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Third Year 🔗 > Oncopathology 1 > Flashcards

Oncopathology 1 Flashcards

1
Q

……………..is a multistep process resulting from the accumulation of multiple genetic
alterations that give raise to transformed cancer cells

A

Carcinogenesis

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2
Q

are mutations that alter the function of cancer genes and
thereby contribute directly to the development or progression of cancer.

A

Driver mutations

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3
Q

are mutations that do not affect cellular behavior

A

Passenger mutations

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4
Q

Passenger mutations usually( more / less) than driver mutations ?

A

More

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5
Q

Example of Over-expression of proto-oncogenes is …..
And between which genes ?

A

t(8:14) in Burkitt Lymphoma

Between MYC gene (chromosome 8) and IG (chromosome14 )

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6
Q

BCR-ABL1 fusion gene, are characteristic of wich disease? (CML).

A

chronic myeloid leukemia

سرCR يعني للأبد chronic

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7
Q

1-Example of Creation of novel fusion proteins ?

2- It’s lead to ……

3- Between which genes?

A

1 -t(9:22) ABL-BCR gene Hybrid gene
2- Chronic Myeloid Leukemia
3- At chromosome 9 there is gene called ( ABL )and at chromosome 22 there is a
gene called (BCR) .

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8
Q

Example of Deletions of genetic lesions in cancer ?

A

loss of particular tumor suppressor genes

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9
Q

What is the common mechanism that Lead to lost tumor suppressor gene ?

A

one allele is lost through inactivating point mutation and the other allele is lost through deletion

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10
Q

Example of Gene Amplification ? And it’s disease

A

Example: NMYC gene in Neuroblastoma

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11
Q

…….is a state of number of chromosomes that is multiple of the
haploid state

A

Euploidy

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12
Q

……….is a state of number of chromosomes that is not a
multiple of the haploid state.

A

Aneuploidy

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13
Q

Aneuploidy occurs mainly from errors in……… when chromosomes separate
into two sides by the mitotic spindle.

A

mitosis

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14
Q

Aneuploidy tends to [increase/decrease] the copy number of oncogenes and
[increase /decrease] the copy number of tumor suppressor genes.

A

1-increase

2-decrease

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15
Q

Example of Aneuploidy ?

A

Loss of chromosome 17 results in loss of TP53 gene, an important tumor suppressor gene.

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16
Q

Loss of chromosome 17 results in loss of…….. an important
tumor suppressor gene.

A

TP53 gene

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17
Q

epigenetic changes include …….

A

The structure around the DNA
include DNA methylation and histone modification
And histone acetylation or deacetylation

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18
Q

(…………….) is overexpressed in most carcinomas of the lung and
head and neck

A

ERBB1 (or EGFR)

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19
Q

(………..) is overexpressed in 20% of breast cancer, due to
gene amplification

A

ERBB2 (or HER2)

Hb

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20
Q

HER2 in which cancer ?

A

breast cancer

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21
Q

ERBB1 (or EGFR) in which cancer ?

A

lung and head and neck

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22
Q

Types of genetic lesions include in the in the growth factor receptor is :

  1. Gene Mutations (Point mutations)
  2. Gene Rearrangements
  3. Gene Deletions
  4. Gene Amplification
  5. Aneuploidy
  6. Lesions affecting MicroRNA
A

4

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23
Q

Which drug can help us to block HER2 for breast cancer?

A

anti-HER2 antibodies (Trustuzumab)

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24
Q

What are the two enabling characteristics that can accelerate the acquisition of genetic and epigenetic alterations responsible for this 8 hallmarks ?

A
  1. Genomic Instability
  2. Tumor-promoting inflammation
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25
Q

………………… are Alterations in genes that regulate some or all of these cellular
functions are seen in every cancer.

A

Hallmarks of Cancer

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26
Q

How I am ?

………..hallmark originates from gain-of-function mutations that
converts proto-oncogenes to oncogenes.

A

Self-Sufficiency in growth signals

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27
Q

What are the functions of Oncoproteins ?

A

promote (cell growth )and (proliferation), even in the
absence of normal growth-promoting signals.

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28
Q

protein product of oncogenes is known as…….
Or which protein is converts proto-oncogenes to oncogenes……..

A

oncoproteins.

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29
Q

In the inactive state, RAS is bound to (GTP /GDP)

A

GDP

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30
Q

When a growth factor binds with
the receptor, it leads to activation of
………..by………… of GDP to
become…………

A

RAS

phosphorylation

GTP

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31
Q

In the active state, RAS is bound to (GTP /GDP)

A

GTP

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32
Q

Activated RAS-GTP activates several
downstream signaling proteins in
growth pathways leading to
….………….of genes responsible for cell growth

A

transcription

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33
Q

Why the activation of RAS-GTP is short-lived ?

A

because RAS has an intrinsic GTPase activity

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34
Q

What is the function of intrinsic GTPase activity?

A

GTP——>GDP

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35
Q

Where we can found the intrinsic GTPase activity?

A

In the RAS

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36
Q

Downstream Signal Transducing Proteins examples include :

4 example

A

include: RAS, NF1, BRAF, and ABL.
• RAS is the most commonly mutated oncogene in human cancers
(around 30% of cancers).

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37
Q

Mutations in RAS usually affect which region ?

A

The region which is response for GTPase activity

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38
Q

Explain for me what will happen if the region of GTPase activity is mutated?

A

GTP—❌—> GDP

causing it to be continuously
activated and leading the cell to
continuously proliferate. ( cancer)

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39
Q

Which protein is responsible for stimulation of the GTPase activity of RAS to prevent its continuous activity?

A

GTPase-Activating Proteins

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40
Q

When there is a mutation in GTPase-Activating Proteins what will happen to

A

1- Loss of GTPase activity,
2- GTP—❌—> GDP
3- resulting in continuous activation of RAS and continuous signalling for cell proliferation.

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41
Q

An example of a GAP (GTPase-Activating Protein) is :

A

Neurofibromin (NF-1)

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42
Q

What is the type of Neurofibromin (NF-1) of gene cancer ?

A

tumor suppressor gene

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43
Q

Transcription factors are………. present in the…… and are
responsible for…….. of genes that drive cell…..

A

proteins

nucleus

transcription

growth

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44
Q

What is the example of Nuclear Transcription Factors ?

A

MYC

Transcription يعني نسخ

كأني اقول انسخ ماي سيدي

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45
Q

Binding of which two proteins to leads to progression of the cell cycle ?

A

cyclin and a CDK

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46
Q

…………. silence CDKs and inhibit progression of cell cycle.

A

CDK inhibitors (CDKI)

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47
Q

In the Cyclins & Cyclin-Dependent Kinases (CDKs) mutation what happen?

gain-of function mutations or loss-of function mutations

A

gain

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48
Q

In the CDK inhibitors (CDKI) mutation what happen?

gain-of function mutations or loss-of function mutations

A

Loss

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49
Q

.……………are the most commonly mutated genes in this
group and occur in many types of cancers. These are responsible for
the G1/S checkpoint

A

Cyclin D and CDK4

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50
Q

What is the commonly mutated genes in the Cyclins & Cyclin-Dependent Kinases (CDKs)?

A

Cyclin D and CDK4

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51
Q

Also, loss-of function mutations in CDKI is a common occurrence in
many cancers Examples include……….

A

CDKN2A (p16) loss

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52
Q

…….occurs in many tumors such as pancreatic cancer

A

CDKN2A ( p16)

53
Q

Genes considered dominant ?

A

Oncogenes

because mutation of one allele is sufficient to produce the oncogenic effect.

54
Q

genes that normally prevent uncontrolled growth.

A

Tumor Suppressor Genes (TSGs)

55
Q

Genes that considered recessive……..

A

Tumor Suppressor Genes (TSGs)

56
Q

Genes that protect against apoptosis are often overexpressed in……..cells.

A

cancer

57
Q

• Point mutations that convert proto-oncogenes to oncogenes are
activating/ inactiving mutations. (Example: genes)

A

Activaing

RAS

58
Q

Point mutations in tumor suppressor genes………..or……. the function
of the protein products, and are therefore activating/inactivating mutations.
(Example: TP53 gene)

A

reduce or disable

inactivating

59
Q

Gene Rearrangements include two mechanisms :

A
  1. Overexpression of proto-oncogenes
  2. Creation of novel fusion proteins
60
Q

Gene Rearrangements include two mechanisms :

A
  1. Overexpression of proto-oncogenes
  2. Creation of novel fusion proteins
61
Q

Gene Rearrangements include two mechanisms :

A
  1. Overexpression of proto-oncogenes
  2. Creation of novel fusion proteins
62
Q

cancer gene is present at the.…….site, in the Gene Rearrangements

A

breakpoint

63
Q

MYC gene (chromosome 8) is proto-oncogene or in tumor suppressor

A

proto-oncogene

64
Q

RAS is proto-oncogene or in tumor suppressor

A

proto-oncogene

65
Q

TP53 gene is proto-oncogene or in tumor suppressor

A

tumor suppressor

66
Q

Amplification leads to……… of the protein product of a gene.
• In cancer, this mainly affects proto-oncogenes and converts them into……..

A

overexpression

oncogenes

67
Q

Amplification leads to……… of the protein product of a gene.
• In cancer, this mainly affects proto-oncogenes and converts them into……..

A

overexpression

oncogenes

68
Q

is a state of number of chromosomes that is multiple of the
haploid state (23 chromosome in humans)

A

Euploidy

69
Q

Epigenetic Modifications and cancer include.……

A

These include DNA methylation and histone modification.

70
Q

The full name of PDGF (Growth Factor) is

A

platelet derived growth factor

71
Q

1-…………These are responsible for the G1/S checkpoint
2-…………protein is to regulate the G1/S checkpoint of the cell cycle

A

1-Cyclin D and CDK4
2-RB

72
Q

Loss of chromosome 17 results in loss of TP53 gene, an important
tumor suppressor gene is which lesion:

  1. Gene Mutations (Point mutations)
  2. Gene Rearrangements
  3. Gene Deletions
  4. Gene Amplification
  5. Aneuploidy
  6. Lesions affecting MicroRNA
A

5

73
Q

What are the pathways of apoptosis?

A
  1. Intrinsic
  2. Extrinsic
74
Q

…………….. is a mechanism whereby the cells activate enzymes that degrade its own DNA and cellular content, followed by cell fragmentation into small apoptotic bodies.

A

Apoptosis

75
Q

……….. : external factors (outside the cell) initiating apoptosis

Examples : …………….
A

1- Extrinsic pathway of apoptosis

Example through death receptors

76
Q

………. internal stressors initiate apoptosis
example : ……………………………………………….

A

Intrinsic pathway of apoptosis

such as DNA damage or loss of growth factors

77
Q

In normal condition, when we have cell damage and we want the cell to undergo apoptosis:
1. pro- apoptotic proteins are ……..
2. Anti- apoptotic proteins are …….

A

activated

inactivated

78
Q

In cancer What happen for genes in the Apoptosis?
In cancerous cell, they don’t want for a damaged cell to die, in order for this cell to survive:
1. pro- apoptotic proteins are …………
2. Anti- apoptotic proteins are ………….

A

inactivated

activated

79
Q

What are the categories of regulatory proteins of apoptosis ?

A
  1. Pro-apoptotic proteins
  2. Anti-apoptotic proteins
80
Q

How to cancer cells evade apoptosis?

A

This happens through (acquired mutations) that (disable key components) of the intrinsic pathway of apoptosis.

81
Q

Example of Pro-apoptotic proteins? باااااااااا

A
  • BAX
  • BAK
    كأنهم متحمسييييين للأكل باااااااااكل (Ba)
82
Q

Example of Anti-apoptotic proteins ?

A

Bcl2

هذا عطاء وياها صريحة قال بكل٢ وهو أصلًا ضد التدمير و الاكل

83
Q

Examples of key molecules that control the intrinsic pathway of apoptosis include……….

A

BCL2
BAK
Bad

84
Q
  • P53 can also initiate apoptosis,how ?
A

By activation of BAX and BAK
- If P53 is mutated it can not initiate apoptosis

Or when the DNA repair is failed

85
Q

MDM2 is an inhibitor of……..

A

p53

86
Q

MDM2 [amplification] leads to loss of P53 function

A

ابغاش تركزي على Amplification

87
Q

Examples of mechanisms of Evasion of Apoptosis ?

A

1-MDM2 amplification (MDM2 is an inhibitor of p53).
2- Loss of p53 function (p53 triggers apoptosis in case of failed DNA repair).
3- Overexpression of BCL2, such as in follicular lymphoma through t(14:18)

88
Q

The release of cytochrome C triggers………

A

apoptosis

89
Q

Which of these proteins increase mitochondrial membrane permeability ?

1-BAX
2-BAK
3- Bcl2

A

1 + 2

90
Q

increase mitochondrial membrane permeability lead to ……..

A

cytochrome c leaves the mitochondria

91
Q

Overexpression of BCL2 lead to which disease?

A

follicular lymphoma

92
Q

………………. is when a cell can not divide any more

A

Senescence

93
Q

Senescence occurs because of progressive shortening of………… with each cell division.

A

telomeres

94
Q

……………….are sequences of DNA present at the ends of chromosomes that protect the chromosomes from degradation

A

Telomeres

95
Q

How do cancer cells avoid senescence & acquire limitless replicative capacity?

A

activation of an enzyme known as Telomerase

96
Q

What is the telomerase function ?

A

Telomerase prevents shortening of telomeres with successive cell divisions

97
Q

A tumour cannot enlarge beyond 1 or 2 mm in diameter unless it has the capacity to………….

A

induce angiogenesis.

98
Q

In normal case the angiogenesis is controlled through a balance between angiogenesis promoters and inhibitors.
• In tumors, the balance is skewed in favor of what …….? promoters or inhibitors

A

promoters

99
Q

How does the tumor acquire the capacity of Sustained Angiogenesis?

This occurs through increased / decreased production of angiogenic factors and
increased / decreased of angiogenic inhibitors,

A

increased

decreased

100
Q

One of the most common mechanism is production of pro angiogenetic factor is ……… give me the full name

A

VEGF (Vascular endothelial growth factor) an
angiogenic factor which is overexpressed in many cancers

101
Q

commonly in tumors you can find hemorrhage and accumulation of blood inside the tumor (why?)

A

Tumor blood vessels are not entirely normal, They are leaky and not well-formed

102
Q

How can we recognise unusual and haphazard appearances of the tumour?

A

We can recognized the appearances by using (Angiograms).

Angiograms is imaging techniques that target blood vessels

103
Q

…………are the major causes of cancer-related morbidity and mortality.

A

Invasion & metastasis

104
Q

Invasion & Metastasis are result from complex interactions between
1- ……………
2-…………….
3-…………….

A

1-cancer cells,
2-stromal cells,
3-extracellular matrix (ECM)

105
Q

The process of Invasion & Metastasis can be subdivided into 2 major phases:

A

• Invasion of the Extracellular matrix.
• Vascular dissemination and homing of tumor cells to distant sites.

106
Q
  • Tumor cells are the parenchyma/stroma
  • Surrounding tissues are the parenchyma/stroma
A

parenchyma

stroma

107
Q

There are 2 types of extracellular matrix:.
1-
2-

A

1-Basement membranes of epithelia
2- interstitial connective tissue

108
Q

In their normal state, the majority of cancer genes have functions related to………,,……….., and…………

A

cell growth

cell division

cell survival

109
Q

Types of Cancer Genes

A
  1. Oncogenes
  2. Tumor suppressor genes
  3. Genes that regulate apoptosis
  4. Genes that regulate interaction between tumor cells and host cells

An additional class is: DNA repair genes

110
Q

Examples of Point Mutations :

A

1-Point mutations that convert proto-oncogenes to oncogenes are
activating mutations. (Example: RAS genes)

2• Point mutations in tumor suppressor genes reduce or disable the
function of the protein products, and are therefore inactivating
mutations. (Example: TP53 gene)

111
Q

Examples of Point Mutations :

A

1-Point mutations that convert proto-oncogenes to oncogenes are
activating mutations. (Example: RAS genes)

2• Point mutations in tumor suppressor genes reduce or disable the
function of the protein products, and are therefore inactivating
mutations. (Example: TP53 gene)

112
Q

Examples of Point Mutations :

A

1-Point mutations that convert proto-oncogenes to oncogenes are
activating mutations. (Example: RAS genes)

2• Point mutations in tumor suppressor genes reduce or disable the
function of the protein products, and are therefore inactivating
mutations. (Example: TP53 gene)

113
Q

Gene rearrangements result mainly from chromosomal ……………..

A

translocations

114
Q

A new gene is created at the site of the translocation by fusion of two
genes present at the breakpoint sites is …………

A

Creation of novel fusion proteins

115
Q

Rearrangements happened between chromosome 9 and 22 resulted in…….. &……… combination (fusion gene), which is a………….

A

BCR & ABL

tyrosine kinase protein

■ For treatment we give tyrosine kinase inhibitor

116
Q

In cancer Gene Amplification this mainly affects ………….. genes

A

(proto-oncogenes) and converts them into oncogenes.

117
Q

In cancer Gene Amplification this mainly affects ………….. genes

A

(proto-oncogenes) and converts them into oncogenes.

118
Q

Two Example of Amplification :
1…….
2……

A

1- NMYC gene in Neuroblastoma
2- liposarcoma with MDM2 gene amplification.

119
Q

Example of Growth Factors :

A

Glioblastoma (A brain tumor) can produce its own growth factor
✨(PDGF) ✨for which it has a receptor.

120
Q

The majority of growth factor receptors function as…………….

A

oncoproteins when they are mutated or overexpressed.

121
Q

Examples of Growth Factor Receptors:

A

Examples: Epidermal growth factor receptor (EGFR) family members
• ERBB1 (or EGFR) is overexpressed in most carcinomas of the lung and head and neck.
• ERBB2 (or HER2) is overexpressed in 20% of breast cancer, due to gene amplification.

122
Q

Examples of Growth Factor Receptors:

A

Examples: Epidermal growth factor receptor (EGFR) family members
• ERBB1 (or EGFR) is overexpressed in most carcinomas of the lung and head and neck.
• ERBB2 (or HER2) is overexpressed in 20% of breast cancer, due to gene amplification.

123
Q

Examples of Growth Factor Receptors:

A

Examples: Epidermal growth factor receptor (EGFR) family members
• ERBB1 (or EGFR) is overexpressed in most carcinomas of the lung and head and neck.
• ERBB2 (or HER2) is overexpressed in 20% of breast cancer, due to gene amplification.

124
Q

An example of GTPase-Activating Proteins is :

A

is Neurofibromin (NF-1).

125
Q

………….is mutated in majority of melanomas and in many thyroid cancers.

A

BRAF

126
Q

Mutation of BRAF leads to …………..of the signaling pathway

A

continuous activation

127
Q

BRAF is a signal transducing protein in the……….

A

MAP Kinase pathway

128
Q

Binding of a cyclin to a CDK leads to
Stop / progression of the cell cycle.

A

progression

Third Year 🔗 (7 decks)

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