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Block 7; Week 1-Michelle > Barsky 1 > Flashcards

Barsky 1 Flashcards

1
Q

What is the progress of a normal cell to a malignant & metastatic cell?

A 
Normal Cell
Transformation Event
Selection Pressure
Tumorigenic
Invasive
Metastatic/Malignant
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2
Q

What are some of the genetic events that are related to tumor progression?

A

mutations
rearrangements
amplifications w/ proto-oncogenes
reduction to homozygosity of tumor suppressor gene deletions or mutations

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3
Q

What is the progression of a normal duct to an invasive ductal cancer?

A 
Normal Duct
Intraductal Hyperplasia
Intraductal hyperplasia with atypic
Intraductal Carcinoma in Situ
Invasive Ductal Cancer
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4
Q

T/F Most cancers are multi hit events, which helps with early detection & screening.

A

True.

This also explains why cancer is a disease of aging.

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5
Q

Why is it difficult for the body to fight cancer, evolutionarily speaking?

A

b/c most cancers occur after the age of procreation

no evolutionary selection pressure that has equipped us to deal with this disease

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6
Q

What are 4 important properties of cancer?

A
  1. uncontrolled growth
  2. invasion & metastasis
  3. clonal dominance-meaning that they all come from one ancestral cell
  4. loss of differentiation
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7
Q

T/F All sub clones are the same.

A

False. There is some heterogeneity amongst the mutant sub clones.

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8
Q

What are the important heterogeneous factors of mutant sub clones?

A 
heterogenous in these ways:
invasiveness
metastatic ability
antigenicity
responsiveness to chemotherapy
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9
Q

What are 5 types of cancer therapy?

A
  1. surgery
  2. radiotherapy
  3. chemotherapy
  4. immunotherapy
  5. gene therapy
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10
Q

What are 3 important limitations in treating cancer?

A
  1. lack of tumor specific antigen
  2. tumor cell heterogeneity
  3. micrometastasis
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11
Q

What are the causes of human cancer?

A 
ENVIRONMENTAL CARCINOGENS
UV RADIATION
OTHER IONIZING RADIATION
VIRUSES
LIFESTYLE, DIET, IMMUNE STATUS
HEREDITARY FACTORS OR GENES
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12
Q

Describe some of the actions of uv radiation in contributing to cancer?

A

ACTION IS SIMILAR TO CHEMICAL CARCINOGENS - FORMATION OF DNA ADDUCTS
ACTION IS CAN BE DIFFERENT FROM CHEMICAL CARCINOGENS: SINGLE AND DOUBLE STRAND DNA BREAKS

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13
Q

Give 3 examples of oncogenic viruses.

A
  1. HPV
  2. EBV
  3. Hep B virus
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14
Q

How many types of HPV are there? Which are responsible for papillomas or warts?

A

80+ types

Papillomas & Warts: 1, 2, 4, 7

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15
Q

Which types of HPV are responsible for invasive squamous cell carcinoma of the cervix?

A

Types 16 & 18

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16
Q

What’s the deal with HPV types 6 & 11?

A

low malignant potential

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17
Q

What are the early products of HPV (bad types) that inactivate tumor suppressor genes?

A

Gene products E6 & 7

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18
Q

What are the tumor suppressor genes that are inactivated by E6 & E7?

A

TP53 & RB

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19
Q

What are the 4 types of tumors that are associated with Epstein Barr Virus?

A

Burkitt’s Lymphoma
B cell lymphoma (if immunosuppressed)
Hodgkin’s Disease
Nasopharyngeal Cancer

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20
Q

What percentage of people have EBV in non endemic areas?

A

20%

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21
Q

What happens with Burkitt’s Lymphoma? Which gene is associated with this?

A

cell proliferation with decreased immunoregulation

MYC gene t(8:14)

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22
Q

Where is nasopharyngeal cancer endemic?

A

south china

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23
Q

What are some examples of lifestyle factors that contribute to the formation of cancers?

A

People who are sun worshippers, go to
tanning salons,etc have a high incidence of
skin cancer
Women who have multiple sexual partners have a higher risk of cervical cancer.
Women who are nulliparous have a high rate of breast cancer
Men who are obese have a higher rate of cancer of the esophagus

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24
Q

What are some diet factors that contribute to cancer?

A

Women who eat fatty foods have a higher rate of breast cancer
Men who drink alcohol and smoke have a higher rate of head and neck cancer
People who eat red meat may have a higher incidence of colon cancer.

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25
Q

Is there ever a hereditary component to cancer?

A

sometimes

Some cancers are inherited (germline) with gene identified
Some cancers are familial with genes not identified
Many cancer have a familial component; fewer cancers have a inherited component

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26
Q

In Li Frameuni Syndrome, what is the contributing inherited gene?

A

p53

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27
Q

In Breast Cancer, what are the contributing inherited genes?

A

BRCA1 & BRCA2

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28
Q

In Lynch syndrome, what are the contributing genes?

A

microsatellite instability genes

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29
Q

T/F Inherited retinoblastoma gene can play a factor in cancer.

A

True.

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30
Q

What is the cause of most cancers?

A

Most cancers are spontaneous, sporadic. Their cause is unknown.

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31
Q

What are the 2 key properties of cancers?

A

Uncontrolled Growth

Invasion & Metastasis

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32
Q

What do oncogenes code for?

A

oncoproteins that are associated with neoplastic transformation
not regulated by normal growth factors & signals

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33
Q

What are protooncogenes?

A

normal genes that affect growth & differentiation
retroviruses can mess with these: create v-onc
can also change in situ to c-oncs.

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34
Q

Cancer comes from what greek word?

A

karkinos
this means crab
**based on how cancers look like the crab on the sign of the zodiac, as it infiltrates neighboring tissues

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35
Q

What is the cancer with the highest incidence in men, as of 2012?

A

prostate cancer

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36
Q

What is the cancer with the highest incidence in females, as of 2012?

A

breast cancer

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37
Q

What are the cancers with the 2nd & 3rd highest incidences for both men & women?

A

2nd: lung & bronchus
3rd: colon & rectum

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38
Q

What is the cancer that causes the most death for both men & women?

A

lung cancer

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39
Q

99% of all cancers are sarcomas/carcinomas.

A

carcinomas! develop from epithelial cells

1% are sarcomas–cancers of the stroma, mesenchyme

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40
Q

T/F The reason that carcinomas are so common is that epithelial cells have the highest rate of turnover.

A

False. If this were the case, then a neonate would get a bunch of cancer. But cancer is a disease of aging.
Another theory is that epithelium is exposed to the external environment-but this is only a part of the picture.

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41
Q

What has happened to lung cancer incidence since the 1930s? What can this be attributed to?

A

it increased rapidly after 1930 & peaked around the 1990s. then it began to decline
this is explained by the rise in smoking + a period of latency. Mainly following a certain degree of smoking cessation–the incidence decreased

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42
Q

What has happened to the rates of gastric cancer since 1930s?

A

it has steadily decreased
one theory is refrigeration, no longer used a carcinogenic substance to keep food fresh
**but people don’t really know

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43
Q

What has happened to the incidence of colorectal cancer & prostate cancer? What could explain this?

A

they have both steadily decreased
prostate peaked around the 1990s and has def decreased since then.
Thought is: PSA & colonoscopies have been successful screening tools.

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44
Q

What has happened to the rates of pancreas cancer, liver cancer, and leukemia since 1930?

A

they have stayed roughly the same!

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45
Q

Breast cancer deaths have steadily decreased since 1930…name 2 factors that may account for this.

A
  1. mammogram screening in post-menopausal women.

2. less hormone replacement therapy

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46
Q

When did lung cancer deaths start to increase for men? For women?

A

For men, after WWI

For women, after WWII. Esp in the 1990s, b/c of latency & peak in women smoking in the 1970s.

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47
Q

Why have cervical cancer deaths decreased since 1930?

A

b/c of the increase in pap smear screenings. but also an unknown factor!

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48
Q

T/F There were serious epidemics of prostate cancer in men & breast cancer in women in the 1990s.

A

False. There was the initiation of PSA & mammogram screenings. Thus, a bunch were detected. Artificial trend.

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49
Q

When should women receive the HPV test?

A

not until their 30s. Has a different significance than for women in their 20s.

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50
Q

Should women who are at a child-bearing age have a mammogram done?

A

probably not b/c their breasts are so dense that it won’t necessarily detect things well
also–it will just expose them to radiation–could cause cancer!

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51
Q

A while back we talked about the possible genetic factors involved in cancer. List some of the epigenetic factors.

A

methylation status for promoter
histone deacetylase status for promoter
**regulate expression of certain cancer genes
Cancer is characterized by a methylation v. histone deacetylation imbalance.

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52
Q

A while back we talked about the stages to go from a normal duct to an invasive ductal cancer. At the stage of intraductal carcinoma in situ…what’s the deal with the positions of the cancer cells?

A

they are confined within the duct

**at the stage of invasive ductal cancer…they have burst thru the basement membrane & invaded.

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53
Q

How long could the process take to get from a normal duct to an invasive ductal cancer?

A

could take up to 12 years b/c it is a multi hit phenomenon.

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54
Q

Does a pap smear detect dysplasia or invasion?

A

detects dysplasia, hopefully before invasion
allows for early detection & treatment
can surgically remove

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55
Q

What are some of the steps involved in an invasive carcinoma?

A

stromal dissolution
basement membrane dissolution
lymphatic invasion
blood vascular invasion

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56
Q

T/F Due to the concept of monoclonal dominance, all cancer cells are the same.

A

False. Like identical twins, cells that come from the same ancestral cell still develop to have different characteristics. Develops thru genetic instability

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57
Q

What are some of the ways that we can see that cancer cells with different characteristics all came from the same ancestral cell?

A

x inactivation
male repeat sequence
microsatellites
**eventually get a picture that we have clones with different features, not cancerous cells from different parents.

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58
Q

Why do we not have a tumor specific antigen that we can use to treat cancer?

A

b/c it is a cancer of our own cells! they look like self

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59
Q

Why does tumor cell heterogeneity make it difficult to treat cancer?

A

b/c the different cancer cells will respond to different treatments.

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60
Q

What’s the deal with micro metastasis in breast cancer?

A

most patients who come to the clinic with a breast mass have already experienced micro metastasis. Unfortunately, only takes a few tumor cells to cause that metastasis.

61
Q

What are some environmental factors that affect cancer rates?

A

chemical carcinogens (direct & indirect)
electrophiles
initiator & promoter
Phase I & Phase II enzymes

62
Q

What makes a chemical carcinogen direct v. indirect?

A

depends on whether it is activated by the body’s cyt p450 or not

63
Q

What is an electrophile?

A

this is something that is neg. charged & binds to DNA’s pos charges.
Ex: initiators are electrophiles

64
Q

What is an initiator?

A

an electrophile that binds DNA & forms a DNA adduct & subsequent mutation.

65
Q

What is the promoter?

A

this is an epigenetic factor that increases cell division after the initiator creates a DNA adduct. It accelerates the response.
If it weren’t for the promoter–the mutation caused by the initiator would die with that cell.

66
Q

What is a DNA adduct?

A

carcinogen + DNA

67
Q

What happens after a DNA adduct is formed?

A

the body tries to remove it by repair mechanisms
if the body’s efforts are unsuccessful then you get a mutation.
if it is in a key gene like an oncogene or tumor suppressor gene–sets cancer into motion with the help of the promoter.

68
Q

What are some things that ionizing & UV radiation can cause?

A

chromosome breakage
translocations
point mutations

69
Q

What can UV radiation lead to?

A

skin cancer

those with xeroderma pigmentosum are at crazy high risk for basal cell carcinomas b/c of a lack of a certain enzyme

70
Q

9% of children who are exposed to significant radiation develop what?

A

thyroid cancer

71
Q

What are some examples of the cancerous & damaging effects of radiation?

A

Hiroshima & Nagasaki

Nevada’s above ground nuclear testing in the 1950s @ area 51

72
Q

Hep B virus puts you at higher risk for which form of cancer?

A

hepatocellular cancer, although this is probably multifactorial

73
Q

What is attributable risk?

A

% of people with the cancer due to a certain factor

74
Q

What is an example of a cancer with a high attributable risk to one factor in the US?

A

smoking–lung cancer.

90% of lung cancers are due to smoking.

75
Q

Which area of the world has a 99% attributable risk of hepatocellular cancer due to Hep B virus?

A

Asian countries

76
Q

What does the Hep B virus do roughly to cause hepatocellular cancer?

A

it makes a protein that disrupts growth control by activating pro to-oncogenes
may also inactivate p53

77
Q

What events in a liver’s life can predispose it to mutations by environmental agents?

A

injury & regeneration

78
Q

Why might it be that men who are obese have higher rates of esophagus cancer?

A

perhaps b/c gastroesophageal reflux can lead to barrette’s metaplasia. Risk factor for carcinoma of the esophagus.

79
Q

A relative risk factor > ___ can suggest that a factor is causative, rather than correlative

A

Greater than 4!

Usu need a double blind prospective randomized study to control all of the random variables & determine causality.

80
Q

Does it take 1 allele mutation or 2 allele mutations to cause the activation of proto-oncogenes to oncogenes?

A

only 1 allele needs to be mutated

81
Q

Where are 3 ways that protooncogenes can be activated into oncogenes? Give examples.

A
  1. Point mutations
    Ex: RAS is an oncogene that is formed this way
  2. chromosomal translocation
    **something moved near the promoter or something gives a chimeric gene product
  3. Gene amplification
    Ex: N-MYC in neuroblastoma
    Her-2-neu in breast carcinoma
82
Q

What are the 5 basic categories of oncogenes? What do they all have in common?

A
  • *all are related to growth
    1. Growth factors
    2. Growth Factor Receptors
    3. Signal Transducing Proteins
    4. Nuclear Transcription Factors
    5. Cyclins & cyclin dependent kinases
83
Q

What is the different b/w oncogenes & antioncogenes? How many mutant alleles are required to form cancer w/ antioncogenes?

A

**need 2 antioncogene mutations to cause cancer

antioncogenes are inactivated cancer suppressor genes

84
Q

Which is an example of gain of fcn & which is an example of loss of fcn?
Oncogenes
Antioncogenes

A

oncogenes: gain of fcn
antioncogenes: loss of fcn

85
Q

What are 4 categories of awesome cancer suppressor genes that can be inactivated forming antioncogenes?

A
  1. Growth inhibitory factors
  2. molecules that regulate cell adhesion
  3. molecules that regulate signal transduction
  4. molecules that regulate nuclear transcription & cell cycle
86
Q

TP53 is called what? What is it?

A

Called the guardian of the genome
**commonly mutated gene in almost all cancers
it has fcns of anti proliferation & apoptosis

87
Q

In more detail, describe what p53 does.

A

p53 senses DNA damage & arrests the cell in G1. It induces DNA repair

  • *increases CDK1 p21 (preventing phosphorylation of RB)
  • *induces GADD45 (to aid DNA repair)
88
Q

What does p53 do if DNA can’t be repaired?

A

apoptosis is induced! Via genes like BAX that are induced

89
Q

WHat’s the deal with Li Fraumeni syndrome?

A

inherit one mutant p43 or RB
you have increased risk of multiple types of cancers
but you need the second hit to get that cancer!
**oddly can be inactivated by certain DNA viruses (oncogenic HPV, HBV, EBV)

90
Q

What is the retinoblastoma gene? WHat is it associated with? What percentage of the people with the RB gene inherit it v. get it sporadically?

A

tumor suppressor gene
associated with childhood tumor retinoblastoma & other types of cancer, like osteosarcoma
40% familial
60% sporadic

91
Q

Is the RB gene (inherited form) aut rec or aut dom?

A

autosomal dominant!

92
Q

So…you have the RB gene–do you automatically have cancer?

A

NO!! 2 hit hypothesis
if you inherit it or get it sporadically to 1 allele–that is 1 hit.
Still need environmental second hit.

93
Q

Why is her-2-neu called that?

A

neu-for neuroblastoma, found in rats

her-family of receptors

94
Q

What is the definition of cancer invasion?

A

active migration of neoplastic cells out of their tissue of origin & across host tissue boundaries
Ex: carcinoma cells thru the basement membrane & into adjacent CT

95
Q

What is the definition of metastasis?

A

a secondary tumor colony discontinuous from the primary tumor
arising from a tumor cell translocated from the primary tumor

96
Q

T/F Invasion is synonymous with metastasis.

A

False. You need invasion to get metastasis. But you just b/c you have invasion doesn’t necessarily mean that you have metastasis.

97
Q

Why is it difficult to differentiate b/w a malignant & a benign sarcoma?

A

sarcomas are tumors of the mesenchyme. Difficult to tell if it has invaded & is malignant b/c there is no basement membrane.

98
Q

Sarcomas tend to invade blood vessels/lymphatics.

Carcinomas tend to invade blood vessels/lymphatics, but can invade either.

A

Sarcomas tend to invade blood vessels.

Carcinomas tend to invade lymphatics.

99
Q

What are the 3 routes that malignant neoplasms tend to spread thru?

A
  1. lymphatics
  2. blood vessels–usu affect lung, liver, brain, bone marrow, adrenals
  3. transcoelomic spread-seeding of body cavities–peritoneal, pleural, pericardial & subarachnoid space
100
Q

Why is it important to grade & stage a cancer?

A

it is vital in estimating aggressiveness & planning therapy

101
Q

What is grading? What are the different grades?

A 
this is done thru microscopy
I--IV
I is good--well differentiated.
II--moderately differentiated
III--poorly differentiated
IV is bad--undifferentiated. cancer that is highly proliferative
102
Q

Describe the staging of a tumor.

A

anatomic extent of the tumor.
TNM (tumor, lymph node, metastases)
AJC

103
Q

What’s the deal with staging the T in TNM?

A 
this is size of the tumor
For breast cancer (different for every cancer):
T1: less than 2 cm
T2: 2-5 cm
T3: greater than 5 cm
104
Q

What’s the deal with staging the N in TNM?

A

Are there lymph nodes involved?
N0: zero nodes
N1: 1-3 lymph nodes involved
N2: more than 3 lymph nodes involved

105
Q

What’s the deal with staging the M in TNM?

A

metastases

if they aren’t overt–M0

106
Q

Can you get a carcinoma that is N0 but M3?

A

Yes, if it chooses to spread via the blood vessels

107
Q

Describe some of the things that must happen in order to get tumor cell dissemination.

A
  1. cells must become less cohesive.
  2. attachment to matrix components must be lessened (like less laminin & fibronectin attachment)
  3. degradation of ECM via metalloproteinases, collagenases, plasmin
  4. migration–done via cytokines & cleavage products of ECM
108
Q

What happens when you get vascular dissemination of tumor cells?

A

they can form emboli with leukocytes & platelets or circulate as single cells
**their end home depends on vascular & lymphatic drainage, tumor adhesion molecules, microenvironment with proteases etc.

109
Q

What is the soil seed hypothesis of Paget?

A

certain cancers like to go to certain parts of the body
Breast cancer–lung
Colon cancer–liver
Lung cancer–brain
**kidney & spleen resistant to metastasis

110
Q

Is systemic metastasis an early event? What is the role of CTCs & DTCs in metastasis?

A

Yes, it is an early event.
CTCs: circulating tumor cells…these are found in the blood & carry the metastatic cells.
DTCs: disseminated tumor cells…these are about to end in an organ (were at one point CTCs).
However, DTC is not synonymous with metastasis.

111
Q

When is DTC indicative of an impending full blown metastasis?

A

it is indicative when there are stem cells present that will cause proliferation after dormancy.

112
Q

When is DTC not indicative of an impending metastasis?

A

when there aren’t stem cells in the DTCs.

113
Q

At an early stage of breast cancer, T1…what is the percentage of women that have CTC or DTC? how can you test for each?

A

33%!
Test for CTC w/ a blood sample.
Test for DTC w/ a bone marrow biopsy.

114
Q

Give an example when doctors are really thankful for CTCs.

A

There has been metastasis, but the metastatic site is difficult to access.
Just draw some blood & test it for chemosensitivity.

115
Q

What are cancer stem cells?

A

a small fraction of cancer cells 1/10 of 1% that are dormant & resistant to cancer treatments. these are the cells that are responsible for growing a tumor back after a period of remission.

116
Q

T/F Every cancer cell is capable of repopulating a tumor.

A

False. Only the stem cells.

117
Q

What are the different types of stem cells?

A

Embryonic Stem Cells
Induced Pluripotent Stem cells (adult ones that are transacted)
Adult Somatic Stem cells (liver)
Stem cells involved in tissue homeostasis
Cancer stem cells

118
Q

What are the common characteristics of all stem cells?

A

self renewal–make a new one of yourself, symmetrical division
asymmetrical division–making a new proliferating terminally differentiated cell
pluripotency–can be a part of all 3 germ line cell types–ectoderm, mesoderm, endoderm.

119
Q

What are 4 important properties of cancer stem cells?

A

exist in a dormant state
resist chemotherapy & radiotherapy
express embryonic stem cell pathways
replenish the dividing cell pop. of a tumor

120
Q 
Hedgehog
Notch
Bmi-1
Wnt
Pten
What are these?
A

these are all embryological stem cell pathways that are activated in cancer
they are activated in cancer stem cells

121
Q

What are some cell markers that indicate–I’m a stem cell who will regrow a breast cancer tumor!

A

CD44+, CD24-

122
Q

What happens if a patient takes a drug that kills cancer cells, but not cancer stem cells?

A

the tumor regresses

the stem cells regenerate the tumor cells again, in time!

123
Q

What happens if a patient is given a drug that kills the cancer stem cells?

A

even if the other cancer cells weren’t killed–>the tumor loses its ability to regenerate & it will eventually degenerate.
Note: this is the goal!

124
Q

If you have a tumor that is only cancer cells, no stem cells…what is the result?

A

No metastasis.

125
Q

If you have a tumor that has cancer stem cells with only partial malignant potential…what is the result?

A

Dormancy followed by metastasis after many years & exposure to multiple oncogenic hits.

126
Q

If you have a tumor that has cancer stem cells with full malignant potential…what is the result?

A

metastasis in months to a couple of years.

& metastases to other sites too!

127
Q

T/F Tumor remission & response rates have little correlation with overall survival.

A

True. B/c of those awful cancer stem cells.

128
Q

What are tumor markers?

A

any gene or gene product that is altered in tumor progression

  • *tumors shed or secrete gene products
  • *source can be tissue, cytology, fluid, or serum
129
Q

What are the 4 categories of biomarkers?

A

Tumor Markers
Prognostic Markers
Surrogate End Point Markers
Predictive Markers

130
Q

What is a paraneoplastic syndrome?

A

these are symptoms experienced by cancer patients that are due to humoral factors secreted by cancer cells, rather than by the presence of the tumor in its surrounding tissue.

131
Q

What % of cancer patients experience paraneoplastic syndrome?

A

10-15%

sometimes the first sign of malignancy

132
Q

What are some initial examples of cancers that produce paraneoplastic syndromes?

A

small cell lung cancer
SIADH
Eaton-Lambert Syndrome
Cerebellar Ataxia

133
Q

Pancreatic, Lung, and other cancers…what end result do these cancers achieve terms of symptoms of paraneoplastic syndrome?

A

venous thrombosis–trousseu’s phenomenon

134
Q

small cell cancer of the lung, pancreatic cancer, neural tumors…what do these cancers release? What is the end result in terms of symptoms of paraneoplastic syndrome?

A

Symptoms: Cushing’s syndrome
Mediator: ACTH or ACTHish thing

135
Q

Breast, renal, and squamous cell cancers cause the release of what? What paraneoplastic syndrome does this create?

A

cause the release of PTHrP & TGFalpha

Get hypercalcemia

136
Q

Cancer of the lung can cause what paraneoplastic syndrome?

A

hypertrophic osteoarthropathy

clubbing of fingers

137
Q

What is cachexia?

A

weight loss etc in a person who is not trying to lose weight!!
includes: weight loss, weakness, anorexia, anemia

138
Q

What causes cachexia?

A

many factors
increased metabolic rate despite reduced caloric intake
may be due to TNF alpha & other cytokines

139
Q

Certain cancers can be detected by certain tumor markers. Give some examples.

A

PSA-prostate cancer
CEA–lung cancer & colon cancer
alpha fetoprotein
**can be used for staging & for therapy

140
Q

What are prognostic markers?

A

these give us info about prognosis, such as disease-free survival, overall survival, length of latency

141
Q

Give some examples of prognostic markers in breast cancer.

A

ER (estrogen receptor): ER+ do better than ER-

Ki-67

142
Q

Give some examples of prognostic markers in colon cancer & prostate cancer.

A

Colon cancer: microsatellite instability gene products

Prostate Cancer: p21 & p27

143
Q

Give a prognostic marker for bladder cancer.

A

Bladder Cancer: p53

144
Q

What are surrogate end point markers?

A

aka intermediate markers

give info about effectiveness & chemopreventive or therapeutic strategy before direct tumoral measurements.

145
Q

Give 2 examples of surrogate end point markers.

A

Minimal residual diseases of the head & neck: mTOR pathway

Bladder Cancer: FvG-actin

146
Q

How could SEMs help drug development?

A

So…have to wait like 15 years to see if a drug helps with a certain type of cancer. These trials are crazy expensive. Sometimes effective therapies on a certain type of person look ineffective in general pop. SEMs will help with immediate feedback for trials.

147
Q

What will predictive markers help with?

A

personalized medicine

match treatment with patients biomarkers.

148
Q

What is an example of a successful predictive marker test for cancer treatments?

A

Hercep Test for her2 screening.
figure out who will respond to herceptin.
**important to have predictive markers b/c it can look like a drug is ineffective, but really it is only effective on certain types of patients.

149
Q

What are some high throughput approaches that could help in the discovery of more biomarkers?

A 
cDNA microarrays
proteomics
array CGH
sequencing
tissue microarrays

Block 7; Week 1-Michelle (7 decks)

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