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PathoPhys > Lecture 4 - Cancer > Flashcards

Lecture 4 - Cancer Flashcards

1
Q

Most common types of cancer in males (Aus)?

A
  1. prostate
  2. colorectal
  3. melanoma
  4. lung
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2
Q

Most common types of cancer in females (Aus)?

A
  1. breast
  2. colorectal
  3. melanoma
  4. lung
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3
Q

~how many cases of cancer annually, worldwide?

A

> 14 million

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4
Q

~how many people die of cancer annually, worldwide?

A

8.2 million

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5
Q

~how many people living with cancer in the world today?

A

21 million

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6
Q

describe the difference between cancer and neoplasia?

A

neoplasia = ‘new growth’, these new growths may be benign or malignant. Cancer implies malignancy, so cancer is a type of neoplasm

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7
Q

define neoplasia?

A
  • disorder of cell growth leading to excessive proliferation of a single cell and its clonal progeny
  • occurs independently of physiologic growth-regulatory stimuli
  • may be benign or malignant
  • due to a series of acquired mutations
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8
Q

explain the 3 key characteristics of a neoplastic growth?

A
  1. Unregulated by normal physiologic mechanisms
  2. Irreversible
  3. Monoclonal (arises from singular abnormal cell)
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9
Q

A neoplasm is colloquially known as?

A

A tumor

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10
Q

State the principle fighter of a bacterial infection in the human body?

A

Neutrophils

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11
Q

What is the fundamental difference between a cancer cell, and a normal cell?

A

Normal cells send, receive and interpret signals which solve as SOCIAL CONTROLS: cells behave responsibly with resting, dividing, dying etc.

Cancer cells do not abide by social controls, they divide without normal constraints and invade territories belonging to other cells

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12
Q

why do cancer cells divide so uncontrollably?

A

due to a mutation in the neoplastic cells giving them a survival and growth advantage

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13
Q

t/f: cancerous growths are always homogenous (all same type of cancer)

A

false - often heterogenous, this is why chemotherapy isn’t always effective and immunotherapy is a better approach

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14
Q

t/f: cancer can be caused by a singular mutation

A

false - needs to be a series of mutations, not just one

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15
Q

define hyperplasia?

A

increased proliferation of cells which is ‘occurring normally’ (observing social controls)

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16
Q

compare or contrast hyperplasia and neoplasia?

A

Main difference = neoplasia involves mutated cell, hyperplasia involves non-mutated cell

  • in hyperplasia growth occurrs normally (social controls) whereas in neoplasia it is abnormal
  • hyperplasia is reversible whereas neoplasia is not
  • neoplasia originates from a single cell, whereas hyperplasia may originate from one or many cells
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17
Q

describe whats meant by the ‘degree of differentiation’ of tumor cells?

A

the extent to which the tumor cells resemble the normal tissue of origin, structurally and functionally

well differentiated= close resemblance to tissue of origin, likely benign

poorly differentiated= minimal resemblance to tissue of origin, likely malignant

(note: normal healthy tissue contains a variety of healthy cells, so the normal cells are well differentiated into their roles, whereas cancerous cells aren’t differentiated into their roles)

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18
Q

explain what’s meant by an ‘anaplastic’ tumor?

A

The worst!
One which is poorly differentiated - so it doesn’t resemble the tissue of origin to the point where it cannot be determined what the tissue of origin is, and is likely malignant

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19
Q

if a tumour is well differentiated, what does this mean in terms of its appearance and apparent threat level?

A

it appears normal - same as original tissue, likely benign

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20
Q

if a tumor is poorly differentiated, what does this mean in terms of its structure and apparent threat level?

A

it appears different to original tissue from which it came, the cells are poorly differentiated meaning they haven’t taken up their normal roles - this is likely a malignant tumor

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21
Q

All neoplasms have 2 components - what are they?

A
  1. Parenchyma - proliferating cells of the tumor, defines the behavior
  2. Supportive stroma - CT, BV, framework from which parenchyma grows

(note: this doesn’t only apply to tumors - parenchyma always means function portion of tissue etc)

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22
Q

Contrast features of benign and malignant neoplasms?

A
  1. benign margins are well defined, malignant are poorly defined and locally invasive
  2. benign growths don’t invade surrounding tissue whereas malignant does, destroying it and spreading (metastasizing)
  3. benign prognosis good (death unlikely), malignant is poor
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23
Q

t/f: benign tumors do not have major abnormalities in the regulation of growth

A

true

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24
Q

t/f: benign tumors grow locally and rapidly

A

false - locally and slowly

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25
can benign tumors cause significant clinical symptoms?
yes - ie. thru compression of adjacent structures (meningioma)
26
can benign tumors be fatal?
yes
27
how can benign tumors affect hormone levels?
tumor within endocrine cells --> excessive levels of hormone secretion
28
t/f: malignant tumors are always poorly differentiated (ie. do not resemble tissue of origin)`
false - malignant tumours can be well differentiated, however they are often poorly differentiated
29
the spread of malignant neoplasms is also known as?
metastasis
30
Describe the mechanisms of metastasis?
1. Direct invasion (into adjacent organs or thru nerves) 2. Spead by lymphatics (to lymph nodes) 3. Haematogenous spread (by blood to distant sites such as liver, lungs, brain, bones, adrenal) 4. Transceolomic spread (abdominal cavity tumors which spread directly across peritoneal spaces by seeding cells which migrate to the surfaces of other organs) note: 4 is technically not considered metastasis
31
what're the most common mechanisms of metastasis?
lymphatic spread & haematogenous
32
t/f: some tumors show a mix of benign and malignant characteristics, and are difficult to classify accordingly
true
33
Basal cell carcinoma: a. ) Risk of metastasis? b. ) Cured by? c. ) If not completely excised, likely activity?
a. ) <0.1% b. ) simple excision c. ) becomes highly invasive and locally destructive
34
A categorically malignant tumor is one which has all 3 malignant qualities of a cancer - what are they?
1. Unlimitied/ uncontrolled growth 2. Invasion of surrounding tissue (direct invasion) 3. Potential for distant spread (metastasis) (note: think of cancer qualities as the things determining cancer movements, this IS different to the 3 characteristics of a neoplasm)
35
A 'categorically benign tumor' is defined as?
lacking all 3 qualities of a categorically malignant tumor (growth, metastasis, invasion)
36
What are tumors which possess 1 or 2 of the 3 qualities of a benign tumor?
May be classified as either malignant or benign depending, often disagreement occurs
37
Breast fibroadenoma: a. ) Growth unlimited? b. ) Invasion? c. ) Metastasis?
No to all 3; categorically benign
38
Breast carcinoma: a. ) Growth unlimited? b. ) Invasion? c. ) Metastasis?
Yes to all 3; categorically malignant
39
Colonic polyp (tubular adenoma): a. ) Growth unlimited? b. ) Invasion? c. ) Metastasis?
a. ) Growth unlimited b. ) Invasion occurrs c. ) No metastasis classified as benign!
40
explain suffix -oma?
benign neoplasm | ie. gland with benign neoplasm becomes adenoma
41
explain suffix -carcinoma?
malignant neoplasm of epithelial tissue (ie. gland with malignant neoplasm becomes adenocarcinoma)
42
explain suffix -sarcoma?
malignant tumor of mesenchymal tissue (CT, muscle, vessels) ie. fibroblasts -> fibrosarcoma, lipocytes -> liposarcoma
43
non-epithelial and non-mesenchymal malignant neoplasms have their own terminology. Explain the terminology for a malignant neoplasm of the blood/ bone marrow?
leukaemia
44
non-epithelial and non-mesenchymal malignant neoplasms have their own terminology. Explain the terminology for a malignant neoplasm of the lymphoid cells (lymph nodes)?
Lymphoma
45
non-epithelial and non-mesenchymal malignant neoplasms have their own terminology. Explain the terminology for a malignant neoplasm of the melanocytes?
melanoma
46
non-epithelial and non-mesenchymal malignant neoplasms have their own terminology. Explain the terminology for a malignant neoplasm of the mesothelial cells?
mesothelioma
47
carcinogenesis AKA?
oncogenesis, tumorigenesis
48
define carcinogenesis
formation of cancer by transformation of normal cells
49
carcinogenesis is a (multi/ uni) step process
multi
50
development of cancer requires accumulation of (multiple/ a singular) mutation(s)
multiple mutations required for cancer, it is a multistep genetic disease which arises from a single abnormal cell
51
State the 7 fundamental changes in cancer cell physiology?
"If she gets cancer the GAL DIES" G - Genomic instability A - Ability to invade/ metastasis L - Limitless replicative potential D - Development sustained angiogenesis I - Insensitivity to growth inhibitory signals E - Evasion apoptosis S - Self sufficiency in growth signals
52
why is genomic instability associated with cancer cell physiology?
genomic instability results from defects in DNA repair
53
how do mutations which cause cancer aid the cancer cells in survival or growth?
mutation allows for production of growth signal from within the cell - usually growth signals are sent from cells surrounding, but cancerous cell makes it for itself
54
state the main growth factors?
``` VEGF EGF FGF PDGF TGF-B ```
55
what cells generally produce growth factors?
macrophages and platelets
56
state the main actions of growth factors?
"growth factors are FASIC" F - fibroblast migration and proliferation A - angiogenesis S - stimulate epithelial proliferation I - increase synthesis extracellular collagen C - chemotaxis (attracting more macrophages)
57
how do growth factors act (mainly)?
1. binding to growth factor receptors 2. stepwise activation of intracellular transcription factors 3. transcription of genes for proliferation
58
state the most important intracellular pathway involves with proliferation, which is stimulated by growth factors?
RAS/ RAF cascade
59
why do genetic mutations cause uncontrollable growth?
because they initiate the process of proliferation without the need for growth factor from other cell being present - some part of the cascade can be switched on indefinitely leading to uncontrolled growth
60
which part(s) of the intracellular pathway associated with proliferation can become 'switched on' permanently, in cancerous cells?
Remember cancer occurs due to a 'series of mutations', so a mutation can occur in... 1. receptor 2. RAS 3. RAF then even when drug inhibits the activation at one point (say it turns off the RAS), cancerous cell still is able to proliferate
61
growth factor receptor alterations account for mutations in what pathologies?
10% of non-small cell lung cancer (EGFR)
62
RAS mutations account for what pathologies?
90% pancreatic cancers 50% colon cancers 30% non-small cell lung cancers
63
RAF mutations account for what pathologies?
70% melanoma | 50% papillary thyroid cancers
64
define a proto-oncogene
a normal gene which when altered (by mutation) promotes autonomous growth
65
examples of structures made by proto-oncogenes?
growth factor receptors, RAF, RAS
66
define an oncogene
mutated proto-oncogene (it has become activated and starts producing protein)
67
define oncoprotein
the protein produced by oncogene
68
generally speaking, oncogenes and their oncoproteins produced cause ____
CANCER duhhh
69
How is it oncoproteins can come about WITHOUT any mutation?
Can be due to overexpression of normal gene (proto-oncogene). For example, in 20% of breast cancer EGFR (growth factor receptor) is overexpressed. This means that even tiny amounts of growth factor causes proliferation of tissue. Thus, when overexpressed, EGFR is classified as an oncoprotein.
70
Alterations to normal EGFR relating to overexpression are the cause of 2 important pathologies - state these?
20% breast cancers | 80% oesophageal adenocarcinomas
71
what does EGFR mean?
Epidermal growth factor receptor
72
t/f: in a tumor the cell cycle is effectively always on
true
73
Growth inhibition of cancerous cells involves ____ of cells from the cell cycle
removal
74
Explain how the cell cycle is involved in DNA monitoring?
- cell cycle involves various 'checkpoints' - at these checkpoints DNA is analysed, looking if damage exists (such as proto-oncogene mutations) - if too much damage exists in DNA the cell cycle halts; a safety mechanism
75
state the 2 'checkpoints' of the cell cycle, as well as what influences them?
1. p53 --> cell size, DNA damage, DNA replication | 2. RB --> cell size, DNA damage, nutrients & growth factors
76
what are the 'checkpoints' of the cell cycle, physically?
tumor suppressor genes
77
state the gene which is "guardian of the genome"?
p53
78
In what scenario may p53 and RB genes be mutated?
cancer
79
p53 mutations are present in __% of cancers
70%
80
cells with defective DNA (beyond repair) are marked for apoptosis by which gene?
p53
81
how is it apoptosis can be evaded by cancerous cells?
p53 mutated, so it cannot mark defective cell
82
most cells have capacity for ____ doublings
60-70
83
after 60-70 doublings, most cells _____
senescence (leave growth cycle)
84
what controls the amount of doublings (replication) a cell can undergo?
Telomeres: Telemeres are present at the end of chromosomes. Every time a cell divides, the telomere shortens. p53 and RB recognise telomere shortening, and induce senescence to the cell if its telomeres are too short
85
How are the telomeres of stem cells different to those of normal cells?
Stem cells possess the telomere repair enzyme telomerase. Thus, the telomeres of stem cells don't shorten
86
How do cancerous cells have 'limitless replicative potential'?
Lots of telomerase so telomeres don't shorten!
87
define senescence
leaving the growth cell cycle
88
t/f: senescent cells can produce molecules which promote the growth of cancer cells
true - this is possibly why older people get more cancer, as oldies have more senescent cells
89
how do tumours stimulate growth of their own blood supply (angiogenesis)?
tumor releases VEGF
90
t/f: VEGF promoters are now approved for treatment of some cancers
false - VEGF inhibitors are approved for treatment of some cancers, as this prevents the tumor from developing sustained angiogenesis
91
Metastasis has 2 phases with regard to tumor growth - explain their steps?
1. Invasion extracellular matrix - proteolysis, migration, adhesion - tumor cells pass through epithelial layer 2. Vascular dissemination and homing of tumor cells - intravasation (invasion BV) - interaction with immune cells, avoid destruction - form tumor embolus - extravasation - metastatic deposit - angiogenesis and growth
92
prediction of metastases site - where likely?
1. regional lymph nodes: from breast carcinoma to axillary lymph nodes 2. distant metastases based on anatomical relationships: gastrointestinal tumor goes to liver 3. non-anatomical tumor specific metastatic patterns: carcinoma prone to bone metastases
93
t/f: some individuals inherit defective copies of genes and are at higher risk of cancer
true
94
t/f: there are no specific genes involved in the repair of DNA damage from mutagens
false - there is
95
examples of genes involved in DNA repair?
BRCA1 and BRCA2, if these defective increased risk of ovarian or breast cancer
96
clinical aggressiveness of tumor largely related to ____?
rate of growth
97
why do faster dividing tumors invade and metastasize earlier?
as they develop genetic alterations faster
98
what determines rate of growth?
1. doubling times of tumor 2. growth fraction (how many tumor cells in growth cycle) 3. rate at which tumor cells lost 4. adequate vascular supply
99
define doubling time
time taken for doubling in cell numbers within neoplasm
100
is doubling time constant
no
101
conventional chemotherapy only targets tumor cells which...
are in the growth fraction
102
t/f: the more aggressive a tumor is, the larger the growth fraction, and the less responsive tumor is to chemotherapy
false - the more aggressive a tumor is, the larger the growth fraction, and the MORE responsive tumor is to chemotherapy

PathoPhys (25 decks)

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