GTP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What happens after RAS is activated?

A

Activated RAS stimulates downstream regulators of proliferation through several pathways that end in the nucleus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the result of RAS signaling on gene expression?

A

It alters the expression of genes that regulate growth, such as MYC.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What happens with continuous stimulation of nuclear transcription factors?

A

Continuous stimulation of nuclear transcription factors drives the expression of growth-promoting genes, leading to growth autonomy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the function of oncoproteins produced by oncogenes?

A

Oncoproteins, such as those encoded by oncogenes like MYC, function as transcription factors that regulate the expression of growth-promoting genes, such as Cyclins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the primary role of cyclins and cyclin-dependent kinases (CDKs) in the cell cycle?

A

Cyclins and CDKs drive cells forward through the cell cycle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What provides negative control over the cell cycle under normal conditions?

A

CDK inhibitors (CDKIs) provide negative control over the cell cycle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How do cancer cells bypass normal cell cycle regulation?

A

Cancer cells have genetic lesions that disable CDK inhibitors, causing cells to continually enter the cell cycle and divide.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the two types of genetic lesions that lead to dysregulated cell cycle in cancer?

A
  1. Gain-of-function mutations involving CDK4 or D cyclins, leading to overexpression of cyclin D or CDK4.
    1. Loss-of-function mutations involving CDK inhibitors (CDKIs).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is an example of a gain-of-function mutation in cancer?

A

Overexpression of cyclin D or CDK4 due to amplification of their genes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Which types of cancers are associated with cyclin D or CDK4 amplification?

A

• Breast cancer
• Esophageal cancer
• Liver cancer
• Melanoma
• Some lymphomas
• Plasma cell tumors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is an example of a loss-of-function mutation in cancer?

A

Mutation of the CDK inhibitor p16, commonly seen in melanoma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the role of tumor suppressor genes (TSGs)?

A

Tumor suppressor genes normally produce products that apply “brakes” to cell proliferation, preventing uncontrolled cell growth.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What happens when there is a loss of function in tumor suppressor genes?

A

A loss of function mutation in tumor suppressor genes results in the failure of growth inhibition, leading to carcinogenesis (the development of cancer).

46
Q

How does a cell become insensitive to growth inhibition?

A

A cell becomes insensitive to growth inhibition when there are mutations in tumor suppressor genes, which prevents the normal “brakes” from being applied to cell proliferation.

47
Q

What are some tumor suppressor genes involved in human neoplasms?7

A
  1. TGF-beta receptor
    1. E-cadherin
    2. NF1 and NF2
    3. PTEN
    4. RB1
    5. P53
    6. BRCA1 and BRCA2
48
Q

What is the significance of the Retinoblastoma (RB) gene in the cell cycle?

A

The Retinoblastoma gene (RB) is a key negative regulator of the cell cycle and acts as a tumor suppressor gene. It is directly or indirectly inactivated in most human cancers.

49
Q

What was the Retinoblastoma (RB) gene the first to be recognized as?

A

The RB gene was the first tumor suppressor gene to be discovered.

50
Q

Where is the RB gene located?

A

The RB gene is mapped to chromosomal locus 13q14.

51
Q

What does the Knudson two-hit hypothesis state?

A

The Knudson two-hit hypothesis states that two mutations (or “hits”) are required to produce retinoblastoma. Both normal alleles of the RB locus must be inactivated for the disease to develop.

52
Q

How does retinoblastoma develop in familial cases?

A

In familial cases, children inherit one defective copy of the RB gene in the germ line, while the other copy is normal. Retinoblastoma develops when the normal RB gene is lost in retinoblasts due to somatic mutation.

53
Q

Why is familial retinoblastoma considered autosomal dominant in inheritance?

A

In familial retinoblastoma, inheriting a single germ line mutation is sufficient to transmit the disease risk because the second “hit” occurs somatically, leading to disease development.

54
Q

What is TP53, and why is it important in cancer?

A

TP53 is the tumor suppressor gene that encodes the p53 protein, which is the most commonly mutated gene in human cancer.

55
Q

What type of protein does TP53 encode, and what is its primary function?

A

TP53 encodes the p53 protein, which is a transcription factor that prevents neoplastic transformation.

56
Q

What are the three mechanisms by which p53 prevents neoplastic transformation?

A
  1. Activation of temporary cell cycle arrest (quiescence).
  2. Induction of permanent cell cycle arrest (senescence).
  3. Triggering programmed cell death (apoptosis).
57
Q

What types of stresses activate p53?

A

p53 is activated by stresses such as DNA damage.

58
Q

How does p53 assist in DNA repair?

A

p53 causes G1 cell cycle arrest and induces the expression of DNA repair genes to facilitate DNA repair.

59
Q

What happens to a cell with damaged DNA that cannot be repaired under normal p53 function?

A

The cell is directed by p53 to either enter senescence or undergo apoptosis.

60
Q

What are the consequences of losing normal p53 function?

A

DNA damage goes unrepaired, mutations become fixed in dividing cells, and the cell undergoes malignant transformation.

61
Q

What is the role of the MDM2 gene in relation to TP53?

A

The MDM2 gene is an inhibitor of TP53.

62
Q

How does overexpression of MDM2 contribute to malignancy?

A

Overexpression of MDM2 inhibits TP53, leading to unchecked cell division and malignancy.

63
Q

What is the Warburg effect?

A

The Warburg effect, also known as aerobic glycolysis, is a phenomenon where cancer cells demonstrate high levels of glucose uptake and increased conversion of glucose to lactate via the glycolytic pathway, even in the presence of ample oxygen.

64
Q

How does aerobic glycolysis benefit cancer cells?

A

Aerobic glycolysis benefits cancer cells by providing them with metabolic intermediates that are needed for the synthesis of essential cellular components, such as proteins, lipids, and nucleic acids, which support their rapid growth and division.

65
Q

Why do cancer cells avoid mitochondrial oxidative phosphorylation?

A

Cancer cells avoid mitochondrial oxidative phosphorylation because it does not provide the necessary metabolic intermediates for synthesizing cellular components, whereas aerobic glycolysis supports their rapid division and growth by supplying these intermediates.

66
Q

Which oncoproteins induce Warburg metabolism?

A

Oncoproteins like RAS, MYC, and mutated growth factor receptors induce Warburg metabolism.

67
Q

Which tumor suppressors oppose Warburg metabolism?

A

Tumor suppressors such as PTEN, NF1, and p53 oppose Warburg metabolism.

68
Q

What is autophagy, and what happens during it?

A

Autophagy is a state of severe nutrient deficiency in which cells arrest their growth and catabolize their own organelles, proteins, and membranes to produce energy.

69
Q

What happens if the autophagy adaptation fails?

A

If the autophagy adaptation fails, the cells die.

70
Q

How do tumor cells survive severe nutrient deficiency without triggering autophagy?

A

Tumor cells often manage to grow in severe nutrient deficiency by entering a state of metabolic hibernation, allowing them to survive for long periods without triggering autophagy.

71
Q

What role do oncoproteins like mutated isocitrate dehydrogenase (IDH) play in tumor cells?

A

Oncoproteins like mutated isocitrate dehydrogenase (IDH) cause the formation of high levels of “oncometabolites” that alter the genome, leading to changes in gene expression and oncogenesis.

72
Q

What happens when cancer cells acquire mutations in genes that regulate apoptosis?

A

Cancer cells acquire mutations in genes that regulate apoptosis, leading to the disabling of apoptotic intrinsic pathways, which results in increased cell survival.

73
Q

What are the major mechanisms that tumor cells use to evade cell death?

A

The major mechanisms include:
1. Loss of p53, either through mutation or antagonism by MDM2 overexpression.
2. Overexpression of anti-apoptotic factors (e.g., BCL2), which reduces the exit of cytochrome c from mitochondria.
3. Upregulation of IAP (inhibitor of apoptosis).

74
Q

How do tumor cells differ from normal cells in terms of replication?

A

Tumor cells are capable of limitless replication, unlike normal cells.

75
Q

What is the limit on the number of divisions in normal cells?

A

Normal cells have a limit of about 70 divisions due to the shortening of telomeres.

76
Q

What happens when telomeres shorten in normal cells?

A

Shortened telomeres in normal cells activate cell cycle checkpoints, such as p53 and RB, which lead to cell senescence.

77
Q

What happens to the checkpoints in tumor cells?

A

Tumor cells have disabled or mutated checkpoints, meaning DNA repair pathways are not activated when telomeres shorten.

78
Q

What is the consequence of disabled checkpoints in tumor cells?

A

The lack of activated DNA repair pathways leads to massive chromosomal instability and a mitotic crisis in tumor cells.

79
Q

What is the maximum size a tumor can reach without inducing angiogenesis?

A

A tumor cannot enlarge beyond 1 to 2 mm in diameter unless it has the capacity to induce angiogenesis.

80
Q

How do growing cancers stimulate neoangiogenesis?

A

Growing cancers stimulate neoangiogenesis by forming vessels that sprout from previously existing capillaries.

81
Q

How do tumors develop neoangiogenesis?

A

Tumors develop neoangiogenesis by breaking the balance between angiogenesis promoters and inhibitors.

82
Q

What role do newly formed endothelial cells play in tumor growth?

A

Newly formed endothelial cells stimulate the growth of tumor cells by secreting growth factors, such as insulin-like growth factors (IGFs) and platelet-derived growth factor (PDGF).

83
Q

What stimulates vascular endothelial growth factor (VEGF)?

A

VEGF is stimulated by hypoxia.

84
Q

What is the role of p53 in angiogenesis?

What happens when p53 is lost?

A

p53 normally stimulates the expression of anti-angiogenic molecules.

Loss of p53 leads to neoangiogenesis.

85
Q

How do gain-of-function mutations of RAS or MYC affect VEGF?

A

Gain-of-function mutations of RAS or MYC upregulate the production of VEGF.

86
Q

What is the function of new blood vessels in tumors?

What are the characteristics of new blood vessels in tumors?

A

New blood vessels deliver oxygen and nutrients and remove wastes from the tumor.

New blood vessels are leaky and dilated, which can cause bleeding and contribute to metastasis.

87
Q

What are the main factors involved in invasion and metastasis?

A

Invasion and metastasis result from complex interactions involving cancer cells, stromal cells, and the extracellular matrix (ECM).

88
Q

What are the two main phases of the metastatic cascade?

A

• (1) Invasion of the ECM.
• (2) Vascular dissemination and homing of tumor cells.

89
Q

What are the key steps in the invasion of the ECM?

A

of cell–cell contacts: Caused by inactivation of E-cadherin.
• Degradation of ECM and BM: Mediated by proteolytic enzymes secreted by tumor cells, such as cathepsins.
• Attachment to ECM components.
• Migration of tumor cells.

90
Q

What happens during vascular dissemination and homing of tumor cells?

A

Many tumors arrest in the first capillary bed they encounter, with the lung and liver being the most common sites.
• Some tumors exhibit organ tropism, likely due to the activation of adhesion receptors whose ligands are expressed by endothelial cells at the metastatic site.

91
Q

Which enzyme secreted by tumor cells is responsible for ECM and BM degradation?

What is the role of E-cadherin in invasion?

A

Proteolytic enzymes such as cathepsins.

E-cadherin is involved in maintaining cell–cell adhesion. Its inactivation leads to the loosening of cell–cell contacts, facilitating invasion.

92
Q

Why do some tumors show organ tropism?

A

Organ tropism is likely due to the activation of specific adhesion receptors that bind to ligands expressed by endothelial cells at the metastatic site.

93
Q

Which organs are most commonly affected by metastatic tumor arrest, and why?

A

The lungs and liver are most commonly affected because they are often the first capillary beds encountered by disseminating tumor cells.

94
Q

How can tumor cells be recognized by the host immune system?

A

Tumor cells can be recognized as “foreign” and eliminated by the host immune system.

95
Q

How can tumor cells be recognized by the host immune system?

A

Tumor cells can be recognized as “foreign” and eliminated by the host immune system.

96
Q

How do cancer cells evade the host immune response?

A

Cancer cells evade the host immune response through various mechanisms.

97
Q

How do cancer cells evade the host immune response?

A

Cancer cells evade the host immune response through various mechanisms.

98
Q

What is the primary mechanism of antitumor activity?

A

Antitumor activity is predominantly mediated by cell-mediated mechanisms.

99
Q

How are tumor antigens presented on the cell surface?

A

Tumor antigens are presented on the cell surface by MHC class I molecules and are recognized by CD8+ cytotoxic T lymphocytes (CTLs).

100
Q

What are the different types of tumor antigens?

A

• Tumor antigens can be:
• Products of mutated genes
• Overexpressed proteins
• Tumor antigens produced by oncogenic viruses

101
Q

What is the risk for cancer in immunosuppressed patients?

A

Immunosuppressed patients have an increased risk for the development of cancer.

102
Q

How can tumors avoid the immune system in immunocompetent patients?

A
  • selective outgrowth of antigen-negative variants tumor cells
  • loss or reduced expression of histocompatibility molecules,
  • immunosuppression mediated by expression of certain factors (e.g.,TGF-β, PD-1 ligands) by the tumor cells
103
Q

What is genomic instability?

A

Genomic instability refers to the increased tendency of an organism’s genome to acquire mutations, leading to an elevated risk of diseases like cancer.

104
Q

What is the relationship between inherited mutations and cancer risk?

A

Individuals with inherited mutations in genes involved in DNA repair systems are at a significantly higher risk for developing cancer.

105
Q

What is the effect of mutations in the mismatch repair system?

A

Patients with Hereditary Nonpolyposis Colorectal Cancer (HNPCC) syndrome have defects in the mismatch repair system, which increases their risk of cancer.

106
Q

What genetic defect causes xeroderma pigmentosum, and how does it affect DNA repair?

A

Xeroderma pigmentosum is caused by a defect in the nucleotide excision repair pathway, which impairs the ability to repair DNA damage caused by UV radiation, leading to an increased risk of skin cancer.

107
Q

What genetic conditions are associated with defects in the DNA repair system?

A

Conditions like Bloom syndrome, ataxia-telangiectasia, and Fanconi anemia are associated with defects in the DNA repair system, leading to genomic instability and an increased risk of cancer.

108
Q

How do mutations in lymphoid cells affect cancer risk?

A

Lymphoid neoplasms, which involve mutations in lymphocytes, are associated with mutations in genes expressing certain gene products, contributing to the development of cancers like lymphomas.

109
Q

What is tumor-promoting inflammation?

A

Tumor-promoting inflammation is a chronic inflammatory reaction provoked by infiltrating cancers. In advanced cancer patients, this inflammation can lead to systemic symptoms such as anemia, fatigue, and cachexia.

110
Q

What are the systemic signs and symptoms of tumor-promoting inflammation in advanced cancer patients?

A

The systemic signs and symptoms can include anemia, fatigue, and cachexia.

111
Q

What are the cancer-enabling effects of inflammatory cells?

A

The cancer-enabling effects of inflammatory cells include:
• Release of factors that promote cell proliferation.
• Removal of growth suppressors.
• Enhanced resistance to cell death.
• Promotion of angiogenesis (formation of new blood vessels).

112
Q

How do inflammatory mediators, cytokines, and chemicals contribute to tumor-promoting inflammation?

A

Inflammatory mediators, cytokines, and chemicals released by inflammatory cells, fibroblasts, and endothelial cells play a role by:
• Promoting cell proliferation.
• Removing growth suppressors.
• Enhancing resistance to cell death.
• Stimulating angiogenesis.

Patho (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions