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PATH300 > neoplasia > Flashcards

neoplasia Flashcards

1
Q

/definition of neoplasia

A

new growth

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2
Q

why has the mortality of non-infectious diseases increased? example

A

due to changes in lifestyle and longer life span.
Neoplasia (cancer) is the number one worldwide killer

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3
Q

most common cancer types in children?

A

leukemia and CNs tumors

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4
Q

what cancers have the highest rates in males and females? name the 3 most frequent

A

1: prostate and breast cancers
2: lung & bronchus
3: colon & rectum

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5
Q

% of hereditary contribution of cancer? what contributes the most?

A

5%
lifestyle and environment contributes the most

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6
Q

what % of cancer patients are cured within 5 years?

A

50%

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7
Q

difference between benign and malignant tumors?

A
  • benign: slow growth, not too dangerous, cells aren’t too weird, does not disseminate
  • malignant: grows rapidly, causes death, invades other tissues
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8
Q

explain tumor nomenclature

A

prefix = location (ex: gland = adeno-, hemangio- = blood vessel)
suffix = benign (oma) or malignant (carcinoma)

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9
Q

what is the oddity in tumor nomenclature?

A

teratoma: mixture of different cell types

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10
Q

tumor cells undergo differentiation while trying to mimic what?

A

the structure of their parent organ, but they are a bit abnormal

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11
Q

describe malignant differentiation?

A

malignant tumors have a haphazard arrangement, little resemblance to origin cell (different size and big nucleus), abnormal function, more abnormal mitoses

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12
Q

What are the changes when the cells go from normal to malignant?

A
  • Loss of contact inhibition
  • Increase in growth factor secretion
  • Increase in oncogene expression
  • Loss of tumor suppression genes
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13
Q

when is cancer more easily cured?

A

when it is still at its site of origin (carcinoma in situ)

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14
Q

what is dysplasia?

A

abnormal growth or development of cells, not yet cancer (Indraductal hyperplasia with atypia)

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15
Q

what is an anaplastic tumor?

A

a tumor that is poorly differentiated

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16
Q

6 phases of cancer

A
  1. normal tissue
  2. intraductal hyperplasia
  3. carcinoma in situ
  4. dysplasia
  5. invasive cancer
  6. anaplastic tumor
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17
Q

what can benign tumors cause? give example about neuroendocrine tumors

A

compression and pain.
Neuroendocrine tumors (benign) can release adrenaline, thus making the patients tachycardic and have an increase in blood pressure

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18
Q

what is the main way how a tumor kills?

A

metastasis -> multiple organ failure

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19
Q

name other actions and consequences of malignant tumors

A

destroy tissue -> organ failure
erode blood vessels -> hemorrhage, anemia
obstruct lumen -> intestine, lung
facilitate infection -> local or systemic
cardiac failure -> terminal events

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20
Q

name the 3 systemic effects of a malignant tumor

A
  1. cachexia: total body wasting (massive loss of weight)
  2. paraneoplastic syndromes: biochemical, neurological, hematological derangements (also caused by compounds released by the tumor)
  3. immunosuppression
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21
Q

describe 5 common tumors

A
  1. papilloma: squamous epithelial benign tumor (wart) or carcinoma
  2. adenoma: glandular epithelial benign tumor (polyp) or adenocarcinoma
  3. liposarcoma: malignant connective tissue tumor that has pleomorphic cells with a coarse emulsion lipid / Lipoma: benign tumor where fat cells accumulate in masses
  4. osteogenic sarcoma: highly malignant and produces metastasis early on, malignant bone tumour
  5. myoma/osteoma: muscle and bone benign tumours
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22
Q

how does angiogenesis increases metastasis? how do tumor increase angiogenesis?

A

newly formed vessels are leaky which makes it easier for the tumor to invade them.
tumor secrete angiogenesis factors.

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23
Q

what makes metastasic prognostic worst?

A

increase in the distance of metastase from the original site

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24
Q

how do tumor cells get past basement membrane to invade blood? (steps)

A
  1. Loosening of intracellular junctions
  2. Attachment: Laminin receptors on the tumor bind laminin in the BM
  3. Degradation: cell secretes collagenase to degrade BM and ECM
  4. Migration: fibronectin help invasion of malignant cells
  5. Extravasation: then invades circulation
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25
Q

what often happens in the middle of a tumor

A

necrosis due to lack of oxygen

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26
Q

what surrounds metastatic tumor cells during migration to avoid immune recognition?

A

platelets

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27
Q

how does cancer get in lymphatics?

A

thin wall. cancer cells can increase lymph flow

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28
Q

what blood vessels are most susceptible to invasion?

A

small veins and venules because thin wall

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29
Q

when does retrograde venous spread happen?

A

lymphatic growth of tumors within a vein may cause reversal of blood flow where veins form a rich plexus and don’t have valves

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30
Q

4 main sites of metastasis + 1 extra

A

liver, lung, brain and bones.
also lymph nodes

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31
Q

where to breast and lung cancer tend to metastasise?

A

to the adrenal glands

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32
Q

why is metastasis hard to treat?

A

The properties of the metastasis may be different from the primary tumor; you may be able to treat tumour cells in one location, that will not be an effective treatment for tumour cells in another location

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33
Q

what is TNM system?

A

Tumor, Nodes, Metastasis: Survival is related to each of these features.
4 stages for tumor and nodes states, only 2 stages for metastasis. stage 2 metastasis automatically = stage 4 cancer

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34
Q

the more undifferentiated a tumor is, the ____ the prognosis

A

the worst the prognosis

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35
Q

what is immunohistochemistry used for?

A

allows a better visualization of
certain markers thus helping the prognosis and treatment

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36
Q

what cancer has the #1 death rate in developed world?

A

lung

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37
Q

why does lung cancer take so long to develop?

A

accumulation of sequential mutations in normal cells caused by carcinogens

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38
Q

describe the steps of lung cancer progression

A
  • activation by carcinogens
  • squamous metaplasia: Squamous cells replace normal ciliated epithelial cells in response to irritation & start multiplying
  • mild dysplasia: Cells looking different from normal cells – appearance & characteristics differ
  • moderate dysplasia
  • severe dysplasia: combine with different cells
  • Carcinoma in situ/anaplasia: accumulated enough mutations to have malignancy, still to small to be detected in situ, basal cells start to multiply
  • invasion: cells erode through BM
  • metastasis
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39
Q

basically whats the normal steps of lung/bronchus carcinoma?

A

metaplasia -> dysplasia -> anaplasia (CIS) -> invasion -> metastasis

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40
Q

what are the 4 major subtypes of lung cancers?

A
  1. Squamous cell carcinoma (30% of all lung cancers in the US)
  2. Small cell (oat cell) carcinoma (15% of all lung cancers in the US)
  3. Large cell (undifferentiated) carcinoma (15% of all lung cancers in the US)
  4. Adenocarcinoma (in the glands of the lung) (40% of all lung cancers in the US)
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41
Q

what is special about small cell carcinoma?

A

small cells have different reactions to therapy & higher likeliness of metastasis

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42
Q

where does squamous cell carcinoma originate from? what is a characteristic of it?

A

from basal cells that form squamous cells. often have necrosis in the center

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43
Q

what type of lung cancers form centrally vs peripherally?

A

central = small and squamous cell carcinomas
periphary = large cell carcinoma (usually spreads to lymph nodes)

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44
Q

what are the survival rates of small vs non-small cell lung cancer? and squamous

A

small = low survival rate
non-small = better survival rate. grows very slowly
squamous = grow very slowly

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45
Q

what are the 3 methods of diagnosis for lung cancer?

A
  1. chest X-ray
  2. bronchoscopy: inserting fiber optic tube into main bronchus to observe the airways
  3. cytology of sputum: detect shedded tumor cells
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46
Q

what is staging of lung cancer based on?

A

T location, N number of lymph nodes involved, M metastasis

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47
Q

what is the % of survival depending of stage of detection?

A

stage 1 = 71%
stage 4 = 5%

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48
Q

what are the 4 types of lung resectomy?

A

wedge resection
segment resection
lobectomy
pneumonectomy

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49
Q

are all lung cancers the same?

A

very much not they’re all so different

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50
Q

what is personalized molecular oncology?

A

Study the abnormalities in that patient’s tumor (molecular signature) to be able to effectively choose the most useful therapy for that particular patient

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51
Q

how does immunotherapy work for lung cancer?

A

create a complex hystological analysis of the tumor and the host and choose the right drig

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52
Q

what is an effective treatment for small cell carcinoma?

A

radiotherapy (mostly relieves the symptoms, not a cure)

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53
Q

what is immunotherapy trying to understand?

A

how lung cancer evades immune system

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54
Q

how do we think malignant cells escape immune response?

A

inactivate T cells once they accumulated enough mutations

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55
Q

how to cancer cells inhibit T cell killing?

A

tumor cell has PD-L1 ligand that binds to PD-1 t cell receptor

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56
Q

what is pembrolizumab?

A

anti-PD-1 drug/ab (?) that increased lung cancer survival

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57
Q

what are the local symptoms of lung cancer? what physical symptoms do these local symptoms cause?

A
  • bronchiectasis: expansion of the airway caused by occlusion causing pleural effusion
  • haemoptysis: coughing up of blood filled with malignant cell
  • causes cough, chest pain, shortness of breath, chest infection, hoarseness, weight loss, infection
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58
Q

what is pleural effusion?

A

infection/inflammation cause by obstructive pneumonia

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59
Q

what are the distal symptoms of lung cancer?

A

compounds released by tumor cause:
- metastasis to brain/bone
- abnormal hormone release
- finger clubbing
- cachexia

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60
Q

what can be caused by tumor growth outside of the lung in thoracic cavity?

A
  • Tracheal obstruction.
  • Esophageal compression
  • Hoarseness because of compression on laryngeal nerve.
  • Lymphatic obstruction, pleural effusion.
  • Obstruction of vena cava
  • heart failure
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61
Q

how can lung cancer spread?

A

through circulation, through PLEURAL SPACE,
- lung metastasis usually -> blood, brain, proximal bone, liver (sometimes adrenal gland and spine)

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62
Q

what is the time gap between when you start smoking until when you are dead?

A

20 years (10 years of a cell accumulating mutations, 10 years for it to divide enough to start metastasis)

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63
Q

what happens if many different mutations happen in different cells

A

many different tumors can arise

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64
Q

can you cure lung cancer by stopping smoking?

A

no you can just decrease the risks

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65
Q

what % of lung cancers are due to cigarette smoking?

A

86%

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66
Q

lung cancer risks can arise from what workplaces?

A
  • asbestos can cause lung cancer and mesothelioma cancer and hardening and scarring of lung
  • arsenic, chromium
  • radon (carcinogenic product of uranium)
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67
Q

what is mesothelioma?

A

cancer of the pleural coverings

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68
Q

how does colorectal carcinoma arise?

A

a single cell multiplies and fill the crypt of the large intestine

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69
Q

describe a benign vs malignant colorectal tumor

A

benign = grows into the lumen and forms an adenoma / adenomatous polyp that can be removed
malignat = grows down through intestinal wall causing sub-growth malignant cells

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70
Q

what is the progression of colorectal cancer? how long can the whole process take?

A

Normal colonic epithelia → small adenoma → large adenoma → pre- malignant changes → colorectal carcinoma
- can take 10-15 years

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71
Q

where is colorectal cancer most common?

A

distal part of colon: sigmoid and rectum (easier to detect)
ascending colon (harder to detect)

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72
Q

why is colorectal cancer easier to detect?

A

it has a well-established pathway of mutations including APC (adenomatous polyposis coli) mutations

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73
Q

what is adenomatous polyposis coli?

A

a tumor suppressor gene mutated in colorectal cancer

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74
Q

mutations of APC can come from what 2 origins?

A

inherited or acquired

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75
Q

what is staging of colorectal cancer based on?

A

how far the tumor has penetrated through the intestine wall

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76
Q

what does stage 4 cancer mean for any type of cancer?

A

metastases to other organs

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77
Q

where does intestine carcinoma first spread? where does it go after?

A

liver because all the blood flow draining from the intestines goes to the liver first.
then goes through portal venous system, brain, lungs

78
Q

how is colorectal cancer detected?

A
  • endoscopy! colonoscopy.
  • blood tests can detect carcinoembryonic antigen CEA (tumor marker)
79
Q

what can CEA mostly help detect?

A

resurgence of the tumor because levels go down when tumor is removed and come back up when it comes back

80
Q

what are the symptoms of cancers on the right side (ascending colon) vs left side (descending colon)

A
  • right = bleeding causing anemia, harder to detect, pain, palpable mass
  • left = rectal bleeding, altered bowel habit, pain, tenesmus
81
Q

what is tenesmus?

A

difficulty in defecation

82
Q

does environment or genes cause colorectal cancer? give example

A

90% caused by environment: high fat, low fiber diet, cigarette, IBD, obesity (adipocyte inflammation)

83
Q

what is familial adenomatous polyposis? how can it be cured?

A

Rare hereditary problem found in families: cause development of hundreds of polyps that become malignant.
cured by removing colon

84
Q

how to prevent colorectal cancer?

A

Test for fecal occult blood,
sigmoidoscopy, colonoscopy, aspirin can decrease risks

85
Q

what does cox-2 inhibition do?

A

diminish size and number of colorectal polyps

86
Q

where else in GI tract can cancers arise?

A

esophagus, stomach, pancreas (biggest killer), liver

87
Q

why is pancreatic cancer so tough?

A

can’t remove surgically, detected late, no cure, early metastasis, no effective chemotherapy

88
Q

what are paraneoplastic syndromes?

A

remote effects of a tumor caused by the mediators released from tumor cells

89
Q

example of paraneoplastic syndromes

A

fever, cachexia, endocrine syndromes, neurological impairment, hematological syndromes

90
Q

what are paraneoplastic syndromes of lung cancer?

A

caused by hormones:
- ADH causes hyponatremia
- ACTH causes cushing syndrome
- para T hormone: hypercalcemia
- calcitonin : hypocalcemia
- gonadotropins : gynecomastia

91
Q

when can paraneoplastic syndrome appear?

A

before tumor is even diagnosed from immune response and abnormal antibodies altering ion channels

92
Q

what relieves cachexia?

A

eradication of the tumor

93
Q

what causes cachexia?

A

cytokine release (IL6, IFN gamma, TNF alpha) from the tumour that act on the hypothalamus causing anorexia, on skeletal muscle causing catabolism, on liver causing release of inflammatory proteins and also on adipose tissue

94
Q

differences between starvation and cachexia

A

Protein degradation is very high in cachexia and resting metabolic rate increases in cachexia instead of going down like in starvation

95
Q

what is the probability of having a prostate (men) or breast (women) cancer?

A

1/8 for both (most common cancers)

96
Q

are genes or environment more important for prostate/breat cancer?

A

environment / lifestyle

97
Q

why is obesity the leading lifestyle risk factor?

A

Obesity impairs the response to therapy

98
Q

in what kind of tissue does breast/prostate cancer occur? what does this mean ab treatment?

A

hormone-dependent tissue.
respond to hormone therapy

99
Q

where does breast/prostate cancer metastase?

A

bone, liver, lungs

100
Q

what are symptoms of male breast cancer

A

lumps, nipple discharge, reddening, inversion of the nipple and skin dimplin

101
Q

explain the two major sites of origin of breast cancer

A
  1. ductal origin: from milk ducts. most common
    - carcinoma will become invasive once proliferate beyond the duct’s BM
  2. lobular origin: originates in the milk-producing glands (lobules)
102
Q

how does TNM work for breast cancer?

A

T = tumour size and type
N = nb of lymphatic vessels involved
M = metastasis

103
Q

what is the survival rate is cancer is found in situ?

A

100% five-year survival rate

104
Q

how does histological grading work?

A

Higher the grade = poorer the prognosis
Grade 4 tissue = anaplastic, disorganized

105
Q

what stain is used in immunohistochemistry? what does it detect in breast cancer?

A

H & E stain.
detects lymphatic invasion

106
Q

where do the lymph vessels drain into? what happens during breast cancer removal surgery?

A

in the sentinel lymph node.
be removed by surgery and examined by a pathologist

107
Q

what do estrogen/progesterone receptor say about prognostic of breast cancer?

A

presence of estrogen or progesterone receptors on the tumour leads to a better prognosis because they respond to hormone manipulation

108
Q

what epidermal GF receptor is associated with poor breast cancer prognostic?

A

HER2

109
Q

% of breast lumps that are benign?

A

90%!

110
Q

50% of breast cancers are found where in breast?

A

in the upper outer quadrant

111
Q

what were the main surgeries for breast cancer then vs now?

A

before = mastectomy
now = lumpectomy

112
Q

how is the sentinel lymph node detected?

A

injecting a radioactive tracer at tumor site. it can be removed during surgery.

113
Q

what hormone therapy is used for breast cancer? why is it better than chemo?

A
  • estrogen blocker (ex tamoxifen (antiestrogen drug)). minimal side-effects.
  • estrogen synthesis inhibiter (letrozole): effective for lobular breast cancer
114
Q

what monoclonal ab therapy is used for breast cancer?

A

HER2 (GF receptor) blockers that slow down tumor progression.
can’t cure the patient, just helps.

115
Q

there is a linear correlation between breast cancer death rate and what?

A

dietary fat intake

116
Q

% of genetic breast cancers

A

5%

117
Q

what therapy can cause a little increase in breast cancer risk?

A

Hormonal replacement therapy that is used after menopause

118
Q

how to determine if there is a lump on the prostate?

A

palpation through rectum

119
Q

is prostate cancer always symptomatic?

A

no Many males have slow-growing prostate cancer that is never diagnosed and remain asymptomatic

120
Q

when does age of prostate cancer diagnosis peak?

A

65-70 yo (same for breast cancer btw)

121
Q

what is benign prostatic hyperplasia? is it cancer?

A

enlarged prostate due to an excess number of prostate cells.
not a tumor, nor a risk factor either

122
Q

whats the problem with benign prostatic hyperplasia?

A

compresses the urethra; urine can flow backward.
also wall thickening of the bladder because it contracts more.

123
Q

complications of benign prostatic hyperplasia

A
  • obstructive uropathy
  • bladder hypertrophy
  • trabeculation
  • diverticula formation (bulging out of the bladder)
  • hydroureter
  • stone
  • secondary infection
124
Q

treatment for benign prostatic hyperplasia

A

transurethral prostatectomy/resection

125
Q

what causes prostate cancer

A

successive mutations.

126
Q

what prostate cancer stages have a high survival rate?

A

stage 1, 2, and 3

127
Q

what is Gleason score?

A

score used to characterize prostate cancer.
well-differentiated tissue = 1
non-glandular tissue = 5 (poor prognostic)

128
Q

where does prostate cancer often metastasizes? how?

A

bones: tumor cells enter the pelvic plexus veins which lack valves, making it easier to migrate to the bones

129
Q

symptom of metastasis to the bones

A

intense pain especially in spinal vertebrae

130
Q

what are therapies for prostate cancer?

A
  • early detection: watchful waiting + individualized treatment
  • late detection: surgery, radiation,
  • hormone block
  • chemotherapy, radiation
  • brachytherapy (radioactive implant kills the tumor)
131
Q

what are the hormone therapies for prostate cancer?

A
  • androgen depletion: inhibition of LH signaling to testicles to stop testosterone synthesis
  • androgen biosynthesis: block testosterone synthesis
  • anti-androgens: blocking testosterone receptor
132
Q

in what cases does hormone therapy not work?

A

when the cancer cells develop resistance ?(androgen independent growth)

133
Q

what can cause androgen independent growth?

A
  • AR is bypassed
  • AR mutation
  • AR overexpression
  • Aberrant AR activation/coactivation
134
Q

4 things that cause abnormal AR activation

A
  1. De novo androgenesis: the tumour can synthesize androgen on its own
  2. Overexpression of AR: tumour can respond to minimal amounts of androgen
  3. Non-specific ligand recognition:activated by ligands that are not androgens
  4. Ligand-independent activation: the ligand is no longer needed for the activation
135
Q

where are androgens and estrogen produced?

A

adrenal glands

136
Q

what is abiraterone?

A

enzyme inhibitor drug that blocks androgen and estrogen production

137
Q

what is prostate specific antigen (PSA)?

A

substance secreted by columnar epithelil cells in prostate that helps maintain semen fluidity. useful to monitor therapy

138
Q

what is PSA level of prostate cancer patient?

A

> 10ng/mL (normal level is 4ng/ml)

139
Q

name a few challenges for prostate cancer therapy

A
  • every tumor is different
  • there can be different tumors in same prostate
  • different cells types in each tumor
  • different mutations involved
  • different methylation and acetylation patterns
140
Q

how can we prevent prostate cancer?

A
  • lower fat intake/obesity
  • lower alcohol
  • routine rectal exams
141
Q

when is testicular cancer diagnosed?

A

late teens, early 20s

142
Q

is testicular cancer curable?

A

yes 100% if detected early enough. one of the highest survival rates

143
Q

what therapy is used for testicular cancer?

A

chemotherapy

144
Q

most early tumors are clonal or monoclonal?

A

clonal

145
Q

explain monoclonal vs polyclonal evolution?

A

Monoclonal evolution of a tumor: from one cell
Polyclonal evolution: you get subclones from the tumor

146
Q

what cells in a tumor are always replicating?

A

stem cells

147
Q

what is the max weight a tumor can reach become killing?

A

1kg

148
Q

what really is the problem with lack of contact inhibition?

A

imbalance between production and elimination

149
Q

what does angiogenesis allow the tumor to do?

A
  • grow exponentially
  • escape in circulation (metastasis)
150
Q

how can the immune system recognize and kill tumor cells?

A

if the cells express tumor antigens.
CD8+ T cells mediate killing

151
Q

what immune mediator can help cancer progression?

A

pro-inflammatory cytokines, pro-inflammatory macrophages, Treg cells help tumor growth.
IFN-y, B cells, NK cells, CTL, CD4+ T cells help tumor immunity.

152
Q

tumor escape (?)

A
  • Self-downregulation of activating receptors: Lack of activation to block antibodies
  • Covering of triggering receptor by soluble counter-ligand
  • Loss of MIC-A/B: impaired recognition
  • Soluble FasL synthesis and exocytosis (i.e., trigger apoptosis of T cells)
153
Q

what are examples of immunotherapy?

A

Chimeric monoclonal antibody, radiolabeled monoclonal-Ab, enzyme locally converts product to drug, etc.

154
Q

what is Herceptin used for?

A

to block receptors that are overexpressed in 20% of breast cancer cells (immunotherapy)

155
Q

what does PD-1 do?

A

When PD-1 is bound to another protein called PD-L1, it helps keep T cells from killing other cells, including cancer cells

156
Q

what drugs related to PD-1 can be good?

A

PD-L1 / PD-1 blockers -> allows T cell killing of tumor cell.
used for non-small cell lung cancer

157
Q

name the mutations associated with the morphological appearance:
hyperproliferative epithelium
early adenoma
intermediate adenoma
late adenoma
carcinoma

A
  • mutation of APC on chromosome 5 = hyperproliferative epithelium
  • loss of DNA methylation = early adenoma
  • RAS gene mutation = intermediate adenoma
  • tumor suppressor loss = late adenoma
  • p53 loss = carcinoma
158
Q

the 6 targets of cell proliferation regulation

A
  1. Growth factors
  2. Growth factor receptors
  3. Signal transduction
  4. Transcription factors
  5. Apoptosis
  6. Cell cycle
159
Q

what are the 2 big changes associates with cancers?

A
  1. Oncogenes (GOF mutations)
  2. Tumor suppressor genes
    (LOF mutations)
160
Q

definition of oncogene

A

Oncogenes are abnormal variants of a normal gene that are involved in cell growth

161
Q

what’s a proto-oncogene?

A

A normal (unmutated) gene promoting cell growth

162
Q

what are the 2 ways how oncogenes accelerate cell growth? what mutations are associated with each?

A
  1. creates normal growth-stimulating proteins in excess (translocation, gene amplification, point mutation)
  2. Proteins are hyperactive or resist degradation/limit apoptosis (point mutation,
  3. block immune regulation
163
Q

2 receptors affected by gene amplification that causes greater expression of their respective proteins?

A
  • MYCN (neuroblastoma) and HER2 (breast cancer)
164
Q

what is gene amplification?

A

amplification of a gene resulting in greater expression of their respective proteins

165
Q

give 2 examples of gene translocation

A
  • increase expression of c-MYC leads to an increased expression of pro-growth genes
  • bcr-abl gene translocation (abnormal protein) activates GF signaling pathways
166
Q

what is the most common mutated proto-oncogene in cancer?

A

Ras: a GPCR that leads to signal transduction and cell proliferation

167
Q

name 2 other proliferation mutations

A
  • cyclins overexpression/inactivation of CDK inhibitors (cyclin D/CDK4)
  • blocking apoptosis (Bcl-2, anti-apoptosis protein)
168
Q

what cell cycle modifications lead to cancer?

A

longer or abnormal cell cycle

169
Q

name 3 mutations that alter cell cycle

A
  1. cyclins/CDKs overexpression
  2. CDK inhibitors inactivation
  3. RB inactivation (regulates the transition from the G1 to S phase)
170
Q

what is the mutation associated with chronic myeloid leukemia?

A

Philadelphia gene translocation (9:22) of Bcr-abl tyrosine kinase (causes altered cellular adhesion, abnormal proliferation, apoptosis inhibition)

171
Q

how many copies of tumor suppressor do you need to lose to completely cause problems?

A

both copies

172
Q

what is hereditary retinoblastoma?

A

born with a defective RB gene (tumor suppressor) on chromosome 13

173
Q

what tumor tumor suppressor gene is responsible for colon cancer, nephroblastoma, and retinoblastoma
responsible for their respective diseases?

A

APC (adenomatous polyposis coli)

174
Q

what does RB protein normally control? what does its mutation do?

A

G1 to S transition in cell cycle.
mutation = hyperphopshorylated by CDKs and cyclins

175
Q

what is familial polyposis?

A

born with one defective APC

176
Q

what is the most commonly mutated tumor suppressor gene? what is its function?

A

p53: temporarily stop cell cycle to allow cell damage repair

177
Q

name epigenetic changes and their effect

A
  • hypomethylation: GF or oncogens overexpression
  • hypermethylation: silencing tumor suppressor genes by blocking protein expression
  • acetylation/deactylation
178
Q

what are microRNAs?

A

small RNAs that bind to messenger RNA and block production of the protein coded by the mRNA

179
Q

2 other things that cancer mutations can increase?

A

glucose and glutamine uptake, cell motility

180
Q

what leads to most cases of cervical cancers?

A

human papilloma virus (inactivates RB and p53)

181
Q

4 viruses that cause like 10-15% of cancers worldwide?

A

HepB, HepC, HPV, EBV

182
Q

what is EBV?

A

Epstein Barr virus: causes mononucleosis, can lead to cancer

183
Q

how does radiation cause cancer?

A

creates free radicals / damage DNA

184
Q

what is cryosurgery? what cancer can it be used for?

A

freezing a small site of the tumor. used for liver cancer

185
Q

what is the standard order of therapies used?

A

surgery -> chemo -> radiation -> hormone

186
Q

what are the main cells targetted by chemo side effects?

A

hair, intestinal cells, skin cells

187
Q

what is galeterone?

A

drug that degrades the whole testosterone signaling

188
Q

what are immunotherapy drugs?

A

drugs linked to an antibody

189
Q

what is rituxan>?

A

first monoclonal antibody approved by FDA to treat lymphomas

190
Q

what is GPR78?

A

a protein that manages apoptosis/cell survival balance. inactive under normal circumstance, increased to promote cell survival

191
Q

what is chemoembolization?

A

blocking blood flow to the tumor and preventing spread of the toxic drug

192
Q

is burkitt lymphoma seen in canada? why?

A

NOT SEEN in Canada because we are not exposed to malaria (EBV)

PATH300 (10 decks)

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