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FunMed Cancer > What is cancer > Flashcards

What is cancer Flashcards

1
Q

define cancer

A
  • An abnormal growth of cells which tend to multiply in an uncontrolled way and in some cases to metastasize(spread), common term for all malignant tumours
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2
Q

how is cancer caused simply

A
  • In general, there is a balance between cell division and cell death but in cancer cell divide in uncontrolled way which results in an imbalance between cell division and cell death
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3
Q

Neoplasm

A
  • An abnormal growth of cells or tissue, specifically one in which cell multiplication is uncontrolled and progressive. Neoplasms may be benign or malignant. This is irreversible.
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4
Q

what is a tumour

A
  • An abnormal mass of tissue which grows in an uncontrolled and uncoordinated manner, it may be benign, malignant or pre-cancerous
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5
Q

what are neoplastic cells

A
  • have lost control of normal processes such as growth and once a neoplasm has started, it is not reversible
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6
Q

what is a mutation

A

an abnormal change in a gene

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7
Q

what is oncology

A

the study of tumours or neoplasia

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8
Q

what is benign

A
  • a group of cells with abnormal growth which grow locally and do not disseminate to other parts of the body to metastasize
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9
Q

what is malignant

A
  • a group of cells with abnormal growth that show characteristics of invasion of other tissues and the ability to spread to distant sites within the body tumours
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10
Q

what is metastasis

A

involves the spread of cancer cells from the primary tumour to surrounding tissues and to distant organs

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11
Q

what is carcinogens

A
  • a multistep process of transformation of a normal cell to a cancer cell.
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12
Q

what is transformation

A
  • the conversion of one cell phenotype to another.
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13
Q

what is carcinogen

A
  • an agent (chemical, radiation or microbial*) that induces changes to a cell population that can cause cancer, these include tobacco and asbestos
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14
Q

what is a carcinoma

A
  • cancer arising from the epithelium of the skin or internal tissue lining organs such as the liver or kidneys(epithelial neoplasia).
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15
Q

what is differentiation

A

the process by which a cell develops or matures which allows it to perform a specific function.

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16
Q

what is histogenesis

A
  • The formation of new tissue from undifferentiated cells (i.e. the three germ layers; mesoderm, ectoderm and endoderm)
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17
Q

what are the three germ layers

A

ectoderm
mesoderm
endoderm

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18
Q

where is the ectoderm found

A

central nervous system(brain and spinal cord) the peripheral nervous system, the sensory epithelia of the eye, ear and nose, the epidermis and its appendages(the nails and hair); the mammary glands the hypophysis; the subcutaneous lands and enamel of the teeth

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19
Q

where is the mesoderm found

A

connective tissue, cartilage, and bone; striated and smooth muscles; the heart walls, blood and lymph vessels and cells; the kidneys; the gonads (ovaries and testes) and genital ducts; the serous membranes lining the body cavities; the spleen; and the suprarenal (adrenal) cortices

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20
Q

where is the endoderm found

A

 epithelial lining of the gastrointestinal and respiratory tracts; the parenchyma of the tonsils, the liver, the thymus, the thyroid, the parathyroids, and the pancreas; the epithelial lining of the urinary bladder and urethra; and the epithelial lining of the tympanic cavity, tympanic antrum, and auditory tube

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21
Q

how many different type of cancers are there

A

200 different types

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22
Q

how is cancer characterised

A
  • Characterised by unregulated growth of malignant tumours
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23
Q

what can localised cancers do

A
  • Invade into surrounding tissues

- Invade into surrounding tissues and metastasise or spread to other sites

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24
Q

what is cancer caused by

A

changes and mutations in DNA

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25
Q

describe the Multi hit idea

A
  • A number of mutations are required to generate a cancer multi-hit – this leads to carcinogenesis which is a multistep process that usually requires several mutations to initiate cancer
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26
Q

not all cancers are …

A

hereditary, most arise form sporadic mutations

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27
Q

what do proteases do in cancer

A

– break through the extracellular matrix, produce filopodia change in the biological character in order for them or metastasis and occur

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28
Q

where are solid cancers derived from

A
  • Solid cancers or haematological malignancies (derived from hematopoietic and lymphoid tissues)
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29
Q

what are the three types of tumours

A
  • Benign
  • Malignant
  • Pre-cancerous
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30
Q

whats the difference between begins and malignant

A
  • Rapidly dividing cells can form tumours, some cancers may spread(metastasise) into other tissues these are malignant
  • Benign tumours are not cancerous as they do not spread
  • Therefore this means that cancer is characterised by unregulated growth of malignant tumours
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31
Q

whats the difference between a primary and secondary tumour

A
  • Primary tumour is formed in the tissues it is the original tumour whereas the secondary tumour is the tumour that forms elsewhere after the primary tumour has formed
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32
Q

what are the common cancers in females

A
  • Breast 25 years +
  • Carcinomas in 15-24
  • Leukaemia’s and then brain tumours in children for both male and female
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33
Q

what are the common cancers in males

A
  • Prostate cancer most common in 50+
  • Testicular cancer in 25-49
  • Germ cell tumours in 15-24
  • Leukaemia and brain tumours in children
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34
Q

a poorly differentiated tumour is..

A

A poorly differentiated tumour is a more aggressive type of tumour

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35
Q

what do cancer cells do in regards to differentiation

A

Cancer cells dedifferentiate – they go back to being more stem cell like, they lose a lot there characteristics that they are required to make them a specific type of cell

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36
Q

what is a difference between normal cells and cancer cells

A
  • Normal cells need signals to survive – signals allow them to survive, divide, differentiate, apoptosis (cell don’t receive signal then apoptosis occurs)
  • Cancer cells can survive without them, they don’t need external growth signals that allow them to grow as the metastatic changes overrule the signals allow the cancer to grow in an uncontrolled way
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37
Q

what can immune inflammatory cells do in tumours

A
  • The immune inflammatory cells present in tumours can include both tumour-promoting as well as tumour-killing subclasses
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38
Q

describe the microenvironment of tissues

A
  • Complex tissues with a rich microenvironment (parenchyma and stroma) made up of several cell types
  • Tumour growth and progression is enabled by interaction between cancer cells, stroma and immune system
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39
Q

Why do the 6 hallmarks of cancer cause cancer

A
  • Most cancer cells require 6 essential cell alterations in cell physiologic that allow malignant growth to occur
  • These enable carcinogenesis, tumour growth and spread and allow the cell to survive and proliferate
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40
Q

what are the 6 hallmarks of cancer

A
  1. Self-sufficiency in growth signals – this means that growth signals are not required for cell survival growth and differentiation
  2. Insensitivity to growth inhibitory signals
  3. Evading apoptosis
  4. Limitless reproductive potential – normal cells undergo a certain number of replications then undergo apoptosis and die therefore cancer cells are immortal
  5. Sustained angiogenesis (blood vessel formation) is sustained and increased
  6. Tissue invasion and metastasis
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41
Q

describe how self sufficiency in growth signals work (6 hall marks of cancer)

A
  • Normal cells require mitogenic growth signals before they move from a quiescent state into an active proliferative state
  • Oncogenes in cancer mimic normal growth signalling and tumour cells generate their own growth signals this is a form of autocrine signalling which allows the tumour to grow faster
  • This means you lose regulation and cannot control cell division and growth
  • No dependent on external growth signals from other tissues and can grow and differentiate without them
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42
Q

describe sensitivity to inhibitor growth signals as a hallmark of cancer

A
  • In normal tissues anti proliferative signals cause cellular quiescence and tissue homeostasis (e.g. soluble growth inhibitors and immobilized inhibitors in the extracellular matrix and on cell membrane)
  • These growth inhibitory signals are received by transmembrane cell surface receptors coupled to intracellular signalling circuits
43
Q

describe how antigrowth signals can block proliferation (sensitivity to inhibitor growth signals 6 hallmarks of cancer)

A
  1. Cell may be forced out of the active proliferative cycle into G0
  2. Cells may be induced to permanently relinquish their proliferative potential by being induced to enter into post mitotic state associated with differentiation
44
Q

describe how invading apoptosis works as the 6 hallmarks of cancer

A

The ability of tumour cell populations to expand in number is determined not only by the rate of cell proliferation but also by the rate of cell attrition. Programmed cell death (apoptosis) — represents a major source of this attrition.

45
Q

describe how limitless replicative potential works as a 6 hall mark of cancer

A

Maintains telomers to prevent apoptosis and senescence

46
Q

what are the emerging hallmarks

A
  1. Modification of metabolism which help support the neoplastic proliferation (abnormal growth)
  2. Evade destruction by the immune system
47
Q

what are the enabling characrestics that lead to cancer

A
  1. Genomic instability promotes mutability and genetic alterations – more genetically unstable the more cancer cells that they make
  2. Inflammation by immune cells is now recognised to be tumour promoting
48
Q

what is the tumorigenic mechanism

A

Variable in cancer types and subtypes
This means that we may increase the number or decrease the number of steps required to complete tumorigenesis but you still end up with the same cell we can do this by changing
1. Order that mutations occur
2. Which mutations occur

49
Q

give examples of the tumorogenic mechanisms

A

Case 1 – p53 loss – angiogenesis and resistance to apoptosis and genetic instability
Case 2 – two or more genetic changes required for invasion/metastasis and resistance to apoptosis

50
Q

How does a tumour develop

A
  1. Uncontrolled growth of abnormal cells
  2. The abnormal cell keeps dividing
  3. Abnormal cells eventually join to form a tumour
  4. As the tumour becomes larger it impedes the function of a tissue or organ
  5. Unless tumour growth is stopped and removed the healthy organs are destroyed
51
Q

when does cancer occur

A
  • Mutation in stimulatory gene goes from a proto oncogene which is mutated and becomes an oncogene
  • Mutation in inhibitory genes – so genes repairing DNA mistakes are suppressed and this forms a tumour suppressor gene
52
Q

what is an oncogene

A

gene that encodes protein capable of inducing cancer, activated by gain of function

53
Q

what is a proto oncogene

A

a normal gene from which an oncogene is derived when mutated, it has the potential to transform a cell into a cancerous state – cacner results when activated GAIN OF FUNCTION

54
Q

What is a tumour suppressor genes

A

encode proteins in their normal state and negatively regulate proliferation, cancerous when there is a loss of function – cancer results when inactivated
LOSS OF FUNCTION

55
Q

what are the 3 main genes that mutate and cause cancer

A
  1. Oncogene
  2. Tumour suppressor gene
  3. DNA repair genes
56
Q

what does a proto oncogene normally do

A
  • Responsible for cell growth, cell division and motility

- They encode growth factors, growth factor receptors or signalling molecules

57
Q

what happens when there is a mutation in the proto oncogene

A
  • Mutations in a proto oncogene gene enhance the signalling pathway in an uncontrolled way leading to uncontrolled cell growth and reduced differentiation
  • it becomes an oncogene
58
Q

what doe a tumour suppressor gene normally do and what happens when it is mutated

A
  • Allow the cell to stop at the checkpoint in the cell cycle and allows DNA repair to occur,
  • If there is a mutation in this gene this means that the cell does not stop at the correct place in the cell cycle and DNA repair does not occur so the cell replicates with the mutation
59
Q

what are the 5 classes of porto oncogenes

A 
I.	Growth factors 
II.	Growth factor receptors  
III.	Signal-transduction proteins 
IV.	Transcription factors 
V.	Pro or anti-apoptotic proteins
60
Q

what do mutations in the 5 classes of proto oncogenes lead to

A

Mutations changing the structure or expression of proteins in classes I-V give rise to dominant active oncogenes leading to a gain on function
Genes are over expressed in cancer

61
Q

whats the difference between Growth factor (type I) and growth factor receptors (type II)

A

Class I (growth factors) and class II proteins (receptors)

62
Q

describe how growth factor a type I protein causes cancer

A

are not mutated by they are overexpressed leading to hyperplasia

63
Q

describe examples of growth factor type I protein causing cancer

A
  • VEGF – benign prostatic hyperplasia – vascular endothelial growth factor,
  • PDGF – glioblastoma - platelet derived growth factor
  • Elevated levels of TGF alpha have been demonstrated in oesophageal cancer – platelet derived growth factor
64
Q

describe how growth factor receptor type II protein causes cancer

A
  • These are overexpressed with unregulated dimerization and activation in the absence of growth signals, this means that activation is caused when the receptor does not have a growth factor molecule in it, leading to unregulated autocrine loops
65
Q

describe an example of growth factor type II protein causing cancer

A

overexpression of HER2 or ErbB2 – lead to invasive breast carcinoma

66
Q

what are the consequences of over expression in type II growth factor protein causing cancer

A
  1. Uncontrolled growth
  2. Survival of cells containing mutations
  3. Invasion of tumour cells
  4. Migration of tumour cells
67
Q

what is signal transduction (protein type III)

A
  • This is the process by which an extracellular signalling molecule activates a membrane receptor that in turn alters intracellular molecules creating a response
68
Q

How does signal transduction (protein type III) cause cancer

A

KRAS is the oncogene, Ras is the proto-oncogene
K-ras – ras Oncogene
- Ras small GTP binding molecule – signal transduction protein type III
1. Mutation in ras results in KRAS this leads to accumulation of active GTP bound state and excess growth signals to the nucleus
2. Leads to continuous proliferation by activation of MAP kinase pathway
- Common in lung, colorectal and pancreatic cancers

69
Q

where is KRAS found

A
  • Found in 15-25% of adenocarcinoma, have tumours associated with KRAS mutations
  • 30-50% of colorectal tumours are known to have a mutated KRAS gene
  • Greater than 95% pancreatic ductal adenocarcinomas have KRAS mutations
70
Q

What kind of cancer does EGFR overexpression cause

A
  • Colorectal cancer
  • Pancreatic cancer
  • Lung cancer
71
Q

What kind of cancer does the Ras mutation cause

A
  • Pancreatic cancer
  • Papillary thyroid cancer
  • Colon cancer
  • Non-small cell lung cancer
72
Q

What kind of caner does B-Raf mutation cause

A
  • Melanoma
  • Papillary thyroid cancer
  • Colon cancer
73
Q

What kind of cancer does the EGFR mutation cause

A
  • NSCLC

- Glioblastoma

74
Q

What is an example of transcript factors (type IV protein) causing cancer

A

c-YMC codes for the transcription factor MYC

75
Q

what does cYMC do

A

Promotes a set of changes that impact cell proliferation:

  • Growth and metabolism
  • DNA replication
  • Cell cycle progression
  • Cell adhesion
  • Differentiation
  • Metastasis
76
Q

What is the frequency of the c-YMC proto oncogene in cancers

A

is one of the most frequently activated oncogenes occurring in 50% of cancers
- Translocation also occurs in some cancers

77
Q

what does elevated levels of c-MYC lead to

A
  • Within cancer cells there is elevated expression of c-MYC this corresponds to bad prognosis as these cancers are highly aggressive and this leads to a more clinical outcome
78
Q

what kind of cancer does c-MYC lead to

A
  • C-MYC translation mutation occurs in some cancers – Burkitt lymphoma – this is cancer in the B cell
  • C-MYC overexpression occurs in breast cancer, colon and lung
79
Q

how does cYMC cancer work (type IV protein)

A

MYC. induces tumorigenesis by evading multiple tumour supressing checkpoints including proliferative arrest, apoptosis, and senescence
MYC overexpression on its own cannot cause tumorigenesis needs to have more than one mutation - this is because it only causes transformation in specific cell lines presumed to have already acquired other oncogenic events that rendered them permissive

80
Q

what are the Class V proteins (apoptotic and anti-apoptotic proteins

A

BAX -
BCL2
- these regulate apoptosis

81
Q

what is BCL2

A
  • BLC2 antiapoptotic – proto – oncogene
82
Q

what is BAX

A
  • BAX – tumour suppressor gene
83
Q

how does cancer develop from apoptotic and anti-apoptotic proteins (type V)

A
  • In the presence of excess BAX apoptosis occurs but in the presence of excess BCL2 the cell is immortalized
  • BAX induces apoptosis – P53 activates it and results in bax homodimers and induction of apoptosis
  • BCL2 blocks apoptosis from occurring – increased levels result from oncogene activation
84
Q

How does apoptosis work in normal cells

A
  • The two gene products are in balance and Bax/BCL2 heterodimers form, this prevents BAX/BAX homodimers from forming which promote apopotisis and the activation of BCL2 which promotes immortality
85
Q

How can some B cell lymphomas evade apoptosis

A
  • Some B cell lymphomas evade apoptosis by using the promoter of an immunoglobulin gene to drive expression of bcl-2 protein in the translocation
86
Q

what do tumour suppressor genes do

A
  • Tumour suppressor genes mainly act to block development of cancer, allows the cell to stop and carry on in the cell cycle
87
Q

How do tumour suppressor genes restrict cell life proliferation

A
  • Control the cell cycle and cell division

- Induce apoptosis when other mechanisms have failed

88
Q

what happens when tumour suppressor genes mutate

A
  • act recessively to release cells from growth control increasing the probability that the mutant cells will become tumour cells.
  • greatly increase the probability of mutations in the other classes.
  • may prevent apoptosis or allow cell division of cells which contain mutations.
89
Q

what does evading apoptosis allow the cancer cells to do

A
  • down regulation of pro-apoptotic signalling pathways (e.g. Bax)
  • allow cancer cells to survive even when challenged with chemotherapeutic or DNA damaging compounds that would normally trigger cytotoxic responses
90
Q

what do gatekeeper genes do

A
  • stop cell cycle progression hen DNA damage is detected
91
Q

what is p53

A

transcription facotr

92
Q

what is pRB

A

transcription inhibitor

93
Q

what are the gatekeeper genes

A

p53,
pRB
P53 - mutations in p53 genes are most common genetic alterations in human cancers

94
Q

when is p53 activated

A

DNA damage
hypoxia
cell injury

95
Q

what does p53 do

A
  • activates p21 – inhibits cyclin complexes and prevents cell leaving G1 and entering S-phase – this checkpoint is for cell cycle arrest for DNA repair or entry into apoptosic pthway
    • cell cycle arrest, allows DNA repair or entry to apoptotic pathway
96
Q

what does a mutation in p53 do

A
  • allows cells to progress through cell cycle with DNA damage, cell will accumulate mutations and cancerous through cycles of DNA damage and cell proliferation
97
Q

what are the caretaker genes

A
  • MMR - mismatch reapir genes

- BRAC1/2

98
Q

what do the caretaker genes do

A
  • repair DNA damage during cell cycle arrest in order to maintain genomic stability
99
Q

what is BRAC1 and BRAC 2 common in

A
  • familial breast and ovarian cancer
  • Responsible for 50% of inherited breast cancers
  • Maybe 70-80% of inherited ovarian cancers
  • carriers of mutant BRCA1 and BRAC2 alleles have a 50-70% risk of developing breast cancer before the age of 70
100
Q

what does BRAC1 normally do

A
  • Interacts with cyclins and CDKs triggerts the activation of CDK inhibitor, p21WAF-1 and p53 thus it can control the cell cycle
  • It is also involved in DNA repair
101
Q

what does BRAC2 normally do

A
  • Facilitate homologous recombination
102
Q

what does a mutant BRAC 2 do

A
  • Cell growth
  • Inhibition of apoptosis
  • Cell migration
  • Angiogenesis
  • Metastasis
103
Q

what are BRAC2 deficient cells do

A
  • BRAC2 deficient cells are defective in recruiting RAD51 ( a ssDNA (single stranded DNA) binding protein) to sites of DSBs and in repairing DSBs by HR
  • DSB – double strand breaks
104
Q

what do BRAC1 deficient cells lead to

A

genomic instability

FunMed Cancer (4 decks)

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