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Pathophysiology > Cancer > Flashcards

Flashcards in Cancer Deck (245)
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1
Q

What is cancer

A

is a class of diseases characterized by altered differentiation and uncontrolled division of cells, caused by an accumulation of genetic mutations

2
Q

What is the outcome of cancer?

A

a malignant growth that may develop to invade other tissues

3
Q

What does tumour mean?

A

literally means ‘swelling’

but primarily used to denote abnormal growth of tissue

4
Q

What does neoplasm mean?

A

abnormal disorganized growth in a tissue or organ usually forming a distinct mass (can be benign or malignant)

5
Q

What does cancer refer to (benign or malignant growths)?

A

malignant growths

6
Q

Neoplasms invade ___ the ______ _____.

A

past the basement membrane

7
Q

Define benign

A

If left untreated or with symptomatic therapy will not be life threatening

8
Q

Define malignant

A

a clinical course that progresses rapidly to death; typically applied to neoplasms that exhibit aggressive behaviour

9
Q

What is the local effect of neoplasms?

A
trivial to lethal
occupy space
OBSTRUCTS PASSAGES
compress healthy tissue
ulcerate and become infected
hemorrhage
10
Q

Common obstructions due to benign neoplasm are ________ and ____.

A

pulmonary and colon

11
Q

When there is a benign neoplasm what does its cells do?

A

preform normal function (often in excess) without responding to negative feedback; remain localized

12
Q

What is the local effect of malignant neoplasms?

A
trivial to lethal
occupy space
obstruct passages
compress healthy tissue
ulcerate and become infected
hemorrhage
- same as benign but…MORE AGRESSIVE (invade and destroy local tissue)
13
Q

What is metastasis?

A

the spread of cancer from one site to another

14
Q

How does the cancer metastasize to other organs?

A
  • blood
  • lymph
  • in a body cavity
15
Q

What criteria is met to be in each of the 5 stages of cancer?

A
  1. size
  2. depth
  3. invades adjacent organs
  4. if and how many lymph nodes effected
  5. spread to distant organs
16
Q

What does the stage indicate?

A

how much the cancer has spread

17
Q

What is the biggest predictor of survival?

A

the spread of the cancer

18
Q

What do malignant neoplasms tissue stop doing;and start doing?

A

stop differentiating, and begin reproducing rapidly

19
Q

What are the characteristics of a benign tumour?

A
  • usually encapsulated
  • no tissue invasion
  • no metastases
  • resemble normal tissue (differentiated)
  • normal nuclei
  • slow growth
  • no new blood vessels
  • little recurrence
  • rarely necrotic areas
20
Q

What are the characteristics of malignant tumours?

A
  • ill defined borders
  • tissue invasion
  • metastases
  • anaplastic (undifferentiated)
  • pleomorphic
  • nuclear irregularities
  • fast growth
  • angiogenesis
  • recurrence if removed
  • necrotic areas common
21
Q

What does -oma indicate?

A

benign

22
Q

What does -carcinoma indicate?

A

malignant epithelial cells

23
Q

What does -sarcoma indicate?

A

malignant mesenchymal cells

24
Q

Benign stratified squamous epithelium

A

squamous papilloma

25
Q

squamous papilloma

A

benign stratified squamous epithelium

26
Q

malignant stratified squamous epithelium

A

squamous cell carcinoma

27
Q

Define carcinoma in situ.

A

Atypical squamous cells that have not advanced through basement membrane; Initially identified (incorrectly) as benign

28
Q

benign glandular epithelium

A

adenoma

29
Q

adenoma

A

benign glandular epithelium (gland or duct)

30
Q

malignant glandular epithelium (gland or duct)

A

adenocarcinoma

31
Q

adenocarcinoma

A

malignant glandular epithelium (glad or duct)

32
Q

benign fibrous connective tissue

A

fibroma

33
Q

malignant fibrous connective tissue

A

fibrosarcoma

34
Q

fibrosarcoma

A

malignant fibrous connective tissue

35
Q

Fibroma

A

Benign fibrous connective tissue

36
Q

‘fibr-‘ is indicative of..

A

collagenous

37
Q

‘lip-‘ indicative of…

A

adipose tissue

38
Q

benign adipose tissue

A

lipoma

39
Q

malignant adipose tissue

A

liposarcoma

40
Q

lipoma

A

benign adipose tissue

41
Q

‘chondro-‘ is indicative of…

A

cartilage

42
Q

chondroma

A

benign cartilage

43
Q

benign cartilage

A

chondroma

44
Q

malignant cartilage

A

chondrosarcoma

45
Q

chondrosarcoma

A

malignant cartilage

46
Q

What is ‘osteo-‘ indicative of?

A

bone

47
Q

Which 2 types of benign tumours are grossly similar?

A

chondromas and osteomas; confirm through histology

48
Q

osteoma

A

benign bone

49
Q

benign bone

A

osteoma

50
Q

malignant bone

A

osteosarcoma

51
Q

osteosarcoma

A

malignant bone

52
Q

What is “-myo-“ indicative of?

A

muscle

53
Q

benign muscle

A

myoma

54
Q

malignant muscle

A

myocarcinoma

55
Q

What is ‘neuro-‘ indicative of?

A

neurons

56
Q

benign nerve fibres

A

neuroma

57
Q

neuroma

A

benign nerve fibres

58
Q

malignant neuron

A

neuroblastoma

59
Q

neuroblastoma

A

malignant neuron

60
Q

benign myelin sheath

A

neurofibroma or NEURILEMMOMA

61
Q

neurilemmoma

A

benign myelin sheath

62
Q

malignant myelin sheaths

A

neurilemmal sarcoma

or neurofibrosarcoma

63
Q

benign meninges

A

meningioma

64
Q

meningioma

A

benign meninge

65
Q

malignant meninges

A

meningeal sarcoma

66
Q

malignant bone marrow

A

leukemia

67
Q

leukemia

A

malignant bone marrow

68
Q

melanoma

A

malignant melanocytes

69
Q

lymphoma

A

malignant lymphnodes

70
Q

Is hematoma a neoplasm?

A

NO

71
Q

malignant melanocytes

A

melanoma

72
Q

malignant lymphocytes

A

lymphoma

73
Q

What are the characteristics of ‘precancerous’ alterations to cells (dysplasia)?

A
  • increased size and density
  • REDUCED COLLAGEN
  • IRREGULAR SHAPED NUCLEUS
  • cytoplasmic immaturity
  • irregular cell size
74
Q

What are the shared characteristics of cancer cells?

A
  • Local increase in cell number
  • Loss of arrangement of cells
  • Variation in cell size and shape (pleomorphism)
  • Increased mitosis
75
Q

What indicates abnormal mitosis

A

(various-shaped cells packed together without organization, many undergoing mitosis)
dark black DNA

76
Q

Define transformation.

A

(aka carcinogenesis)

process by which a normal cell becomes a cancer cell

77
Q

What are the 9 diverse behaviours of cancer cells?

A
  1. ANAPLASIA (no differentiation
  2. genetically unstable (due to quick mutations)
  3. grow independent of external growth factors
  4. AUTONOMOUS (no longer communicates with neighbouring cells
  5. loss of contact inhibition and anchorage dependence
  6. Tissue invasion and metastasis
  7. Limitless replication
  8. avoidance of apoptosis
  9. promote ANGIOGENESIS
78
Q

Define angiogenesis.

A

blood vessel formation

79
Q

What is the histological grade?

A

an evaluation of the aggressiveness of the tumour; marks the level of differentiation and number of mitoses (grade 1-4)

80
Q

Define anaplasia.

A

loss of differentiation; marked cellular and nuclear pleomorphism, heavily stained nuclei, and tumour giant cells

81
Q

Medium grade histological grade

A

cells begin to look less typical and change shape

82
Q

High grade histological grade

A

very aggressive, normal cells die off as the compete with cancer cells for nutrients; surrounding ducts and glands are lost

83
Q

Cancer cells become genetically unstable because of…

A

“proof-reading” genome gets deactivated, which allows mutations to accumulate more quickly

84
Q

How does the cell cycle control gene contribute to cancer?

A

cancer cells develop a mutation of the ‘cell cycle control genes’ real easing cells from normal growth constrains

85
Q

Cancer cells divide without _____ or they ____ their own

A

growth factor

produce

86
Q

Define autonomous in regards to cancer.

A

lost much of their contact with surrounding cells (cell to cell communication is lost)

87
Q

Why do cancer cells become autonomous?

A

cadherins are cell membrane molecules that bind adjacent cells

88
Q

What does the loss of density-dependent inhibition do to cancer cells?

A

removes the limits to proliferation

89
Q

When normal epithelial cells detach from neighbouring cells what happens?

A

undergo apoptosis

90
Q

What contributes the cancers limitless replication?

A

telomerase

91
Q

With normal cell divisions what happens?

A

there is non coding DNA is found at the end of each chromosome; each time a cell divides the chromosomal telomere shortens, leading to apoptosis after 50 divisions

92
Q

What does telomerase do?

A

adds DNA back (normally at the ends of stem cells); a mutation in telomerase gene may produce this enzyme in cancer cells

93
Q

How do cancer cells avoid apoptosis?

A

There are many genes responsible for apoptosis so any one having a mutation may prevent self-destruct signals

94
Q

What is angiogenesis?

A

development of new blood vessels

95
Q

What causes angiogenesis in cancer

A

mutation in angiogenic factor may allow cancers to continually produce signals for new blood vessel growth

96
Q

What are the 2 most potent angiogenic factors?

A

FGF- fibroblast growth factor

VEGF- vascular endothelial growth factor

97
Q

What does a mutation of angiogenic factors do to the rate of cancer growth?

A

this would allow cancer to grow faster and spread throughout the body

98
Q

When do tumours become clinically relevant?

A

when they develop a blood supply

99
Q

When are new vessels needed by a tumour?

A

when they consist of 100-300 cells (~2mm)

100
Q

Where are we more likely to get cancer?

A

where cells divide rapidly; epithelial (90%)

101
Q

Which cancer most commonly causes death?

A

lung

102
Q

The most common cancers are dependant on what?

A

hormones

103
Q

What is carcinogenesis?

A

literally means ‘creation of cancer’; multistage process involving genetic damage (mutation) that affect cell cycle

104
Q

All cells with a ____ have access to the same ____

A

nucleus

genes

105
Q

If ____ ____ are blocked then cells will keep _____

A

signalling pathways

dividing

106
Q

What regulates the development, growth, differentiation and death of cells?

A

cell cycle control gene

107
Q

What does the cell cycle control gene do?

A

has growth factors that turn the cells division and proliferation on or off

108
Q

When would a cell be turned on?

A

when there is damage it needs to repair/replace

109
Q

When is a cell turned off?

A

when repair is complete

110
Q

What is responsible for turning cells on and off?

A

cell cycle control genes

111
Q

What 2 main mechanisms are involved with transformation to cancer cells?

A
  1. Proto-oncogene activation

2. Tumor suppressor gene inactivation

112
Q

What do proto-oncogenes activation cause?

A

stimulates inappropriate growth /activity (dominant mutation - needs only one copy of gene mutated)

113
Q

What do tumor suppressor genes inactivation cause?

A

prevents the arrest of the cell cycle (recessive mutation - both copies must be mutated)

114
Q

What are mutated pro to-oncogenes called?

A

oncogenes

115
Q

What are proto-oncogenes responsible for?

A

produce growth factor that control cell size, differentiation and proliferation; typically activate cells to divide

116
Q

What is ras protein?

A
  • found on the inner surface of the plasma membrane of proto-oncogenes
  • ras signals the nucleus when growth receptors are stimulated
  • ras can be mutated to always convey the message to divide
117
Q

What percentage of cancer have the ras gene mutation?

A

30 %

118
Q

Define oncogene.

A

cancer causing gene

119
Q

Ras gets converted to an ______ that tells cells to continually ____

A

oncogene

divide

120
Q

What do tumour suppressor genes do?

A

suppress growth

121
Q

When tumour suppressor genes are inactivated or deleted the…

A

tumour forms

122
Q

What are 3 examples of tumour suppressor genes?

A

p53
retinoblastoma (Rb)
BRCA1

123
Q

What is p53 involved in?

A

involved in producing DNA repair, growth inhibition and APOPTOSIS

124
Q

How does p53 hep with DNA repair?

A
  • helps with normal growth control (which maintains integrity)
  • blocks DNA production until DNA can repair
125
Q

How is p53 activated?

A
  • by DNA damage
126
Q

What is p53’s role in growth inhibition?

A
  • encodes for protein that suppress growth
127
Q

What is p53’s role in apoptosis?

A

induces apoptosis when DNA damage is irreversible

128
Q

What is the prevalence of p53 gene mutations?

A

50% of cancers contain it

129
Q

What happens when p53 gene is mutated?

A
  • loss of DNA repair, growth suppression and apoptotic factors
  • DNA replication and cell division without correction of DNA mutations causing genetic instability and increasing risk of cancer formation
130
Q

What does DNA replication and cell division without correction of DNA mutations cause?

A

causing genetic instability and increasing risk of cancer formation

131
Q

Can cancer develop with one mutation?

A

no, needs multiple.

132
Q

What are some mutations that affect cancer development?

A
  • oncogenes (self sufficient growth signals)

- tumour suppressor (insensitivity to antigrowth signals)

133
Q

What are the hallmarks of cancer?

A
  • self sufficient growth signals
  • insensitivity to antigrowth signals
  • evades apoptosis
  • limitless replication potential
  • sustained angiogenesis
  • tumour invasions and metastasis
  • prevent DNA repair
134
Q

What is tumour heterogeneity?

A

tumours having different kinds of cells

135
Q

Human cancers arise ______

A

sponatneously

136
Q

frequency of mutations can be increased by exposure to _____

A

carcinogens or mutagens

137
Q

Cancer incidences ___ with age.

A

increases

138
Q

What cells are oncogenes inherited from?

A

geminal cells

139
Q

What cells are oncogenes NOT inherited from?

A

somatic cells

140
Q

What is BRCA1/2 known for?

A

mutation in breast cancer

141
Q

____ and ____ effect your changes of getting cancer.

A

genes and environment

142
Q

What accounts for varying cancer rates in different countries?

A

environmental factors

143
Q

Gene environment interactions include…

A
  • tobacco
  • diet
  • alcohol
  • sexual/reproductive behaviour
  • air pollution
  • occupational hazards
  • UV/ionizing radiation
  • hormones
144
Q

Can viruses cause cancer?

A

yes, accounts for 15% of cases

145
Q

What kind of virus would cause cancer?

A

one that integrates into host genome, and carry oncogenes (more provirus)

146
Q

What are some examples of viruses that cause cancer?

A
  • human heroes virus (HHV)
  • Hepatitis B or C (80% of cases with liver cancer)
  • HPV (nearly 100% of cases of cervical cancer)
147
Q

What is relevant in 80% of liver cancer?

A

hepatitis B or C

148
Q

What kinds of cancers can result from human herpes virus (HHV)?

A
  • kaposi’s sarcoma (connective tissue)

- burkitt lymphoma (bcells)

149
Q

What kind of bacteria causes cancer?

A
  • helicobacter plori
  • infects 50% of the worlds population
  • infects stomach- leads to gastric lymphomas and carcinomas
150
Q

How does bacteria cause cancer?

A
  • Formation of carcinogens
  • Alter secretion of cytokines and growth factors
  • Disrupts gastric epithelial cell cycles
  • Generation of free radicals
  • Decrease protective gastric secretions
151
Q

How do cancer cells get from one spot to another?

A
  • local spread by direct invasion (which is the first step in metastasis)
  • malignant cells break through their basement membrane and surround connective tissue
152
Q

What are the mechanisms required for metastasis to occur?

A
  1. Cellular multiplication
  2. Mechanical pressure
  3. Release of lytic enzymes
  4. Decrease cell-to-cell adhesion
  5. Increase motility of tumor cells
153
Q
  1. Cellular multiplication:

Invasion depends on the rate of _____ _____.

A

tumour growth

154
Q

How do you calculate tumour growth?

A

amount of cells replicating - the amount of cells dying= tumour growth

155
Q

What is the mechanism of pressure for metastasis?

A
  • builds up and forces sheets or fingers of tumor cells along paths of least resistance
  • pressure can result in local tissue necrosis making it easier for the tumour to spread
156
Q

What is the lytic enzyme mechanism of metastasis?

A

malignant tumour cells secrete lytic enzymes to breakdown extra cellular matrix (ECM); decreases local pressure allowing tumour to invade local tissues

157
Q

What is the decreased adhesion mechanism of metastasis?

A

cancer cells do not adhere due to lack of or defect in cadherins

158
Q

What are cadherins responsible for?

A

adhesion of neighbouring cells

159
Q

What is the increased motility mechanism of metastasis?

A

secretion of AUTOCRINE MOTILITY FACTOR (AMF) allows tumour cells to stimulate own movement

160
Q

Cancer cells take the path of ____ _______.

A

least resistance

161
Q

How do malignancies spread?

A

move through body cavities, lymph, or blood

162
Q

What is a primary neoplasm?

A

the original neoplasm

163
Q

What is metastasis?

A

a secondary neoplasm; subpopulation that has detached, spread, & formed secondary mass

164
Q

Metastases often resemble the ____ _______ histology.

A

primary neoplasm

165
Q

What are the pathways of metastatic spread?

A
  1. seeding across body cavity
  2. via lymph channels
  3. via blood vessels
166
Q

What is lymphatic spread?

A

metastasis via lymphatic channels

167
Q

What is hematogenous spread?

A

metastasis via blood vessels

168
Q

What is trans-coelomic spread?

A

metastasis seeding across body cavities

169
Q

Where is seeding likely to occur?

A

peritoneal cavity

170
Q

What is a concern when surgically removing a cancer?

A

metastasis via seeding (in body cavities)

171
Q

What is the most common route of metastasis?

A

lymphatics

172
Q

Once metastatic emboli are in the lymph they travel to…

A

regional lymph nodes

173
Q

What happens when cancer cells get lodged in lymph nodes?

A
  • get KILLED (local inflammation or incompatible local environment)
  • become DORMAT
  • detach and enter afferent vessels
  • grow into noticeable lump
174
Q

What do manifestations typically depend on?(slide 41)

A

location and extent of metastasis

175
Q

What are the 9 main manifestations?

A
  • Local Effects
  • Pain
  • Fatigue
  • Cachexia (general weakness)
  • Anemia
  • Leukopenia/ Thrombocytopenia
  • Infection
  • Paraneoplastic Syndromes
176
Q

What is the local effect of cancer?

A
  • ulcerations and necrosis

- when with a serous membrane commonly leads to effusion (excreting fluid or gas)

177
Q

How many terminally ill patients feel pain?

A

60-80%

178
Q

Is there pain in the early stages of cancer?

A

little to none

179
Q

What about cancer causes pain?

A
  • PRESSURE
  • stretching visceral surfaces
  • tissue destruction
  • inflammation
180
Q

Pain can be due to ____ factors, ___ and ____

A

psych factors

infections and necrosis

181
Q

What is the most common symptom of cancer?

A

fatigue not releived by more sleep

182
Q

What may fatigue involve?

A
  • sleep disturbances
  • biochmical changes due to disease or txt
  • nutritional disrution
  • LEVEL OF ACTIVITY
  • psych factors
183
Q

What is cachexia?

A

most severe form of malnutrition associated with cancer

184
Q

What percentage of cancer patients die from cachexia?

A

20%

185
Q

What percent of patients present with cachexia?

A

80%

186
Q

What is involved in cachexia?

A
ANOREXIA 
ANEMIA (low RBC count)
ASTHENIA (weakness)
taste alterations
altered metabolism of nutrients
187
Q

What is the anorexia due to in cachexia?

A

pain, depression, chemo- or radiation-therapy

188
Q

Define emaciation

A

to be come very thin, loss of ~80% of adipose tissue and skeletal muscle

189
Q

Does food decrease with cachexia?

A

food intake may increase

190
Q

Why does the same or decreased fluid intake not effect the decrease in weight of cancer patients?

A

 protein synthesis and protein degradation in some cells (skeletal muscle) – more like patients suffering from sepsis or severe trauma

191
Q

How is cachexia treated?

A

high calorie intake

192
Q

Why do we see anemia in cancer patients?

A
chronic bleeding
severe malnutrition 
medical therapies
impaired production
malignancies of 
  blood-forming 
  tissues
193
Q

How do we treat anemia?

A

EPO- erythropoietin

194
Q

What is leukopenia?

A

decreased WBC’s

195
Q

What is thrombocytopenia?

A

decreased platelets

196
Q

What about cancer causes leukopenia and thrombocytopenia?

A

direct tumor invasion of bone marrow

chemotherapy or radiation of bone marrow

197
Q

Why is infection risk increased when you have cancer?

A
  • decreased WBCs, increased immune function - immunosuppression due to chemo/radiation
  • decreased resistance due to surgery
  • age
198
Q

What are paraneoplastic syndromes

A

When mutations result in PRODUCTION OF HORMONES (such as ADH (leads to SIADH), ACTH (leads to Crushing syndrome)
PTH (leads to hypercalsemia)
- procoagulants (increase venous thrombosis)
- come cause weakness or pigmentation

199
Q

What is preformed to screen for cancer?

A
observation
palpation 
imaging 
histologic sampling
blood tests
200
Q

Cancer generally has a ________ prior to treatment.

A

headstart

201
Q

After how many doublings is the tumour at 1 billion cells and approx 1cm

A

30 doublings

202
Q

After 35 doublings how many cells does the tumour contain?

A

1 trillian

203
Q

What are 6 treatment options for cancer?

A
  1. Surgery
  2. Radiation
  3. Chemotherapy
  4. Hormone Therapy
  5. Immunotherapy
  6. New possibilities on the horizon
204
Q

What roles can surgery play in management of cancer?

A

diagnosis
prognosis
treatment
prevention

205
Q

Surgery to obtain viable neoplasm tissue allows ____ diagnosis and obdservation needed for ___ and ___

A

histologic diagnosis

staging and grading

206
Q

What ways may we retrieve tissue from cancer.

A
  • aspiration biopsy
  • needle (core) biopsy
  • incisional biopsy (remove a piece of tumor)
  • excisional biopsy (remove the entire tumor)
  • endoscope methods
207
Q

Surgery is used for treatment of…

A

solid cancer

(may have necrotic centres and poor vascular supply rendering radiation and chemo less effective

208
Q

How can surgery be used preventatively?

A

to remove congenital some times cancer causing parts of the body

209
Q

What is debulking?

A

(remove as much as possible – increases success of alternate therapies)

210
Q

What is radiation?

A

Utilizes high energy radiation from a variety of sources which can be precisely aimed at neoplastic; without excessive toxixity

211
Q

What kind of rays are caused for radiation?

A

xray and gamma rays

212
Q

How does radiation work?

A

generates free radicals leads to tumour cel death

213
Q

What percentage of cases is radiation useful for?

A

50-60%

214
Q

How many doses are typically used to minimize damage to healthy cells and increase chance cell dividing?

A

30+

215
Q

How is radiation typically used?

A
  • vital or inaccessible areas

- in combination with surgery and or chemo

216
Q

What is the device used in radiation treatment?

A

linear accelerators

217
Q

What is palliative radiotherapy used for?

A
  • painful bone and soft tissue metastases
  • brain metastases
  • malignant spinal cord compression
  • airway obstruction, hemoptysis, ulcerating or bleeding lesions, etc.
218
Q

What percentage of palliative radiotherapy patients notice a significant difference in symptoms

A

60-80%

219
Q

When is chemotherapy used?

A
  • widespread
  • rapidly growing
  • at high risk of micro- metastatic deposits (clinically undetectable)
220
Q

Chemotherapy is a _____ treatment.

A

systemic (effecting the whole body)

221
Q

Chemotherapy is typically done with a combination of drugs because…

A
  • ONE type may NOT BE EFFECTIVE
  • AVOID RESISTANCE
  • allows individual doses to be smaller, which typically produces LESS SIDE EFFECTS
222
Q

What are cytotoxic drugs?

A

they target viral cellular machinery or metabolic pathways required for malignancy

223
Q

Most chemo agents interfere with ____ and _____ of DNA

A

synthesis or function

224
Q

What are cytotoxic drugs more toxic too?

A

proliferating cels

225
Q

What 4 main things does chemo do?

A
  1. prevents vessel growth
  2. stops cels division/replication
  3. causes spontaneous cell death
  4. creates a non-dividing cell by altering cell structre
226
Q

Different chemo drugs stop replication in different ____, making it more effective

A

stages

227
Q

Define therapeutic index.

A

refers to the relative amount of the drug required to kill cancer cells, compared to the dose that is harmful to normal cells

228
Q

Chemo treats proliferating cells, however cells responsible for persistence and growth is often largely in __ ___ ____.

A

cell cycle arrest

229
Q

Cells that are in cell cycle arrest ___ ___ _.

A

stimulate later growth

230
Q

Define first order kinetics.

A

a dose of the drug kills the same percentage of cells are not the same number of cells each time is it given

231
Q

What impact does first order kinetics have on cancer treatment?

A

must use multiple courses of therapy

232
Q

What effect does tumour heterogeneity and chemotherapy have?

A

creates sub-clones making cancer more heterogenous and adapts to host defences making it MORE AGGRESSIVE

233
Q

What are some side effects of chemo and radiation?

A
  • aging
  • discomfort
  • fatigue and anemia
  • risk of infection
    -risk of hemorrhage
  • effect on rapidly dividing cells
    (bone marrow, GI, skin and nails, and reproductive system)
234
Q

What are the GI effects of chemo and radiation?

A
  • ULCERS
  • INFECTION
  • malabsorption
  • diarrhea
  • nausea
235
Q

What are the skin and nail side effects of chemo and radiation?

A
  • alopecia

- dryness

236
Q

What are the reproductive system effects of chemo and radiation?

A
  • decrease number of gametes

- affects indirectly through the hypothalamus

237
Q

How does hormone therapy work?

A

alters hormonal environment through suppression or receptor changes which may slow cancer

238
Q

How does immunotherapy work?

A
  • use bacterial strains locally induce immune response

- or antibodies injected directly (antibodies injected with radioactive isotopes)

239
Q

How do interferons effect tumours?

A

They are
- Anti-proliferative (prevent cell division but prolonging cell cycle, making cells more susceptible to chemo.)
- Pro-apoptotic (initiate cell death pathways)
Immunostimulatic (trigger immune response)
- Anti-angiogenic (stop new blood vessel formation)

240
Q

What are some potentially new cancer therapies?

A
  • block angiogenesis
  • initiate apoptotic pathways
  • virus
241
Q

What are the components responsible for blocking angiogenesis?

A

anti-VEGF compounds to block angiogenesis
- EGFR (epidermal growth factor receptors)- tyosine kinase inhibitors
to block angiogenesis

242
Q

What apoptotic pathways could be initiated for cancer therapy?

A

Gemin X- INITIATES APOPTOSIS regardless of their p53 status

currently in phase 2 of clinical trials under the name obatoclax

243
Q

How can viruses be used as cancer therapy?

A

Viruses are able to infect human cells and replicate, induce cell death, and release viral particles that spread through tissues (self-amplifying dose)
- cancer cells are extremely vulnerable to viral attach

244
Q

Viruses that are extremely sensative to ___ pathwayss of normal cells are able to only effect cancer cells

A

interferon

245
Q

What is the down side to cancer treatment?

A

become immune to the virus